A species of POLYOMAVIRUS, originally isolated from the brain of a patient with progressive multifocal leukoencephalopathy. The patient's initials J.C. gave the virus its name. Infection is not accompanied by any apparent illness but serious demyelinating disease can appear later, probably following reactivation of latent virus.
An opportunistic viral infection of the central nervous system associated with conditions that impair cell-mediated immunity (e.g., ACQUIRED IMMUNODEFICIENCY SYNDROME and other IMMUNOLOGIC DEFICIENCY SYNDROMES; HEMATOLOGIC NEOPLASMS; IMMUNOSUPPRESSION; and COLLAGEN DISEASES). The causative organism is JC Polyomavirus (JC VIRUS) which primarily affects oligodendrocytes, resulting in multiple areas of demyelination. Clinical manifestations include DEMENTIA; ATAXIA; visual disturbances; and other focal neurologic deficits, generally progressing to a vegetative state within 6 months. (From Joynt, Clinical Neurology, 1996, Ch26, pp36-7)
A species of POLYOMAVIRUS apparently infecting over 90% of children but not clearly associated with any clinical illness in childhood. The virus remains latent in the body throughout life and can be reactivated under certain circumstances.
Infections with POLYOMAVIRUS, which are often cultured from the urine of kidney transplant patients. Excretion of BK VIRUS is associated with ureteral strictures and CYSTITIS, and that of JC VIRUS with progressive multifocal leukoencephalopathy (LEUKOENCEPHALOPATHY, PROGRESSIVE MULTIFOCAL).
Infections produced by oncogenic viruses. The infections caused by DNA viruses are less numerous but more diverse than those caused by the RNA oncogenic viruses.
A genus of potentially oncogenic viruses of the family POLYOMAVIRIDAE. These viruses are normally present in their natural hosts as latent infections. The virus is oncogenic in hosts different from the species of origin.
Viruses whose genetic material is RNA.
A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.
Those proteins recognized by antibodies from serum of animals bearing tumors induced by viruses; these proteins are presumably coded for by the nucleic acids of the same viruses that caused the neoplastic transformation.
Deoxyribonucleic acid that makes up the genetic material of viruses.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
The type species of ORTHOPOXVIRUS, related to COWPOX VIRUS, but whose true origin is unknown. It has been used as a live vaccine against SMALLPOX. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of VACCINIA VIRUS.
Specific molecular components of the cell capable of recognizing and interacting with a virus, and which, after binding it, are capable of generating some signal that initiates the chain of events leading to the biological response.
Process of growing viruses in live animals, plants, or cultured cells.
The expelling of virus particles from the body. Important routes include the respiratory tract, genital tract, and intestinal tract. Virus shedding is an important means of vertical transmission (INFECTIOUS DISEASE TRANSMISSION, VERTICAL).
The mechanism by which latent viruses, such as genetically transmitted tumor viruses (PROVIRUSES) or PROPHAGES of lysogenic bacteria, are induced to replicate and then released as infectious viruses. It may be effected by various endogenous and exogenous stimuli, including B-cell LIPOPOLYSACCHARIDES, glucocorticoid hormones, halogenated pyrimidines, IONIZING RADIATION, ultraviolet light, and superinfecting viruses.
A general term for diseases produced by viruses.
Polyomavirus antigens which cause infection and cellular transformation. The large T antigen is necessary for the initiation of viral DNA synthesis, repression of transcription of the early region and is responsible in conjunction with the middle T antigen for the transformation of primary cells. Small T antigen is necessary for the completion of the productive infection cycle.
The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.
A family of small, non-enveloped DNA viruses, infecting mainly MAMMALS, and containing a single genus: POLYOMAVIRUS.
The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.
Viruses parasitic on plants higher than bacteria.
The functional hereditary units of VIRUSES.
Viruses whose nucleic acid is DNA.
Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.
Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. Some are host-dependent defectives, meaning they can replicate only in cell systems which provide the particular genetic function which they lack. Others, called SATELLITE VIRUSES, are able to replicate only when their genetic defect is complemented by a helper virus.
The type species of ALPHAVIRUS normally transmitted to birds by CULEX mosquitoes in Egypt, South Africa, India, Malaya, the Philippines, and Australia. It may be associated with fever in humans. Serotypes (differing by less than 17% in nucleotide sequence) include Babanki, Kyzylagach, and Ockelbo viruses.
The type species of MORBILLIVIRUS and the cause of the highly infectious human disease MEASLES, which affects mostly children.
A subtype of INFLUENZA A VIRUS with the surface proteins hemagglutinin 1 and neuraminidase 1. The H1N1 subtype was responsible for the Spanish flu pandemic of 1918.
Proteins that form the CAPSID of VIRUSES.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Substances elaborated by viruses that have antigenic activity.
The type species of LYSSAVIRUS causing rabies in humans and other animals. Transmission is mostly by animal bites through saliva. The virus is neurotropic multiplying in neurons and myotubes of vertebrates.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 5 and neuraminidase 1. The H5N1 subtype, frequently referred to as the bird flu virus, is endemic in wild birds and very contagious among both domestic (POULTRY) and wild birds. It does not usually infect humans, but some cases have been reported.
Proteins found in any species of virus.
Transcription factors that were originally identified as site-specific DNA-binding proteins essential for DNA REPLICATION by ADENOVIRUSES. They play important roles in MAMMARY GLAND function and development.
Ribonucleic acid that makes up the genetic material of viruses.
The ability of a pathogenic virus to lie dormant within a cell (latent infection). In eukaryotes, subsequent activation and viral replication is thought to be caused by extracellular stimulation of cellular transcription factors. Latency in bacteriophage is maintained by the expression of virally encoded repressors.
A broad category of viral proteins that play indirect roles in the biological processes and activities of viruses. Included here are proteins that either regulate the expression of viral genes or are involved in modifying host cell functions. Many of the proteins in this category serve multiple functions.
Established cell cultures that have the potential to propagate indefinitely.
A subtype of INFLUENZA A VIRUS comprised of the surface proteins hemagglutinin 3 and neuraminidase 2. The H3N2 subtype was responsible for the Hong Kong flu pandemic of 1968.
The type species of the genus ORTHOHEPADNAVIRUS which causes human HEPATITIS B and is also apparently a causal agent in human HEPATOCELLULAR CARCINOMA. The Dane particle is an intact hepatitis virion, named after its discoverer. Non-infectious spherical and tubular particles are also seen in the serum.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
A species of FLAVIVIRUS, one of the Japanese encephalitis virus group (ENCEPHALITIS VIRUSES, JAPANESE). It can infect birds and mammals. In humans, it is seen most frequently in Africa, Asia, and Europe presenting as a silent infection or undifferentiated fever (WEST NILE FEVER). The virus appeared in North America for the first time in 1999. It is transmitted mainly by CULEX spp mosquitoes which feed primarily on birds, but it can also be carried by the Asian Tiger mosquito, AEDES albopictus, which feeds mainly on mammals.
The infective system of a virus, composed of the viral genome, a protein core, and a protein coat called a capsid, which may be naked or enclosed in a lipoprotein envelope called the peplos.
A group of viruses in the PNEUMOVIRUS genus causing respiratory infections in various mammals. Humans and cattle are most affected but infections in goats and sheep have also been reported.
Liquid by-product of excretion produced in the kidneys, temporarily stored in the bladder until discharge through the URETHRA.
Y-box-binding protein 1 was originally identified as a DNA-binding protein that interacts with Y-box PROMOTER REGIONS of MHC CLASS II GENES. It is a highly conserved transcription factor that regulates expression of a wide variety of GENES.
The outer protein protective shell of a virus, which protects the viral nucleic acid.
The type species of VESICULOVIRUS causing a disease symptomatically similar to FOOT-AND-MOUTH DISEASE in cattle, horses, and pigs. It may be transmitted to other species including humans, where it causes influenza-like symptoms.
A watery fluid that is continuously produced in the CHOROID PLEXUS and circulates around the surface of the BRAIN; SPINAL CORD; and in the CEREBRAL VENTRICLES.
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.
Membrane glycoproteins from influenza viruses which are involved in hemagglutination, virus attachment, and envelope fusion. Fourteen distinct subtypes of HA glycoproteins and nine of NA glycoproteins have been identified from INFLUENZA A VIRUS; no subtypes have been identified for Influenza B or Influenza C viruses.
The relationships of groups of organisms as reflected by their genetic makeup.
Viruses that produce tumors.
A CELL LINE derived from the kidney of the African green (vervet) monkey, (CERCOPITHECUS AETHIOPS) used primarily in virus replication studies and plaque assays.
Species of the genus LENTIVIRUS, subgenus primate immunodeficiency viruses (IMMUNODEFICIENCY VIRUSES, PRIMATE), that induces acquired immunodeficiency syndrome in monkeys and apes (SAIDS). The genetic organization of SIV is virtually identical to HIV.
A species of CERCOPITHECUS containing three subspecies: C. tantalus, C. pygerythrus, and C. sabeus. They are found in the forests and savannah of Africa. The African green monkey (C. pygerythrus) is the natural host of SIMIAN IMMUNODEFICIENCY VIRUS and is used in AIDS research.
Immunoglobulins produced in response to VIRAL ANTIGENS.
The type species of RUBULAVIRUS that causes an acute infectious disease in humans, affecting mainly children. Transmission occurs by droplet infection.
A species of RESPIROVIRUS also called hemadsorption virus 2 (HA2), which causes laryngotracheitis in humans, especially children.
Viruses which produce a mottled appearance of the leaves of plants.

Immunohistochemical detection of JC virus in nontumorous renal tissue of a patient with renal cancer but without progressive multifocal leukoencephalopathy. (1/512)

We performed immunohistochemical staining on the nontumorous renal tissue of 45 patients with renal cancer but without progressive multifocal encephalopathy using JCV-specific antibody. For one patient we found positive staining of the nuclei of the renal collecting ducts. Immunoelectron microscopic examination of the positive cell nuclei revealed electron-dense polyomavirus-like particles.  (+info)

The J domain of papovaviral large tumor antigen is required for synergistic interaction with the POU-domain protein Tst-1/Oct6/SCIP. (2/512)

Large T antigens from polyomaviruses are multifunctional proteins with roles in transcriptional regulation, viral DNA replication, and cellular transformation. They have been shown to enhance the activity of various cellular transcription factors. In the case of the POU protein Tst-1/Oct6/SCIP, this enhancement involves a direct physical interaction between the POU domain of the transcription factor and the amino-terminal region of large T antigen. Here we have analyzed the structural requirements for synergistic interaction between the two proteins in greater detail. Tst-1/Oct6/SCIP and the related POU protein Brn-1 were both capable of direct physical interaction with large T antigen. Nevertheless, only Tst-1/Oct6/SCIP functioned synergistically with large T antigen. This differential behavior was due to differences in the amino-terminal regions of the proteins, as evident from chimeras between Tst-1/Oct6/SCIP and Brn-1. Synergy was specifically observed for constructs containing the amino-terminal region of Tst-1/Oct6/SCIP. Large T antigen, on the other hand, functioned synergistically with Tst-1/Oct6/SCIP only when the integrity of its J-domain-containing amino terminus was maintained. Mutations that disrupted the J domain concomitantly abolished the ability to enhance the function of Tst-1/Oct6/SCIP. The J domain of T antigen was also responsible for the physical interaction with Tst-1/Oct6/SCIP and could be replaced in this property by other J domains. Intriguingly, a heterologous J domain from a human DnaJ protein partially substituted for the amino terminus of T antigen even with regard to the synergistic enhancement of Tst-1/Oct6/SCIP function. Given the general role of J domains, we propose chaperone activity as the underlying mechanism for synergy between Tst-1/Oct6/SCIP and large T antigens.  (+info)

Reciprocal interaction between two cellular proteins, Puralpha and YB-1, modulates transcriptional activity of JCVCY in glial cells. (3/512)

Cross communication between regulatory proteins is an important event in the control of eukaryotic gene transcription. Here we have examined the structural and functional interaction between two cellular regulatory proteins, YB-1 and Puralpha, on the 23-bp sequence element derived from the enhancer-promoter of the human polyomavirus JCV. YB-1 and Puralpha are single-stranded DNA binding proteins which recognize C/T- and GC/GA-rich sequences, respectively. Results from band shift studies demonstrated that while both proteins interact directly with their DNA target sequences within the 23-bp motif, each protein can regulate the association of the other one with the DNA. Affinity chromatography and coimmunoprecipitation provide evidence for a direct interaction between Puralpha and YB-1 in the absence of the DNA sequence. Ectopic expression of YB-1 and Puralpha in glial cells synergistically stimulated viral promoter activity via the 23-bp sequence element. Results from mutational studies revealed that residues between amino acids 75 and 203 of YB-1 and between amino acids 85 and 215 of Puralpha are important for the interaction between these two proteins. Functional studies with glial cells indicated that the region within Puralpha which mediates its association with YB-1 and binding to the 23-bp sequence is important for the observed activation of the JCV promoter by the Puralpha and YB-1 proteins. The results of this study suggest that the cooperative interaction between YB-1 and Puralpha mediates the synergistic activation of the human polyomavirus JCV genome by these cellular proteins. The importance of these findings for cellular and viral genes which are regulated by Puralpha and YB-1 is discussed.  (+info)

Clinical and virological monitoring during treatment with intrathecal cytarabine in patients with AIDS-associated progressive multifocal leukoencephalopathy. (4/512)

We describe the clinical and virological outcome of human immunodeficiency virus-infected patients with progressive multifocal leukoencephalopathy (PML) treated with cytarabine. Twenty-seven patients received intrathecal cytarabine, 5 received concomitant intravenous cytarabine, and 20 received concomitant antiretroviral therapy. The median baseline CD4+ cell count was 28/mm3. After 4 weeks, 4 (19%) of 21 evaluable patients had stable disease, whereas the others progressed. The median survival from diagnosis and from onset was 66 and 128 days, respectively. Patients with Karnofsky scores of >50 and those previously taking antiretroviral medications had a higher probability of survival 3 months after diagnosis (P = .003 and P = .05, respectively). Overall, after 4 weeks, median JC virus load in CSF increased by 0.7 log10 copies/mL from baseline (P = NS). The mean JC virus load at 4 weeks was lower in patients with stable disease than in progressors (3.47 vs. 4.47 log10 copies/mL; P = .027). JC virus became undetectable in the only patient who had a long-term stable condition. The concentration of JC virus in CSF showed a correlation with clinical outcome.  (+info)

Molecular cloning and expression of major structural protein VP1 of the human polyomavirus JC virus: formation of virus-like particles useful for immunological and therapeutic studies. (5/512)

The major structural viral protein, VP1, of the human polyomavirus JC virus (JCV), the causative agent of progressive multifocal leukoencephalopathy (PML), was expressed by using recombinant baculoviruses. Recombinant VP1 formed virus-like particles (VLP) with the typical morphology of empty JCV capsids. Purified VP1 VLP bind to SVG, B, and T cells, as well as to monkey kidney cells. After binding, VP1 VLP were also internalized with high efficiency and transported to the nucleus. Immunization studies revealed these particles as highly immunogenic when administered with adjuvant, while immunization without adjuvant induced no immune response. VP1 VLP hyperimmune serum inhibits binding to SVG cells and neutralizes natural JCV. Furthermore, the potential of VP1 VLP as an efficient transporter system for gene therapy was demonstrated. Exogenous DNA could be efficiently packaged into VP1 VLP, and the packaged DNA was transferred into COS-7 cells as shown by the expression of a marker gene. Thus, VP1 VLP are useful for PML vaccine development and represent a potential new transporter system for human gene therapy.  (+info)

Viral variant nucleotide sequences help expose leukocytic positioning in the JC virus pathway to the CNS. (6/512)

The human polyomavirus JCV lytically infects oligodendrocytes of immunosuppressed individuals leading to the fatal demyelinating disease termed progressive multifocal leukoencephalopathy (PML). Dementia, hemiparesis, and hemianopsia are the predominant presenting signs of PML. Asymptomatic JCV infection is common worldwide with approximately 80% of adults testing positive for JCV antibodies. In addition to the brain, JCV has been shown to infect tonsil, lymphoid, bone marrow, and kidney tissues. Viral variants, classified according to the nucleotide sequences of their regulatory regions, are being mapped in human tissues and cell types to help trace the pathway of JCV from a site of initial infection to target oligodendrocytes. In most literature, a dichotomy of the JCV regulatory region structure exists by tissue. B lymphocytes, however, have demonstrated the capacity to harbor JCV of diverse regulatory regions, which helps position their interaction with virus amid every stage of infection and implicates a lymphocytic role in latency.  (+info)

Archetypal and rearranged sequences of human polyomavirus JC transcription control region in peripheral blood leukocytes and in cerebrospinal fluid. (7/512)

Two forms of human polyomavirus JC (JCV) genome are known based upon the structure of the transcriptional control region (TCR) of the virus: the archetypal form, which is commonly detected in urine, and the rearranged form, which was first detected in brain tissue from progressive multifocal leukoencephalopathy (PML) patients. The latter actually includes a group of TCR variants that, relative to the former, are characterized by various deletions and/or duplications. The aim of this study was to establish whether or not a correlation exists among the TCR type, the spreading of the virus within the host and its ability to cause PML. JCV TCR sequences from peripheral blood leukocytes (PBL) and cerebrospinal fluid (CSF) obtained from various groups of patients were compared. JCV with archetypal TCR was detected in CSF and PBL specimens from patients without neurological disorders or who eventually received a diagnosis of a non-PML neurological disorder. Rearranged TCR sequences were detected in all the CSF and PBL specimens from PML patients. The high similarity observed between the TCR structure detected in PBL and CSF specimens from individual patients could strengthen the hypothesis that PBL has a role in spreading JCV to the brain. Moreover, heterogeneous TCR patterns have been shown in individual PBL specimens from PML patients. This supports the hypothesis that, in PBL, JCV may replicate and undergo rearrangements of the TCR. The detection of JCV DNA by PCR in CSF independently from PML, although rare, could suggest that this assay is not sufficient for a virological diagnosis of PML. Further studies are required to assess the usefulness of quantitative assays or TCR typing in combination with PCR for diagnostic purposes.  (+info)

Progressive multifocal leukoencephalopathy in a patient with acquired immunodeficiency syndrome (AIDS) manifesting Gerstmann's syndrome. (8/512)

We reported a case of acquired immunodeficiency syndrome (AIDS) via multiple blood transfusions, who manifested progressive multifocal leukoencephalopathy (PML) about 18 months after the development of AIDS. PML initiated with right hemiparesis, dysphasia, and Gerstmann's syndrome and resulted in death within 2 months after the onset. Neuroimaging examinations revealed white matter lesions mainly in the left posterior parietal lobe. The cortical gray matter also showed abnormal signal intensity. Peripheral CD4+ lymphocyte count was 81/microl. Routine cerebrospinal fluid (CSF) examinations were negative. CSF antibodies against herpes simplex virus, varicella-zoster virus, cytomegalovirus, Epstein-Barr virus as well as serum antibody against toxoplasma gondii were negative. Though autopsy or biopsy of the brain was not performed, JC virus genomes were detected in the CSF sample by a polymerase chain reaction, and their sequencing showed unique alterations of the regulatory regions, characteristic to PML-type JC virus.  (+info)

Our laboratory studies the host-pathogen relationship between viruses and cells to better understand cellular and molecular mechanisms underlying the complexities of viral disease. In particular, we study the human JC polyomavirus, which infects the majority of the population and causes the fatal demyelinating disease progressive multifocal leukoencephalopathy in the brain of immunosuppressed individuals. Our goal is to understand the basic biology of the virus and JCPyV pathogenesis in order to develop novel treatment options, which are currently very limited.. The Maginnis laboratory is committed to excellence in biomedical research and educational training. We aim to provide a collegial, supportive atmosphere that promotes a passion for scientific curiosity and research excellence in an environment where scientific research is fun and rewarding. We emphasize the importance of asking key scientific questions with creative, open minds to provide meaningful contributions in the fields of ...
JC virus (JCV) is a common human polyomavirus responsible for the fatal demyelinating disease progressive multifocal leukoencephalopathy (PML), in immunocompromised individuals. About 5% of AIDS patients develop this currently untreatable fatal disease. Typical and atypical antipsychotic drugs inhibit JCV infection of glial cells. Elphick et al. now find that the cellular receptor for JCV on glial cells is a serotonin receptor. The findings contribute to the understanding of the pathogenesis of PML in AIDS patients and suggest that therapy based on existing serotonin receptor inhibitors may be feasible.. G. F. Elphick, W. Querbes, J. A. Jordan, G. V. Gee, S. Eash, K. Manley, A. Dugan, M. Stanifer, A. Bhatnagar, W. K. Kroeze, B. L. Roth, W. J. Atwood, The human polyomavirus, JCV, uses serotonin receptors to infect cells. Science 306, 1380-1383 (2004). [Abstract] [Full Text]. ...
Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease caused by human neurotropic JC virus. JCV infects more than 80% of human popul...
One of the major limitations of highly active antiretroviral therapy is its inability to inhibit the replication of polyomavirus JC (JCV), the etiologic agent of progressive multifocal leukoencephalopathy (PML), an acquired immunodeficiency syndromeâ€defining illness. We previously demonstrated the induction of interferon (IFN)â€stimulated genes (ISGs) by JCV. In the present study, we characterize the specific viral events required to induce ISGs and the potential antiviral effects of type I IFN on JCV replication in human fetal glial cells in the presence and absence of type I IFNs. Productive JCV replication was essential for the induction of the antiviral host response. JCV replication at all steps was significantly inhibited in the presence of IFN, and neutralizing anti-IFN antibody rescued the inhibitory effect of IFN. These results support the use of IFN as an adjunct therapy for patients with PML. Because IFN cannot cross the blood-brain barrier to achieve its direct antiviral ...
JC virus can cause the serious neurological disease progressive multifocal leukoencephalopathy (PML) in patients who are immunocompromised. Presence of JC virus antibodies alone is not enough to diagnose PML, however, because the majority of adults who have been exposed to the virus dont develop symptoms
John Cunningham virus (JCV) constitutes a family of polyoma viruses, which plays important roles in the progressive multifocal leukoencephalopathy (PML) and tumorigenesis. However, no bibliometric investigation has been reported to guide the researchers and potential readers. Papers were collected from database Sci-expanded and Pubmed until May 22, 2008. The highly-productive authors, institutes and countries, highly-cited authors and journals were ranked. The highly-cited articles were subjected to co-citation and chronological analysis with highly-frequent MeSH words for co-occurrence analysis. Until now, 1785 articles about JCV were indexed in Sci-expanded and 1506 in Pubmed. The main document type was original article. USA, Japan and Italy were the largest three producers about JCV. Temple University published 128 papers and ranked the top, followed by University of Tokyo. Khalili K and Yogo Y became the core authors due to more than 20 documents produced. Journal of Neurovirology published more
The JC virus belongs to the polyoma virus group of the papovavirus family, which are double-stranded DNA viruses without an envelope. BK virus is also in the polyoma virus group. It appears that infection by both viruses occurs during childhood or adolescence, with about 50% of the population demonstrating antibody before adulthood, rising later to 80%-90%. The JC virus localizes to and remains latent in the kidney, from whence it occasionally may reactivate. If a patient becomes immunosuppressed, especially during AIDS, reactivated JC virus can infect lymphocytes, be carried to the brain, infect oligodendroglia glial cells, and produce a demyelinating disease called progressive multifocal leukoencephalopathy. This occurs in about 4% of patients with AIDS. Diagnosis is made through biopsy using immunologic stains containing antibody against polyomavirus. One report applied a homemade nucleic acid probe with PCR amplification to urine of JC virus patients and obtained an excellent detection ...
Treatment with natalizumab in patients with multiple sclerosis (MS) appears linked with JC virus (JCV) infection, which can lead to a rare and often fatal demyelinating disease of the central nervous system called progressive multifocal leukoencephalopathy (PML) that destroys the myelin that protects nerve cells.
Human JC polyomavirus (JCV) causes progressive multifocal leukoencephalopathy (PML), a rare but life-threatening demyelinating disease in patients under profound immunosuppression and those receiving therapeutic immunomodulation for autoimmune and inflammatory disorders. Using persistent mouse polyomavirus (MPyV) infection in mice, we are developing a model of PyV-induced CNS disease to elucidate the role of immunosuppression in PML pathogenesis. Histology revealed corpus callosum demyelination in 100% of persistently infected mice. Following intracerebral injection with MPyV, immunocompetent C57BL/6 mice showed robust infiltration by MPyV-specific CD8 T cells with minimal contraction. During persistent CNS infection, a significant population of CD8 T cells exhibited a tissue-resident memory (Trm) phenotype (CD103+CD69+CD62Llo), as reported for acute VSV and latent HSV-1 infections, and incorporated BrdU in situ, suggesting capacity for self-renewal. Furthermore, these Trm cells develop and ...
On my website I have invited medical practitioners and other health professionals to debate the information that I am providing on Australias vaccination policies. John Cunningham decided to take up this offer in February/March 2014. He is a leader of the Stop the Australian Vaccination Network (SAVN) lobby group and a medical practitioner. When responding to my request he chose to send his opinions in unsolicited emails to members of the public, including UOW academics involved with my research and journalists. This occurred whilst I was a student at the University of Wollongong (UOW).. Here are the corrections to the personal opinions and misinformation provided by John Cunningham in unsolicited emails to members of the public and UOW academics in 2014.. Further, in July 2014 John Cunningham, made a complaint to the University of Wollongong about my research project completed in 2006. This research project was a critique of the Australian governments whooping cough policy and the research ...
Igor Koralnik, MD is an American physician, neurologist and scientist. He is one of the first physicians to study the neurologic complications caused by the human immunodeficiency virus (HIV) and is a leading researcher in the investigation of the polyomavirus JC (JC virus), which causes progressive multifocal leukoencephalopathy (PML), a disease of the central nervous system that occurs in immunosuppressed individuals. Koralnik was born in Geneva, Switzerland on July 20, 1962. He moved to the United States in 1990 and became a naturalized U.S. citizen. He received his medical degree at the University of Geneva Medical School, Switzerland, in 1987. While a medical student, he became interested in a new disease - acquired immune deficiency syndrome (AIDS), whose origin in the HIV virus was discovered in 1983. Koralniks doctoral dissertation focused on the early neurological complications of AIDS. He used magnetic resonance imaging, electroencephalography and other electrophysiologic diagnostic ...
Diseases that result in injury to oligodendrocytes include demyelinating diseases such as multiple sclerosis and various leukodystrophies. Trauma to the body, e.g. spinal cord injury, can also cause demyelination. The immature oligodendrocytes, which increase in number during mid-gestation, are more vulnerable to hypoxic injury and are involved in periventricular leukomalacia.[26] This largely congenital condition of damage to the newly forming brain can therefore lead to cerebral palsy. In cerebral palsy, spinal cord injury, stroke and possibly multiple sclerosis, oligodendrocytes are thought to be damaged by excessive release of the neurotransmitter, glutamate.[27] Damage has also been shown to be mediated by N-methyl-D-aspartate receptors.[27] Oligodendrocyte dysfunction may also be implicated in the pathophysiology of schizophrenia and bipolar disorder.[28]. Oligodendrocytes are also susceptible to infection by the JC virus, which causes progressive multifocal leukoencephalopathy (PML), a ...
the jc virus, or john cunningham virus, is a germ so common that the majority of adults have been exposed to it. the virus was first discovered in 1971, when a doctor found it in the brain of a man wi
For a comprehensive list of publications, see the PubMed link above. Below is a selection of publications:. Cabral HJ, Tobias C, Rajabiun S, Sohler NL, Cunningham CO, Wong MD, Cunningham WE. Outreach program contacts: Do they increase the likelihood of engagement and retention in HIV primary care for hard-to-reach patients? AIDS Patient Care STDs. 2007 Jun;21(S1):S59-S56.. Cunningham CO, Kunins HV, Roose RJ,Elam RT, Sohler NL. Barriers to Obtaining Waivers to Prescribe Buprenorphine for Opioid Addiction Treatment Among HIV Physicians. J Gen Intern Med. 2007 Sep;22(9):1325-9. Epub 2007 Jul 10. PMC2219773. Cunningham CO, Sanchez JP, Heller D, Sohler NL. Assessment of a medical outreach program to improve access to HIV care among marginalized individuals. Am J Public Health. 2007 Oct;97(10):1758-61. Epub 2007 Aug 29. PMC1994196. Cunningham CO, Giovanniello A, Sacajiu G, Whitley S, Mund P, Beil R, Sohler NL. Buprenorphine treatment in an urban community health center: What to expect. Fam Med. 2008 ...
The JC virus is a virus which infects the brain of advanced cancer patients and causes PML-- progressive multifocal leukoencephalopathy. PML can lead to neurologic deficits as indicated in your...
Background and aims: Anti-α4 integrin therapy with natalizumab is efficacious in refractory Crohns disease and in multiple sclerosis, but carries an estimated 1/1000 risk of progressive multifocal leukoencephalopathy (PML) caused by reactivation of latent JC virus infection. Athough anti-α4 integrin therapies are likely to be introduced in the clinic, screening for the risk of PML has not been developed.. Methods: We prospectively collected urine, serum, plasma and buffy coats from 125 patients with Crohns disease, 100 control subjects with gastrointestinal (GI) disease, and 106 healthy volunteers. Four to eight weeks after this first sample collection, we additionally collected a set of urine, serum, plasma and buffy coat samples from the 125 patients with Crohns disease, and a next set of samples was collected 12-16 weeks after the first collection. JC viral loads were determined with quantitative real-time polymerase chain reaction (PCR), and JC virus seroprevalence with a specific ...
The initial site of infection may be the tonsils,[4] or possibly the gastrointestinal tract.[5] The virus then remains latent in the gastrointestinal tract[6] and can also infect the tubular epithelial cells in the kidneys,[7] where it continues to reproduce, shedding virus particles in the urine. JCV can cross the blood-brain barrier into the central nervous system, where it infects oligodendrocytes and astrocytes, possibly through the 5-HT2A serotonin receptor.[8] JC viral DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue.[9] JCV found in the central nervous system of PML patients almost invariably have differences in promoter sequence to the JCV found in healthy individuals. It is thought that these differences in promoter sequence contribute to the fitness of the virus in the CNS and thus to the development of PML.[3] Certain transcription factors present in the early promoter sequences of the JC virus can induce trophism and viral proliferation that ...
Rapid restoration of virus-specific T immunity via adoptive transfer of ex vivo generated T cells has been proven as a powerful therapy for patients with advanced cancers and refractory viral infections such as cytomegalovirus (CMV) and Epstein-Barr virus (EBV). BK virus (BKV), John Cunningham virus (JCV), and Merkel cell carcinoma virus (MCV) are the members of the rapidly growing human polyomavirus (hPyV) family that commonly infects most healthy humans. These viruses have a clearly established potential for causing severe end-organ damage or malignant transformation, especially in individuals with weakened immunity who are unable to mount or regain endogenous T-cell responses as a result of underlying leukemia or iatrogenic immunosuppression in autoimmunity, bone marrow and solid organ transplant settings ...
Of 41 HIV+ patients, 38 were male (93%) and indications for BM biopsies were lymphoma (20), pancytopenia (8), anemia (6), MGUS (2), polycythemia (2), leucopenia (1), splenomegaly (1), and thrombocytopenia (1). Mean age was 47 (range 32-71), mean CD4 count 211 (2-928), 27% had undetectable plasma HIV RNA, and 75% were on HAART. The 47 HIV- controls, matched for indications for BM biopsy, included 32 males (65%), and mean age was 56 (range 27-93). Quantitative PCR detected JCV DNA in BM samples of 19/41 (46%) HIV+ vs 3/47 (6%) of HIV- (p , 0.001). Preliminary immunohistochemistry (IHC) experiments suggest that JCV T antigen is detectable in a fraction of JCV DNA positive bone marrows samples, while JCV VP1 protein was not. Furthermore, JCV was detected by double IHC in some of the plasma cells, myeloid, and lymphoid cells. We then tested fresh BM aspirates, blood and urine samples from 30 HIV- and 6 HIV+ patients. JCV DNA was detectable in 10/36 (28%) fresh BM aspirates, 7/26 (27%) peripheral ...
Last night I took part in an extraordinary event in Musselburgh Grammar School. Organised by Maya, a pupil in S4, One World Night featured an imaginative mix of pupil performance and presentations on humanitarian themes by guest speakers and pupils of MGS and Campie Primary School. The event was warmly compèred by Fiona ODonnell, MP for East Lothian.. MGS Orchestra opened with the Prelude from Charpentiers Te Deum, followed by an arrangement of Over The Rainbow. John Cunningham then gave a presentation on the work of Mercy Corps. MGS Guitar Group performed Tárregas Recuerdos de la Alhambra before Katherine and Roanna described the work of the MGS Amnesty Group and the necessity of speaking out against injustice.. After the interval, six pupil members the local branch of the Alpha Dance Academy gave a fantastic performance of Jai Ho from the film, Slum Dog Millionaire. This was an energetic and impressive mix of Indian and en pointe styles.. P7 pupils from Campie PS spoke eloquently about ...
Online etext Cunninghams manual of practical anatomy (Volume 1) by D. J. (Daniel John) Cunningham (page 7 of 44) : the collection of free ebooks
Once Dr. Cunningham discovered Ophthalmology, he says, there was no second-guessing. He knew he had found his passion, and was determined to use his medical knowledge, curiosity about advanced technologies, and genuine interest in others to help people of all ages achieve the best possible vision. In 1991, Dr. Cunningham joined the Knoxville Ophthalmology practice started by Dr. J. Ed Campbell in 1952, and has been an integral part of a number of firsts achieved by the practice ever since, including: first in the Southeast to perform the Crystalens® procedure, a cataract replacement lens that is also designed to correct vision at all distances and East Tennessees first onsite Custom LASIK surgical facility, the Campbell Cunningham Laser Center.. While hes accomplished a lifetime of goals in less than 25 years in Ophthalmology, Dr. Cunningham is quick to point out that in his precision, technology-based specialty, there is always something new to learn and accomplish. Some of his best teachers ...
Human polyomaviruses (JC virus, BK virus and simian virus 40) are causative agents of some human diseases and, interestingly, are involved in processes of cell transformation and oncogenesis. These viruses need the cell cycle machinery of the host cell to complete their replication; so they evolved mechanisms that can interfere with the growth control of infected cells and force them into DNA replication. The retinoblastoma family of proteins (pRb), which includes pRb/p105, p107 and pRb2/p130, acts as one of the most important regulators of the G1/S transition of the cell cycle. Rb proteins represent an important target for viral oncoproteins. Early viral T antigens can bind all members of the pRb family, promoting the activation of the E2F family of transcription factors, thus inducing the expression of genes required for the entry to the S phase. The interaction between early viral antigens and cell cycle regulators represents an important mechanism through which viruses deregulate cell cycle ...
The JC virus, or John Cunningham virus, is a member of the polyomavirus family. When youre exposed to it as a kid or young adult, you might not even notice it, or you might notice cold-like symptoms which are self-limiting. Not a huge deal at all. You get infected, you make antibodies, life goes on. As long as youre immunocompetent. But thats not the case in patients with impaired cellular immunity, as in cases of Hodgkins lymphoma (HL).. Although the gold standard for diagnosis is brain biopsy, you dont need tissue to make the diagnosis of PML. In an immunocompromised patient with progressive neurologic changes, youll always need the MRI. This can exclude opportunistic processes like toxoplasmosis, cryptococcal meningitis, or CNS lymphoma, but will also be important to confirm the presence of white matter disease, which may or may not have enhancement 10-20% of the time, and may or may not have mass effect. Our patient had faint enhancement, as you can see from the images on the blog. Once ...
As many patients are keenly aware, Tysabri is among the most effective MS drugs available, but the treatment comes with some troubling potential side effects. Chief among these is PML, a horrendous and often fatal brain infection caused by the JC virus. Although the JC virus is quite common in humans, infecting between 70%-90% of the general population (click here), the immune system typically keeps the virus in check. However, the same immunosuppressive properties that makes Tysabri so effective in combating MS can also allow the JC virus to become active and lead to PML. Since Tysabri became widely available to the public in 2006, neurologists have attempted to reduce the risk of PML by carefully monitoring patients for the presence of JC virus antibodies in their blood, and these efforts have lessened the dangers associated with Tysabri treatment. For patients currently on Tysabri or considering starting the drug, the folks at the Barts and London Medical School in England have come up with a ...
Laura Cunningham has very strong communication skills. She is very good explaining complex and sometimes esoteric concepts in simple terms. Her dedication and commitment to meeting deadlines and completing the transaction was exceptional.. IFLR 1000: The Guide to the Worlds Leading Financial Law Firms, 2021. Excellent client relationship management, knowledge of the subject and problem solving skills.. IFLR 1000: The Guide to the Worlds Leading Financial Law Firms, 2021. Laura Cunningham and the team have done a great job on a difficult transaction with us this year, and have shown strength and flexibility at all times.. The Legal 500: Europe, Middle East & Africa, 2020. Laura Cunningham is a fantastic lawyer. She commits herself to any given deal and works tirelessly until the transaction is brought to a successful close.. The Legal 500: Europe, Middle East & Africa, 2020. ...
Cunningham earned an undergraduate degree at Mississippi State College for Women and a Ph.D. in both microbiology and immunology from the University of Tennessee Center for Health Sciences.. Today, she is a George Lynn Cross Research Professor and Presbyterian Health Foundation Presidential Professor in the Department of Microbiology and Immunology at the University of Oklahoma College of Medicine, where she has taught and conducted research into infection and autoimmune diseases for 33 years.. My training was in Group A streptococcal disease, but I also love immunology, which is our bodys response to infections, she said.. After researching rheumatic fever, myocarditis and other heart-related diseases for 15 years, Cunningham received a call from the National Institutes of Mental Health. They wanted her to investigate a puzzling condition affecting children known as pediatric autoimmune neuropsychiatric disorder associated with strep, commonly known as PANDAS.. Cunningham became a ...
Dear Friends,. In March of 2014, the New-York Historical Society mounted Facades, an exhibition of photographs taken by Bill Cunningham as part of an eight-year project, begun in the late 1960s, to document the architectural riches and fashion history of New York City. The photographs had been gifted to New-York Historical by Mr. Cunningham, who used our Patricia D. Klingenstein Library for much of his research. We were delighted when, in the course of the shows development, Mr. Cunningham agreed to add another photograph to our collection, which depicted his muse, Editta Sherman dressed in exquisite period costume against the backdrop of a graffiti-covered New York City subway car. That photograph might seem emblematic of hard times in 1970s New York. But truly it was vivid proof of Mr. Cunninghams ability to see beauty where others saw only despair. As we mourn Bill Cunninghams passing, we treasure this photograph above all.. In advance of Facades opening, we planned a VIP reception for ...
Dr. Matthew Cunningham, MD is a Vitreoretinal Disease Specialist in Clermont, FL and has over 17 years of experience in the medical field. Dr. Cunningham has more experience with Eye Conditions than other specialists in his area. He graduated from University Of Florida College Of Medicine medical school in 2004. He is affiliated with medical facilities such as AdventHealth Altamonte Springs and Adventhealth Orlando. He is accepting new patients and has indicated that he accepts telehealth appointments. Be sure to call ahead with Dr. Cunningham to book an appointment.
Cunningham, rundles S.; Feller, W F.; Cunningham, rundles C.; Dupont, B; Wanebo, H; Oreilly, R; and Good, R A., Lymphocyte transformation in vitro to riii mouse milk antigen among woman with breast disease. (1976). Subject Strain Bibliography 1976. 2295 ...
EMS ISO Merchant Services Agent Program in Cunningham, gets you into the verticals you need for success. Get 24/7 support & grow your portfolio! Boost your residual income when you partner with the leading ISO agent program. See how the leading payment processor can help you take your merchant services business to the next level when you become an EMS ISO Agent In Cunningham, Illinois. Join today and get access to state-of-the-art credit card processing products and services. When youre selling merchant services as an EMS merchant services reseller youll get the success you deserve and be a leader in the payments industry. See why our merchant services agent program will help give you the edge in the payments industry that you need.
CUNNINGHAM genealogy, discover the coat of arms, family crest, family history, ancestry, the surname meaning and the name origin for the CUNNINGHAM Tribe
Andy Cunningham is the founder of Cunningham Collective, a marketing, brand and communication strategy firm. She has played a role in the launch of many technology categories and products, including the Apple Macintosh. Her new book is Get to Aha!: Discover Your Positioning DNA and Dominate Your Competition.
Prosecutors allege Cunningham violated a law that forbids disclosing photos or videos without the consent of someone whose intimate parts are exposed or who is engaged in a sexual act. They say the woman and Cunningham lived together.. ...
Issuu is a digital publishing platform that makes it simple to publish magazines, catalogs, newspapers, books, and more online. Easily share your publications and get them in front of Issuus millions of monthly readers. Title: Paul James Cunningham // Untitled 2.0 // Geometry of Fear, Author: Untitled 2.0, Name: Paul James Cunningham // Untitled 2.0 // Geometry of Fear, Length: 106 pages, Page: 1, Published: 2017-12-23
Scott stopped by Ward Cunningham (you know, the guy who invented the Wiki. Yes, that Ward Cunningham) to hang out, and discovered Wards treasure trove of electronics, software, soldering guns and we
Dr. Matthew Cunningham, MD of New York, NY patient reviews, appointments, phone number and quality report. Compare Dr. Cunningham to other nearby Orthopedic Surgeons in New York.
Obituary for Joan Cunningham Heidelberg | JOAN CUNNINGHAM HEIDELBERG, age 87, of Troy, Ohio passed away on Friday, August 14, 2020 at Hospice of Miami County Inpatient Unit in Troy surrounded by love. She was born on October 27,...
The principal CNS targets for JCV infection are oligodendrocytes (the brain cells that produce myelin). A stable human oligodendrocyte cell line for studies of JCV dependent PML was, however, not previously available. Therefore, we were delighted to report in Peterson et al, 2017 that a human stem cell line termed G144 (Pollard et al, 2009) undergoes differentiation by removal of growth factors (Fig. 1A), express oligodendrocyte specific surface markers (Fig. 1B), has a rapid doubling time (3-5 days) and is stable during passage. Furthermore, we reported that G144 cells support robust levels of JCV DNA replication and infection by JC virus. Thus, we have established the first oligodendrocyte based model system for studies of JCV dependent PML.. ...
Not a very heartening picture, but there is good news.. The parasites have to go through a free swimming stage, and during this stage they are vulnerable. It is during this stage that the conventional copper treatment is effective, and the same applies to UV sterilization.. When the parasites pass by the UV light, they are either killed outright or are badly damaged and no longer a problem. It is important that the parasites receive the correct amount of radiation, and that is why the manufacturers instructions for pump size must be followed.. There is a potential downside to this: if free swimming parasites can be killed, then is anything good also killed?. Unfortunately, the answer is yes, but it is not necessarily a problem. If the aquarist is fortunate enough to have plankton, then if this passes through the sterilizer it will be killed. Plankton is not usually present in any quantity in an aquarium, so that is why it is not a problem. Any other minute beneficial organism will meet the same ...
Progressive brain disorder that slowly destroys a persons ability to learn, reason, make judgments, communicate and perform daily activities. As this disease progressives the individuals may experience memory loss, this usually occurs more in the short-term memory, changes in personality and behavior, such as anxiety, suspiciousness or agitation, as well as delusions or hallucinations. Brain cells are gradually destroyed and leads to progressive decline in mental functions, No cure is available at this time but their are treatments that can slow the progress of the disease.
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Jangan sampai kemudian seseorang mengajukan JC perbuatannya tidak diakui tetapi perbuatan pihak lain disampaikan…. Jakarta - Komisi Pemberantasan Korupsi (KPK) mempertimbangkan banyak hal terkait permohonan justice collaborator (JC) yang diajukan terdakwa perkara korupsi proyek pengadaan KTP-elektronik Setya Novanto.. Permohonan JC tersebut masih diproses. Analisisnya tidak mudah karena perlu mempertimbangkan banyak hal, kata Juru Bicara KPK Febri Diansyah di gedung KPK, Jakarta, Kamis.. Menurut Febri, KPK masih harus melihat apakah memang ada keseriusan dan itikad baik dari terdakwa Novanto soal pengajuan JC tersebut.. Indikator yang pertama kali dilihat, menurut Febri, apakah terdakwa Novanto mengakui atau tidak perbuatannya.. Jangan sampai kemudian seseorang mengajukan JC perbuatannya tidak diakui tetapi perbuatan pihak lain disampaikan. Bahwa kemudian terdakwa nanti akan terbuka, saya kira itu positif saja untuk proses persidangan. Positif untuk terdakwa, juga positif untuk penanganan ...
Different studies suggested an oncogenic potential of the polyomaviruses JC virus, BK virus and simian virus 40, particularly in brain tumors and neuroblastoma, which belong to the most frequent malignancies in children. However, currently available data are controversial, possibly due to the different regional prevalence of the viruses and the detection techniques used.
While it would be extremely concerning if the patient in question developed PML while her lymphocyte counts remained at acceptable levels, the facts as now known indicate that this simply was not the case. Given the immunosuppressive properties of Tecfidera, it would appear to be vitally important that patients be regularly tested to check their white blood cell counts. It would seem that the FDA suggestion of once yearly blood tests is insufficient, and I know many neurologists are checking their patients much more frequently, more on the order of at least once every three months. Monitoring for JC virus might make sense if PML were to be seen in Tecfidera patients not experiencing severe lymphopenia, but at this point the available evidence doesnt seem to merit the taking of this extra step. Then again, any extra bit of information is valuable, and Id imagine that some neurologists might Institute testing for JC virus in their Tecfidera patients on their own. Tecfidera is proving to be quite ...
Specimen Type: Formalin-fixed, paraffin-embedded tissue block. Supplies: Pathology Packaging Kit (T554). Specimen Volume: Entire block. Specimen Type: Slides. Slides: 4 Unstained glass, positively charged slides with 5 (+ or - 1)-microns formalin-fixed, paraffin-embedded tissue. ...
Verma S, Ziegler K, Ananthula P, Co J K G, Frisque R J, Yanagihara R, Nerurkar V R (2006); Virology, 345:457-467. doi: 10.1016/j.virol.2005.10.012. ...
CLINICAL IMAGES. Progressive multifocal leucoencephalopathy - a case report. Mala Modi. Dr Modi is a senior radiologist and senior lecturer in the Department of Radiology, Chris Hani Baragwanath Hospital, Johannesburg. She is author of numerous papers in national and international peer-reviewed journals and is assistant editor of the South African Journal of Radiology.. Correspondence. Progressive multifocal leucoencephalopathy (PML) is a demyelinating disease caused by the human neurotropic JC (John Cunningham) virus, a polyomavirus.1,2. Following on the worldwide HIV/AIDS pandemic there has been a dramatic increase in the incidence of PML. However, cases of PML, an AIDS-defining illness, have rarely been reported from Africa, an area where HIV-1 clade C infection predominates.3-5. Clinical and imaging details. A 27-year-old woman presented to Chris Hani Baragwanath Hospital, Johannesburg, with new-onset seizures. She was heterosexual, did not abuse intravenous drugs, and was retroviral ...
Niche market research report on Global Progressive Multifocal Leukoencephalopathy Drug Market 2019-2025 by industry driving factors, size, trends & key players.. LOS ANGELES, CALIFORNIA, UNITED STATES, December 10, 2019 /EINPresswire.com/ - The report comes out as an intelligent and thorough assessment tool as well as a great resource that will help you to secure a position of strength in the global Progressive Multifocal Leukoencephalopathy Drug market. It includes Porters Five Forces and PESTLE analysis to equip your business with critical information and comparative data about the Global Progressive Multifocal Leukoencephalopathy Drug Market. We have provided deep analysis of the vendor landscape to give you a complete picture of current and future competitive scenarios of the global Progressive Multifocal Leukoencephalopathy Drug market. Our analysts use the latest primary and secondary research techniques and tools to prepare comprehensive and accurate market research reports.. Each ...
TY - JOUR. T1 - Progressive multifocal leukoencephalopathy. T2 - Investigation of three cases using in situ hybridization with JC virus biotinylated DNA probe. AU - Aksamit, Allen J.. AU - Mourrain, Pascale. AU - Sever, John L.. AU - Major, Eugene O.. PY - 1985/10. Y1 - 1985/10. N2 - Using the technique of in situ DNA‐to‐DNA hybridization, a JC virus biotinylated DNA probe was developed and applied to formalin‐fixed, paraffin‐embedded, or fixed, frozen sections of brain tissue from three subjects with progressive multifocal leukoencephalopathy (PML). Light microscopy was carried out to correlate the presence of JC virus DNA with the selective infection of oligodendrocytes and astrocytes in PML. Oligodendrocytes (lytically infected) showed the greatest evidence of viral DNA. More astrocytes showing bizarre morphological changes had evidence of viral DNA than did astrocytes that were simply reactive. Viral DNA was not evident in vascular endothelial cells using this technique. Viral DNA ...
By McCalmont, Vicki Bennett, Kristi Progressive multifocal leukoencephalopathy is a rare, highly fatal demyelinating brain infection caused by the JC virus. This infection is associated with immunosuppressive agents and is emerging in the transplant population. There has never been a documented case of progressive multifocal leukoencephalopathy in a transplant recipient receiving sirolimus. We present a study, in which the JC virus was found in a 68-year-old man who had received a postorthotopic heart transplant 3 years earlier and who was receiving sirolimus and prednisone for immunosuppression. We review the clinical presentation, diagnosis, current treatment options, and the outcomes of progressive multifocal leukoencephalopathy in transplant recipients. (Progress in Transplantation. 2007; 17:157- 160) CASE Study A 65-year-old white man received an orthotopic heart transplant for idiopathic cardiomyopathy. Triple immunosuppression with cyclosporine, mycophenolate mofetil (MMF), and prednisone ...
By Stan Deresinski, MD, FACP, FIDSA Clinical Professor of Medicine, Stanford University Dr. Deresinski reports no financial relationships relevant to this field of study. SYNOPSIS: Enhancing the immune response with checkpoint inhibitors may be beneficial in the management of progressive multifocal leukoencephalopathy, a viral disease previously recalcitrant to therapy. SOURCE: Cortese I, Muranski P, Enose-Akahata Y, et al. Pembrolizumab treatment for progressive multifocal leukoencephalopathy. N Engl J Med 2019;380:1597-1605. Progressive multifocal leukoencephalopathy (PML) is a rare infection caused by the John Cunningham virus (JCV) that . . .
Progressive multifocal leukoencephalopathy (PML) is a rare, life-threatening disease that is characterized by focal neurological deficits. It is caused by the John Cunningham virus (JC virus), which is usually contracted during childhood but is asymptomatic until the virus is reactivated later in life due to weakened immune status. The clinical manifestations are consistent with findings on brain imaging or biopsy. Since this disease is fatal, early diagnosis and prompt treatment are imperative.… Progressive Multifocal Leukoencephalopathy (Progressive Multifocal Leukoencephalitis): Read more about Symptoms, Diagnosis, Treatment, Complications, Causes and Prognosis.
TY - JOUR. T1 - Progressive multifocal leukoencephalopathy associated with human immunodeficiency virus infection. T2 - A review of the literature with a report of sixteen cases. AU - Berger, J. R.. AU - Kaszovitz, B.. AU - Post, M. J.D.. AU - Dickinson, G.. PY - 1987/1/1. Y1 - 1987/1/1. N2 - Progressive multifocal leukoencephalopathy, a common complication of infections with human immunodeficiency virus (HIV), occurs in as many as 3.8% of patients with the acquired immunodeficiency syndrome (AIDS). We report 16 cases and review 12 previously reported cases of progressive multifocal leukoencephalopathy associated with HIV infection. This illness was the presenting manifestation of HIV infection in 8 cases. Limb weakness, gait abnormalities, visual loss, and altered mental status were the commonest initial complaints. Computed tomography of the brain frequently showed hypodense, nonenhancing white matter lesions. Magnetic resonance imaging was more sensitive than computed tomography in detecting ...
A case of developing progressive multifocal leukoencephalopathy while using rituximab and mycophenolate mofetil in refractory systemic lupus erythematosus Yuichi Ishikawa, Tadamichi Kasuya, Junichi Ishikawa, Michio Fujiwara, Yasuhiko Kita Department of Rheumatology, Yokohama Rosai Hospital, Kohoku-ku, Yokohama, Kanagawa, Japan Abstract: Progressive multifocal leukoencephalopathy (PML) is a central nervous system infection caused by John Cunningham (JC) virus reactivation in an immunocompromised patient. PML has various neurologic symptoms and has very poor prognosis. A 36-year-old man developed transverse myelitis and had a psychiatric disorder at the age of 26. He was diagnosed with systemic lupus erythematosus (SLE) and neuropsychiatric SLE (NPSLE), on the basis of leukopenia and presence of anti-DNA and anti-nuclear antibodies. Treatment with glucocorticoid (GC) was started, and remission was introduced. Six months before PML onset, his condition was complicated with hemophagocytic
Progressive multifocal leukoencephalopathy (PML) is a highly fatal, demyelinating disease of the brain caused by lytic infection of oligodendrocytes with the JC polyomavirus (JCPyV). Emergence of PML is considered rare and is always associated with an underlying deficit in immune surveillance. In accordance, the majority of PML cases are detected ... read more in patients with HIV-induced severe immunodeficiencies. Fortunately, the introduction of cART significantly reduced the incidence of PML in HIV-infected patients. In 2005, however, a surprising increase in PML cases was observed with the use of monoclonal antibodies, including natalizumab and rituximab. As these therapies modulate the immune system rather than suppressing it, questions were raised regarding the conventional route of JCPyV pathogenesis. Owing to the lack of both animal models, and sufficient in vitro models to sustain effective replication of JCPyV, the mechanisms of JC virus infection remain largely uncertain and current ...
certain hiv drugs may make your immune system stronger and help prevent the virus from causing progressive multifocal leukoencephalopathy (pml). these drugs have become more common, so the number of p
TY - JOUR. T1 - Topotecan in the treatment of acquired immunodeficiency syndrome-related progressive multifocal leukoencephalopathy. AU - Royal, Walter. AU - Dupont, B.. AU - McGuire, D.. AU - Chang, L.. AU - Goodkin, K.. AU - Ernst, T.. AU - Post, M. J.. AU - Fish, D.. AU - Pailloux, G.. AU - Poncelet, H.. AU - Concha, M.. AU - Apuzzo, L.. AU - Singer, E.. PY - 2003/6/1. Y1 - 2003/6/1. N2 - Progressive multifocal leukoencephalopathy (PML) affects about 1 in 20 individuals with the acquired immunodeficiency syndrome (AIDS) and has been associated with poor survival. This report describes the results of a phase II clinical trial using the drug topotecan, a semisynthetic analogue of camptothecan, administered to a cohort of subjects with AIDS-related PML. Data were evaluated on 11 of 12 subjects enrolled in the study. Three responded to therapy. Additionally, one patient was treated off-protocol and showed a response to treatment. Progression occurred after the first course; however, a partial ...
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease which results from the reactivation of John Cunningham virus (JC virus) infecting oligodendrocytes in patients with compromised immune systems. It is considered the most ...
CiteSeerX - Scientific documents that cite the following paper: JC virus load in progressive multifocal leukoencephalopathy: analysis of the correlation between the viral burden in cerebrospinal fluid, patient survival, and the volume of neurological lesions. Clin. Infect. Dis
Progressive multifocal leukoencephalopathy is a demyelinating disease which results from the JC virus infecting oligodendrocytes. It is considered the most common clinical manifestation of JC virus infection in the brain.
Progressive multifocal leukoencephalopathy (PML) is a neurological disorder characterized by the destruction of myelin-producing cells responsible for protecting nerve cells in the brain and spinal cord. The disease is caused by the JC virus and is typically fatal. Over the past few years, the use of pembrolizumab has increased to strengthen the immunity in patients with PML. The objective of this study is to analyze the efficacy of pembrolizumab in the treatment of PML.. This study included a total of eight adult patients with PML and with different underlying predisposing conditions. Each participant was assigned to a 2 mg per kg BW dose of pembrolizumab every four to six weeks. The primary outcomes were the JC viral load and CD4+ and CD8+ activity against the JC virus. Pembrolizumab resulted in a down-regulation of PD-1 expression on lymphocytes and cerebrospinal fluid in all eight patients. Five patients showed clinical improvement or stabilization of PML with reduced JC viral load and an ...
Progressive multifocal leukoencephalopathy is caused by human polyomavirus ( JC virus). JC virus is detected by polymerase chain reaction of the brain biopsy or cerebral spinal fluid of the patient.
Progressive Multifocal Leukoencephalopathy (PML) is a demyelinating disease of the brain caused by the polyomavirus JC (JCV) in immunosuppressed people. There is no cure for PML but 1-year survival has increased from 10% to 50% in HIV-infected individuals treated with highly active antiretroviral therapy. We describe herein the clinical outcome of 24 PML patients whose survival exceeded 5 years, with a mean follow-up of 94.2 months (range, 60-188 months). Of all patients, only two were females including one who had non-Hodgkins lymphoma and was HIV negative. All 23 HIV-positive patients received highly active antiretroviral therapy, and additional experimental therapies were not associated with a better clinical outcome.. Marked neurological improvement occurred in 4/24 (17%) of patients, while 11/24 (46%) had partial improvement and 9/24 (37%) remained stable. By the end of the period of observation, 8/24 (33%) of patients had no significant disability despite persistent symptoms (modified ...
This study will identify genetic factors associated with the development of progressive multifocal leukoencephalopathy (PML) in patients with acquired immunodeficiency syndrome (AIDS). PML is a life-threatening infection of the brain that affects about 5 percent of untreated patients with AIDS. Its symptoms include mental deterioration, vision loss, speech disturbances, ataxia (inability to coordinate movements), paralysis, and coma. PML is caused by a polyomavirus called the JC virus.. It is estimated that up to 80 percent of the human population has been exposed to the JC virus, but the disease is very rare. The virus only becomes active in people who have compromised immune systems, such as those undergoing immune suppressive chemotherapy for cancer and those with damaged immune systems due to HIV.. Patients who have participated in the Multicenter AIDS Cohort Study may be eligible for this study, as well as healthy normal volunteers who will serve as controls. The study will review clinical ...
This study will identify genetic factors associated with the development of progressive multifocal leukoencephalopathy (PML) in patients with acquired immunodeficiency syndrome (AIDS). PML is a life-threatening infection of the brain that affects about 5 percent of untreated patients with AIDS. Its symptoms include mental deterioration, vision loss, speech disturbances, ataxia (inability to coordinate movements), paralysis, and coma. PML is caused by a polyomavirus called the JC virus.. It is estimated that up to 80 percent of the human population has been exposed to the JC virus, but the disease is very rare. The virus only becomes active in people who have compromised immune systems, such as those undergoing immune suppressive chemotherapy for cancer and those with damaged immune systems due to HIV.. Patients who have participated in the Multicenter AIDS Cohort Study may be eligible for this study, as well as healthy normal volunteers who will serve as controls. The study will review clinical ...
Progressive multifocal leukoencephalopathy (PML) is a frequently fatal demyelinating condition of the central nervous system in which reactivation of the human polyomavir..
Progressive multifocal leukoencephalopathy (PML) is a neurological disorder that damages the myelin that covers and protects nerves in the white matter of the brain. It is caused by the JC virus (JCV). By age 10, most people have been infected with this virus, but it rarely causes symptoms unless the immune system becomes severely weakened. The disease occurs, rarely, in organ transplant patients; people undergoing chronic corticosteroid or immunosuppressive therapy; and individuals with cancer, such as HodgkinÕs disease, lymphoma, and sarcoidosis. PML is most common among individuals with acquired immune deficiency syndrome (AIDS ...
Natalizumab provides rapid and high-efficacy control of multiple sclerosis disease activity with long-term stabilization. However, the benefits of the drug are countered by a risk of developing progressive multifocal leukoencephalopathy in patients infected with the John Cunningham Virus. Close monitoring is required in patients with increased progressive multifocal leukoencephalopathy risk receiving natalizumab in the long-term for an optimal benefit-risk evaluation. Standardized high-quality monitoring procedures may provide a superior basis for individual benefit and risk evaluation and thus improve treatment decisions. The non-interventional study TRUST was designed to capture natalizumab effectiveness under real-life conditions and to examine alternate approaches for clinical assessments, magnetic resonance imaging monitoring and use of biomarkers for progressive multifocal leukoencephalopathy risk stratification. TRUST is a non-interventional, multicenter, prospective cohort study conducted at
INTRODUCTION. Progressive multifocal leukoencephalopathy (PML) is a disease of the central nervous system (CNS) caused by the virus JC and characterized by lytic infection of the oligodendrocytes and demyelination10, tipically occuring in the context of severe immunodepression. After the advent of the HIV epidemic, acquired immunodeficiency syndrome (AIDS) became the most common predisposing disorder for PML1. This disease has been diagnosed in up to 5% of HIV-infected patients in developed countries in the pre highly active antiretroviral therapy (HAART) era10. However, the incidence of PML has decreased less dramatically when compared to other CNS diseases in the HAART era6,21. Interestingly, PML has rarely been reported in HIV-infected patients from developing countries8,11,12. The objectives of this study were to describe the clinical and radiological features of patients with PML and estimate its frequency among AIDS patients with CNS opportunistic diseases admitted in a referral center in ...
Madelungs disease - progressive, excessive, and symmetrical deposition of adipose tissue in the subcutaneous layer: case report and literature review Monika Szewc,1 Robert Sitarz,1-3 Nina Moroz,2 Ryszard Maciejewski,1,* Ryszard Wierzbicki2,4,* 1Department of Human Anatomy, Medical University of Lublin, Lublin, Poland; 2Department of Surgery with Trauma, Orthopaedic and Urological Subunit, Independent Public Health Care Center of the Ministry of Interior and Administration in Lublin, Lublin, Poland; 3Department of Surgery, St Johns Cancer Center, Lublin, Poland; 4Department of Surgical Oncology, Medical University of Lublin, Lublin, Poland *These authors contributed equally to this work Abstract: Madelungs disease is a rare disorder described for the first time in the year 1846 by Brodie. It is characterized by the occurrence of progressive, excessive, and symmetrical deposits of adipose tissue in the subcutaneous layer. Most often, these changes concern the neck, the nape of the neck, arms, and upper
Author(s): Berger, Joseph R; Cree, Bruce A; Greenberg, Benjamin; Hemmer, Bernhard; Ward, Brian J; Dong, Victor M; Merschhemke, Martin | Abstract: OBJECTIVE:We describe the characteristics of the 15 patients with fingolimod-associated progressive multifocal leukoencephalopathy (PML) identified from the Novartis data safety base and provide risk estimates for the disorder. METHODS:The Novartis safety database was searched for PML cases with a data lock point of August 31, 2017. PML classification was based on previously published criteria. The risk and incidence were estimated using the 15 patients with confirmed PML and the overall population of patients treated with fingolimod. RESULTS:As of August 31, 2017, 15 fingolimod-treated patients had developed PML in the absence of natalizumab treatment in the preceding 6 months. Eleven (73%) were women and the mean age was 53 years (median: 53 years). Fourteen of the 15 patients were treated with fingolimod for >2 years. Two patients had confounding medical
Progressive multifocal leukoencephalopathy is a demyelinating disease ( AIDS defining illness) which affect the brain. Patient may complain with vision and speech abnormalities and alteration of the mental function.Patient may fall into coma and death.
Progressive multifocal leukoencephalopathy (PML) answers are found in the Johns Hopkins HIV Guide powered by Unbound Medicine. Available for iPhone, iPad, Android, and Web.
Progressive Multifocal Leukoencephalopathy (PML) - Learn about the causes, symptoms, diagnosis & treatment from the Merck Manuals - Medical Consumer Version.
AIDS generated a significantly increased interest in the pathogenesis, clinical manifestations, and treatment of progressive multifocal leukoencephalopathy (PML), a disease previously considered to be very rare. Scrutiny increased after a second wave of PML following the introduction of biological a …
Progressive Multifocal Leukoencephalopathy, also known as PML, is a neurological disorder that affects the cells that produce myelin (better known as the white matter of the brain), the substance that envelops the neurons.
Diagnosis of progressive multifocal leukoencephalopathy relies on assessing the white matter of the brain on a computed tomography scan or a magnetic resonance imaging (MRI).
Progressive Multifocal Leukoencephalopathy - Pipeline Insight, 2017 is a market research report available at US $1250 for a Single User PDF License from RnR Market Research Reports Library.
Learn more about Progressive Multifocal Leukoencephalopathy at Blake Medical Center DefinitionCausesRisk FactorsSymptomsDiagnosisTreatmentPreventionrevision ...
LIMA, Marcus Aurelho de; ANDRADE, Fabiana Valente de; ETCHEBEHERE, Renata Margarida and SILVA-VERGARA, Mario León. Progressive multifocal leukoencephalopathy as initial manifestation of acquired immunodeficiency syndrome. Rev. Soc. Bras. Med. Trop. [online]. 1998, vol.31, n.6, pp.569-574. ISSN 0037-8682. http://dx.doi.org/10.1590/S0037-86821998000600011.. This is a report of a man with acquired immunodeficiency syndrome (AIDS) who presented acutely ill with severe progressive multifocal leukoencephalopathy (PML) as the first manifestation of AIDS. PML was diagnosed in the brain after gross and microscopical examination as well as by immunohistochemistry with an antibody against JC virus.. Keywords : Progressive multifocal leukoencephalopathy; Acquired immunodeficiency syndrome; Central nervous system; JC virus. ...
Author Summary Progressive multifocal leukoencephalopathy (PML) is a complication of treatment with natalizumab in patients with multiple sclerosis (MS) and Crohns disease. PML results from a failure of the immune system to control replication of JC virus (JCV) in the brain. We studied the T cell responses of 8 patients with MS who were starting treatment with natalizumab, 10 healthy volunteers, and 4 patients with natalizumab-associated PML. The magnitude and quality of JCV-specific immune responses remained unchanged after starting natalizumab. However, applying the same methods and antigens, we found that immune responses in the individuals who developed PML differed from those in the MS patients and healthy volunteers. In the four patients with PML from whom the laboratory had identified JCV DNA in the cerebrospinal fluid (CSF), two had no measurable T cell response to JCV and two had T cells that produced IL-10, an anti-inflammatory mediator. Furthermore, we studied the CSF of 10 patients with
We previously showed that, in addition to human glial cells, JCV could infect tonsillar lymphocytes and stromal cells in vitro (29). The anatomical location of tonsils and the susceptibility of lymphocytes and stromal cells, both of which are present in tonsils, to JCV infection make it plausible that JCV infection can occur via a respiratory route. We used n-PCR amplification to determine whether DNA from nondissected tonsillar tissue, isolated tonsillar lymphocytes, and isolated stromal cells of healthy individuals contained JCV-specific nucleotide sequences. Of 54 tonsils from immunocompetent children and adult donors, 19 (35%) were positive for the JCV T-protein sequences and 21 (39%) were positive for the regulatory-region sequences. We also showed by n-PCR amplification that DNA of isolated tonsillar lymphocytes and stromal cells contained JCV-specific T-protein and regulatory-region sequences (Table 1). The lower percentage of n-PCR products found in tonsillar stromal cells could be ...
JC viral infection normally tends to take place during early childhood; however, this archetype remains asymptomatic taking sanctuary in the kidneys and B. lymphocytes throughout later years [5]. The JC virus belongs to the Polyomaviridae family of viruses and is closely related to four other polyomaviruses: BKV, WUV, KIV, and MCV. The degree of homology (69-75%) between the JC viral genome and that of the simian virus 40 and BK virus confirms the close evolutionary relationship of these three polyoma viruses [5]. Theses viruses biologically differ with respect to the extent of divergence pertaining to the promoter-enhancer sequences [5]. The JC virus has a closed, circular genome containing double stranded ...
Perinuclear clearing, or haloes, is a typical feature of oligodendrogliomas, but it can also decorate the cells of astrocytomas. In such cases, nuclear pleomorphism and irregularity favor astrocytic differentiation. By definition, necrosis and endothelial proliferation are absent. According to WHO grading, a single mitotic figure is not sufficient to raise the grade of an infiltrating astrocytoma to grade III. This practice is based on a large series by Giannini et al. who found no significant difference in survival between ordinary grade II lesions and those that showed a single mitotic figure [14]. Progressive multifocal leukoencephalopathy in 47 HIV-seropositive patients: neuroimaging with clinical and pathologic correlation. Radiology. 1993; 187(1):233-40. 65. , Incidence and outcome of progressive multifocal leukoencephalopathy over 20 years of the Swiss HIV Cohort Study. Clin Infect Dis. 2009;48(10):1459-66. 66. , Determinants of survival in progressive multifocal leukoencephalopathy. ...
A 40-year-old woman (patient 3) had an 8-year history of SLE, along with leukocytopenia and a lupus profundus on her face and arms. She developed dysarthria, left-side hemiplegia, and a disturbance of consciousness; she had been taking 10 mg/day of prednisolone. An MRI examination revealed a low-intensity area on T1-weighted images and a high-intensity area on T2-weighted images in the right front parietal and left parietal white matter (Figure 1B). A PCR analysis of a CSF sample detected a PML-type JC virus DNA, confirming the diagnosis. Despite 4 times monthly administration of 250 mg of cidofovir, her neurologic findings worsened to those of a vegetative state. She died 20 months after the onset of her neurologic symptoms.. In all 3 patients, a CSF examination showed normal numbers of cells and normal levels of protein and glucose. The IgG index and albumin index were not elevated. Serologic testing for HIV yielded negative results. The patients were negative for antiphospholipid antibodies, ...
In immunocompromised individuals, JC polyomavirus (JCPyV) may mutate and gain access to the central nervous system resulting in progressive multifocal leukoencephalopathy (PML), an often fatal opportunistic infection for which no treatments are currently available. Despite recent progress, the contribution of JCPyV-specific humoral immunity to controlling asymptomatic infection throughout life and to eliminating JCPyV from the brain is poorly understood. We examined antibody responses against JCPyV major capsid protein VP1 (viral protein 1) variants in the serum and cerebrospinal fluid (CSF) of healthy donors (HDs), JCPyV-positive multiple sclerosis patients treated with the anti-VLA-4 monoclonal antibody natalizumab (NAT), and patients with NAT-associated PML. Before and during PML, CSF antibody responses against JCPyV VP1 variants show recognition holes; however, upon immune reconstitution, CSF antibody titers rise, then recognize PML-associated JCPyV VP1 variants, and may be involved in ...
As per American Academy of Neurology diagnostic criteria, definite PML is a symptomatic disease confirmed by MRI and the detection of JCV DNA in CSF.3 This view is challenged by the application of MRI as a screening tool for early detection of PML. These patients can show localised disease on MRI (not multifocal as the acronym PML may imply), and a majority is asymptomatic. Furthermore, in our study half of the patients had negative JCV DNA findings in CSF at time of first MRI suspicion of PML. Importantly, if JCV DNA remains undetectable and brain biopsy is not performed, such cases classify as possible or not PML, despite the strong MRI suspicion of PML. Consequently, these cases will not appear in PML statistics of confirmed cases, and consecutive management decisions (eg, plasma exchange in case of PML; continuation/switch of immune suppression in case of MS relapse) may be challenging. Our data suggests that detection of an intrathecal IgG antibody response towards JCV (positive AIJCV) ...
Abstract Following the development of progressive multifocal leukoencephalopathy (PML) in two multiple sclerosis (MS) patients treated with natalizumab and interferon-beta (IFNbeta), a possible correlation between JC virus (JCV), the etiological agent of PML, and MS has received heightened interest. In particular, attention has focused on assessing whether IFNbeta treatment could affect the replication of JCV and thus its frequency in the peripheral blood of MS patients and whether the presence of JCV DNA in peripheral blood could be a predictive marker of the risk of developing PML. In order to answer to these questions, peripheral blood samples were collected from 59 INFbeta-treated, 39 untreated relapsing-remitting MS patients, and 98 healthy controls (HCs) and JCV DNA levels were determined and quantified by means of a real-time polymerase chain reaction (Q-PCR) assay. Overall, no differences were found in the presence or viral load of JCV DNA of MS patients and the HCs, but JCV DNA was ...
進行性多發性腦白質病變、人類多瘤性病毒、血清抗JC 病毒抗體、Progressive multifocal leukoencephalopathy、Human polyomavirus、Levamisole ...
As published in the New England Journal of Medicine, positive results have been seen in a small study of pembrolizumab (Keytruda; Merck, Kenilworth, NJ) for treatment of progressive multifocal le…
Alemtuzumab is a highly efficacious therapy used in the treatment of multiple sclerosis (MS), but uncoupling of T and B cell repopulation during immune reconstitution associates with an increasing range of secondary B cell-mediated autoimmune complications. A 34-year-old woman developed Graves disease 11 months following an initial course of alemtuzumab treatment for MS. Nine months following the second treatment with alemtuzumab, the patient presented with spontaneous intramuscular and subcutaneous haemorrhage due to development of an inhibitory autoantibody to coagulation factor VIII. Acquired haemophilia A (AHA) is an extremely rare complication in patients treated with alemtuzumab. Treatment with rituximab may induce a rapid remission of AHA; however, the patients high John Cunningham virus (JCV) antibody index and alemtuzumab-induced T cell lymphopenia may lead to an increased risk of progressive multifocal leucoencephalopathy, a potential complication which was unacceptable to the ...
How long do I need to take natalizumab (Tysabri). Tysabri is designed to be taken as maintenance treatment to treat and prevent flares of Crohns disease. But the longer you are on Tysabri, the greater the risk of developing progressive multifocal leukoencephalopathy (PML), a rare brain disorder caused by the activation of the polyomavirus JC virus in people with suppressed immune systems.. You and your care team will need to weigh the risks and benefits of long-term use of Tysabri.. Taking probiotics while Pregnant. Women planning to become pregnant should discuss their treatment options with their care team in clinic. It is generally advised that you continue with maintenance treatment throughout pregnancy. An uncontrolled flare can be harmful to the fetus and increase the risk of miscarriage.. Yet the safety data on the use of natalizumab (Tysabri) during pregnancy and breastfeeding is limited.. A Tysabri pregnancy registry has been established to monitor maternal-fetal outcomes of pregnant ...

No data available that match "jc virus"

  • The JC virus or John Cunningham virus is a type of human polyomavirus (formerly known as papovavirus ). (wikipedia.org)
  • The JC virus, or John Cunningham virus, is a germ so common that the majority of adults have been exposed to it. (webmd.com)
  • If you have multiple sclerosis (MS), you need to know about the John Cunningham (JC) virus. (everydayhealth.com)
  • John Cunningham or JC virus (JCV) is a non-enveloped, double-stranded DNA virus that, following primary infection, undergoes latency in tonsillar tissue, renal tubular cells, bone marrow, or the brain. (aacc.org)
  • A mutation in a mouse model of the John Cunningham (JC) virus, which causes progressive multifocal leukoencephalopathy (PML), allows the virus to evade the host immune responses in people with multiple sclerosis (MS), according to a study into the mechanisms of PML. (thisisms.com)
  • JC virus, or John Cunningham polyomavirus, infects between 50 and 70 percent of the human population, most often during early childhood or adolescence. (psu.edu)
  • John Cunningham (JC) virus is a (RNA/DNA) polyomavirus that causes progressive multifocal leukoencephalopathy in HIV patients. (osmosis.org)
  • The cause of progressive multifocal leukoencephalopathy is the John Cunningham virus, or simply JC virus , named after the first patient in whom the virus was identified. (osmosis.org)
  • JC virus (JCV) is a DNA polyomavirus discovered in 1971, isolated from patient John Cunningham. (hopkinsguides.com)
  • The virus was named after the patient from whom the virus was initially cultivated, John Cunningham. (kartalozelders.com)
  • The John Cunningham virus, known more commonly as the JC virus, is a very common virus in the United States. (kartalozelders.com)
  • It is caused by reactivation of the John Cunningham virus (JCV) and infection of glial cells. (kartalozelders.com)
  • Human polyomavirus 2, commonly referred to as the JC virus or John Cunningham virus, is a type of human polyomavirus (formerly known as papovavirus). (kartalozelders.com)
  • JC virus granule cell neuronopathy results from the reactivation of the John Cunningham virus (JC virus) , infecting granule cell neurons in the cerebellum, in patients with compromised immune systems. (radiopaedia.org)
  • John Cunningham virus (JCV)is a type of human polyomavirus . (bvsalud.org)
  • Aetna considers polymerase chain reaction (PCR) testing of cerebrospinal fluid for John Cunningham (JC) polyomavirus, for diagnosis of progressive multifocal leukoencephalopathy in persons before initiating natalizumab treatment not medically necessary. (aetna.com)
  • Genomic sequences of the human polyomaviruses, JC virus (JCV) and BK virus (BKV), and simian virus 40 (SV40) have been reported from several types of human brain tumors, but there have been no population-based seroepidemiologic studies to evaluate the association between polyomavirus infection and brain tumors. (aacrjournals.org)
  • Knowles, "Discovery and epidemiology of the human polyomaviruses BK virus (BKV) and JC virus (JCV)," Advances in Experimental Medicine and Biology, vol. (thefreedictionary.com)
  • Taken together with well-established evidence that SV40, as well as the human polyomaviruses JC virus (JCV) and BK virus (BKV), are oncogenic in several animal models, new interest has resurfaced regarding a possible role for these viruses in human tumors. (elsevier.com)
  • Sequential changes in the non-coding control region sequences of JC polyomaviruses from the cerebrospinal fluid of patients with progressive multifocal leukoencephalopathy. (cdc.gov)
  • The item Malaria and some polyomaviruses (SV40, BK, JC, and merkel cell viruses), (electronic resource) represents a specific, individual, material embodiment of a distinct intellectual or artistic creation found in University of Missouri-St. Louis Libraries . (umsl.edu)
  • This Volume of the IARC Monographs provides evaluations of malaria (a disease caused by infection with Plasmodium parasites) and four polyomaviruses--simian virus 40 (SV40), and BK, JC and Merkel cell viruses. (umsl.edu)
  • METHODS: A pair of primers (JC1 and JC2) were designed to be complementary to the early and late regions of JC and BK polyomaviruses, respectively. (ox.ac.uk)
  • Polyomaviruses are a group of small DNA viruses, which have long been studied as a model for eukaryotic DNA replication. (springer.com)
  • Polyomaviruses including JCV, and BKV are prevalent small and non-enveloped viruses that contain a 5Kb circular double-stranded DNA genome (Pinto and Dobson 2014 ). (exeley.com)
  • People who have antibodies to the JC virus and take certain MS medications are at higher risk of a serious brain infection. (everydayhealth.com)
  • In the age range when most people tend to develop MS - typically young- to middle adulthood - somewhere around 58 percent of the population has antiviral antibodies to the JC virus in their blood, Cortese says, indicating exposure to the virus. (everydayhealth.com)
  • Up to 80% of humans express serum antibodies to JC virus (JCV), yet considerably fewer people develop PML--predominantly those under. (ebscohost.com)
  • 50% of adults have been exposed to JCV and will be positive for IgG-class antibodies to this virus (Eur J Neurol 2014;21:299-304), even though the vast majority will never experience any symptoms. (aacc.org)
  • STRATIFY JCV allows neurologists to determine their MS patients' anti-JCV antibody status and is the first blood test to be FDA authorized for the qualitative detection of antibodies to the polyomavirus JC virus. (fiercebiotech.com)
  • The infection generally occurs during childhood, with specific antibodies to the virus developing subsequent to infection ( 23 , 37 , 39 ). (asm.org)
  • Anti-JC virus antibodies: implications for PML risk stratification. (semanticscholar.org)
  • A new assay for serum antibodies to JC virus (indicating past exposure) may prove to be a guide to PML risk. (thefreedictionary.com)
  • Recent publications indicate 39 [3] to 58% [4] of the general population are seropositive for antibodies to JCV, indicating current or previous infection with the virus. (wikipedia.org)
  • Risk of natalizumab-related progressive multifocal leukoencephalopathy is associated with the presence of anti-JC-virus (JCV) antibodies. (blogspot.com)
  • A map of the genome of JC virus, indicating the position of the tumor antigen genes (red), the three capsid protein genes (green and blue), the agnogene (yellow), and the non-coding control region (NCCR). (wikipedia.org)
  • Human polyomavirus JC virus genome. (semanticscholar.org)
  • A two-year grant from the PML Consortium awarded to scientists in the Eberly College of Science aims to unravel sequence variations within the JC virus genome that could case the development of a rare fatal brain disease. (psu.edu)
  • In collaboration with Vivek Nerurkar's lab at the University of Hawaii, Frisque will use the $314,000 grant to investigate three forms of sequence variation identified in the JC virus genome, which are hypothesized to contribute to the pathogenic potential of this human virus. (psu.edu)
  • JC virus is a non-enveloped virus with closed circular double-stranded DNA genome. (osmosis.org)
  • Some of these may already have been present within the initial virus, and others may be coded for by the viral genome for production within the host cell. (thefreedictionary.com)
  • Viral architecture is very complex, but every virus contains at least a genome and a capsid. (tabers.com)
  • The 400 known viruses are classified in several ways: by genome core (RNA or DNA), host (animals, plants, or bacteria), method of reproduction (such as retrovirus), mode of transmission (such as enterovirus), and disease produced (such as hepatitis virus). (tabers.com)
  • Sensitivity was estimated by titration of a plasmid containing JC virus genome. (ox.ac.uk)
  • 2009. Simian virus 40 large T antigen disrupts genome integrity and activates a DNA damage response via Bub1 binding. (springer.com)
  • The presence of JC virus, which results in p53 protein accumulation, was also examined. (biomedcentral.com)
  • Light microscopy was carried out to correlate the presence of JC virus DNA with the selective infection of oligodendrocytes and astrocytes in PML. (elsevier.com)
  • Presence of JC virus-specific CTL in the cerebrospinal fluid of PML patients: rationale for immune-based therapeutic strategies. (rush.edu)
  • In urine from 29 LUTS cases and 9 controls from Wisconsin, we found a statistically significant association between a diagnosis of LUTS and the presence of JC virus (JCV), a common neurotropic human polyomavirus (Polyomaviridae, Betapolyomavirus) linked to severe neurologic disease in rare cases. (elsevier.com)
  • A correction to the article "Asymptomatic Reactivation of JC Virus in Patients Treated with Natalizumab," which appeared in the September 10, 2009 issue is presented. (ebscohost.com)
  • Unfortunately, an unanticipated side effect of these drugs has been the reactivation of JC virus in the patient, resulting in the appearance of the rare, fatal brain disease progressive multifocal leukoencephalopathy (PML). (psu.edu)
  • Progressive multifocal leukoencephalopathy (PML) is caused by reactivation of JC virus (JCV) infection. (beds.ac.uk)
  • Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease caused by human neurotropic JC virus. (grantome.com)
  • JC virus remains latent in the host, and in profoundly immunosuppressed patients, JC virus can cause PML, a fatal disease associated with neurotropic JC virus that lytically infects oligodendrocytes. (clinicaltrials.gov)
  • In people with very weak immune systems, the virus can bring on a serious brain infection called progressive multifocal leukoencephalopathy (PML). (webmd.com)
  • JC virus (JCV) seropositivity is a risk factor for progressive multifocal leukoencephalopathy (PML) in patients on natalizumab. (nih.gov)
  • Although polyomavirus JC (JCV) is the proven pathogen of progressive multifocal leukoencephalopathy, the fatal demyelinating disease, this virus is ubiquitous as a usually harmless symbiote among human beings. (pnas.org)
  • The polyomavirus JC (JCV), the proven pathogen of the fatal demyelinating disease known as progressive multifocal leukoencephalopathy (PML) ( 1 ), is ubiquitous in human beings, infecting children asymptomatically ( 2 , 3 ). (pnas.org)
  • The JC virus is a virus which infects the brain of advanced cancer patients and causes PML-- progressive multifocal leukoencephalopathy. (thebody.com)
  • Critical role of JC virus-specific CD4 T-cell responses in preventing progressive multifocal leukoencephalopathy. (nih.gov)
  • The human neurotropic polyomavirus JC (JCV) causes the fatal CNS demyelinating disease progressive multifocal leukoencephalopathy (PML). (ebscohost.com)
  • Traffic of JC Virus from Sites of Initial Infection to the Brain: The Path to Progressive Multifocal Leukoencephalopathy. (ebscohost.com)
  • Progressive multifocal leukoencephalopathy (PML) is a demyelinating disorder of the human brain caused by infection with the human polyomavirus, JC. (ebscohost.com)
  • Although infection with JCV is typically mild or subclinical in immunocompetent patients, reactivation of latent virus may result in progressive multifocal leukoencephalopathy (PML) in patients who are immunocompromised (such as AIDS patients) or taking immune-modulating therapy. (aacc.org)
  • Citation Query JC virus load in progressive multifocal leukoencephalopathy: analysis of the correlation between the viral burden in cerebrospinal fluid, patient survival, and the volume of neurological lesions. (psu.edu)
  • Progressive multifocal leukoencephalopathy is a demyelinating disease of the human central nervous system that results from lytic infection of oligodendrocytes by the polyomavirus JC (JCV). (asm.org)
  • Stoner, G. L. 1997-04-01 00:00:00 The central demyelinating disease progressive multifocal leukoencephalopathy (PML) is caused by the human polyomavirus JC virus (JCV). (deepdyve.com)
  • JC Virus is the cause of progressive multifocal leukoencephalopathy (PML), a severe demyelinating disease of the central nervous system. (specialtylabs.com)
  • MRI brain showed characteristic appearances of progressive multifocal leukoencephalopathy (PML), confirmed by detection of the JC virus in CSF, despite the absence of any evidence of immunosuppression. (readbyqxmd.com)
  • Using the technique of in situ DNA‐to‐DNA hybridization, a JC virus biotinylated DNA probe was developed and applied to formalin‐fixed, paraffin‐embedded, or fixed, frozen sections of brain tissue from three subjects with progressive multifocal leukoencephalopathy (PML). (elsevier.com)
  • In a retrospective review of data from 168 patients with suspected progressive multifocal leukoencephalopathy (PML) between 1996 and 2006, JC virus (JCV) PCR on cerebrospinal fluid (CSF) samples was positive only in human immunodeficiency virus (HIV)-infected patients with low CD4 cell counts and in severely immunocompromised patients with radiographic lesions consistent with PML or infectious processes generally. (microbiologyresearch.org)
  • Progressive multifocal leukoencephalopathy associated with human immunodeficiency virus infection. (microbiologyresearch.org)
  • JC virus DNA load in patients with and without progressive multifocal leukoencephalopathy. (microbiologyresearch.org)
  • Reduced rate of diagnostic positive detection of JC virus DNA in cerebrospinal fluid in cases of suspected progressive multifocal leukoencephalopathy in the era of potent antiretroviral therapy. (microbiologyresearch.org)
  • The human polyomavirus JC (JCV) infects glial cells and causes progressive multifocal leukoencephalopathy (PML), a demyelinating disease of the brain, in immunosuppressed individuals. (northwestern.edu)
  • If a patient becomes immunosuppressed, especially during AIDS, reactivated JC virus can infect lymphocytes, be carried to the brain, infect oligodendroglia glial cells, and produce a demyelinating disease called progressive multifocal leukoencephalopathy . (med-life.net)
  • While up to 51% of patients with progressive multifocal leukoencephalopathy (PML) show infection of granule cells by JC virus on autopsy, GCN is thought to be a distinct entity caused by mutation in the VP1 gene of the JC virus leading to a shift in viral tropism from glial cells to cerebellar granule cells [ 1 ]. (biomedcentral.com)
  • JC virus granule cell neuronopathy is considered a rare manifestation of JC virus reactivation, thought to be much less common than progressive multifocal leukoencephalopathy 1-4 . (radiopaedia.org)
  • There is conjecture whether these white matter changes are truly due to JC virus granule cell neuronopathy, or due to concurrent infratentorial progressive multifocal leukoencephalopathy 1-3 . (radiopaedia.org)
  • Regardless, supratentorial white matter involvement, on the other hand, is not a feature of JC virus granule cell neuronopathy, and its involvement may be due to other manifestations of the JC virus such as progressive multifocal leukoencephalopathy or immune reconstitution inflammatory syndrome , which are known to manifest concurrently with JC virus granule cell neuronopathy 1-3 . (radiopaedia.org)
  • Progressive multifocal leukoencephalopathy and other disorders caused by JC virus: clinical features and pathogenesis. (radiopaedia.org)
  • 4. Brew BJ, Davies NW, Cinque P, Clifford DB, Nath A. Progressive multifocal leukoencephalopathy and other forms of JC virus disease. (radiopaedia.org)
  • Progressive multifocal leukoencephalopathy (PML) is a rare but fatal demyelinating disease of the central nervous system (CNS) caused by JC virus (JCV). (cdc.gov)
  • High-resolution melting analysis for mutation scanning in the non-coding control region of JC polyomavirus from patients with progressive multifocal leukoencephalopathy. (cdc.gov)
  • Analysis of PCR as a tool for detection of JC virus DNA in cerebrospinal fluid for diagnosis of progressive multifocal leukoencephalopathy. (cdc.gov)
  • Patients undergoing immune modulatory therapies for the treatment of autoimmune diseases such as multiple sclerosis, and individuals with an impaired-immune system, most notably AIDS patients, are in the high risk group of developing progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease of the white matter caused by human neurotropic polyomavirus, JC virus. (grantome.com)
  • Treatment with natalizumab in patients with multiple sclerosis (MS) appears linked with JC virus (JCV) infection, which can lead to a rare and often fatal demyelinating disease of the central nervous system called progressive multifocal leukoencephalopathy (PML) that destroys the myelin that protects nerve cells. (liberationtreatmentccsvi.com)
  • Progressive multifocal leukoencephalopathy is a rare, highly fatal demyelinating brain infection caused by the JC virus. (redorbit.com)
  • The purpose of this study is to identify host genetic factors that contribute to the development of Progressive Multifocal Leukoencephalopathy (PML) associated with JC virus. (clinicaltrials.gov)
  • The human polyomavirus JC virus is the etiologic agent of the fatal disease demyelinating progressive multifocal leukoencephalopathy. (elsevier.com)
  • The human polyomavirus JC virus (JCV) is the causative agent of the fatal demyelinating disease progressive multifocal leukoencephalopathy (PML), which is commonly seen in AIDS patients. (nntc.org)
  • Natalizumab is a new and efficient treatment for multiple sclerosis (MS). The risk of developing progressive multifocal leukoencephalopathy (PML) during the use of this drug has created the need for better comprehension of JC virus (JCV) infection . (bvsalud.org)
  • In the last several years, studies have reported the detection of sequences similar to the polyomavirus, Simian Virus 40 (SV40) in human tumors including choroid plexus papillomas and ependymomas. (elsevier.com)
  • JCV is genetically closely related to BK and SV40 viruses. (hopkinsguides.com)
  • Polymerase chain reaction on cerebrospinal fluid for diagnosis of virus-associated opportunistic diseases of the central nervous system in HIV-infected patients. (microbiologyresearch.org)
  • Central nervous system (e.g., meningitis and encephalitis): For diagnosis of meningitis, cerebrospinal fluid (CSF) and serum, as well as stool or throat swabs, can be collected because viruses are sometimes shed into these sites. (issuu.com)
  • In order to identify natalizumab-treated patients at risk of developing PML, we assayed for anti-JC virus (JCV) antibody levels in cerebrospinal fluid (CSF). (tischms.org)
  • It results when JC virus infects oligodendrocytes, cells that insulate nerve cells with myelin. (everydayhealth.com)
  • PML occurs when immune control of persistent infection with JCPyV fails, the virus mutates and changes its cellular tropism, enters the brain and infects astrocytes, oligodendrocytes and, in particular cases, also neurones. (readbyqxmd.com)
  • The virus reactivates under immunomodulatory conditions with an unknown mechanism, resulting in productive infection of oligodendrocytes and astrocytes in the central nervous system (CNS). (grantome.com)
  • We are now engaged in a number of studies designed to determine how infection of oligodendrocytes with JC virus leads to the death of these cells and demyelination of neurons. (tufts.edu)
  • For about 30 percent of those who are exposed to JC virus, it will remain latent in their kidneys, notes Dr. Major. (everydayhealth.com)
  • T/F: Most people are infected by 15 years of age via respiratory and latent viruses can be reactivated under suppressed imunity ( prenancy, AIDS, organ transplant). (quizlet.com)
  • So to be clear, the virus is not eliminated, but instead it remains latent in the kidneys, meaning that it isn't dividing and causing disease. (osmosis.org)
  • Most people with a healthy immune system are able to keep JC virus in the latent phase in the kidney epithelial cells for their entire life. (osmosis.org)
  • The JC virus localizes to and remains latent in the kidney, from whence it occasionally may reactivate. (med-life.net)
  • Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. (thefreedictionary.com)
  • Viruses are also responsible for the common cold, childhood exanthems (such as chickenpox, measles, rubella), latent infections (such as herpes simplex), some cancers or lymphomas (such as Epstein-Barr virus), and diseases of all organ systems. (tabers.com)
  • Timeline: Polyoma virus middle T antigen and its role in identifying cancer-related molecules. (ebscohost.com)
  • Virus-specific CD4(+) T cells play a central role in control of viral pathogens including JC polyoma virus (JCV) infection. (uzh.ch)
  • The JC virus belongs to the polyoma virus group of the papovavirus family, which are double-stranded DNA viruses without an envelope. (med-life.net)
  • BK virus is also in the polyoma virus group. (med-life.net)
  • 2013. A cornucopia of human polyoma-viruses. (springer.com)
  • Although JC virus infection is classically associated with white matter demyelination and PML pathogenesis, recent literature has identified viral variants as etiological agents of other novel syndromes. (wikipedia.org)
  • Findings in this study do not support the hypothesis that vascular endothelial replication is important in the pathogenesis of JC virus-induced PML. (elsevier.com)
  • Owing to the lack of both animal models, and sufficient in vitro models to sustain effective replication of JCPyV, the mechanisms of JC virus infection remain largely uncertain and current understanding in pathogenesis is obtained from human autopsy material. (uu.nl)
  • [3] Certain transcription factors present in the early promoter sequences of the JC virus can induce trophism and viral proliferation that leads to PML. (wikipedia.org)
  • [10] The protein encoded by these early sequences, T-antigen, also plays a key role in viral proliferation, [11] directing the initiation of DNA replication for the virus as well as performing a transcriptional switch to allow for the formation of the various capsid and regulatory proteins needed for viral fitness. (wikipedia.org)
  • Using a cut-off of 5% allele fraction for junctional reads, 7 different rearrangements were present in the JC virus sequences present in the WHO standard across multiple library preparations and sequencing runs. (physiciansweekly.com)
  • Differences in regulatory sequences of naturally occurring JC virus variants. (semanticscholar.org)
  • Persistence of DNA sequences of BK virus and JC virus in normal human tissues and in diseased tissues. (semanticscholar.org)
  • JC viral sequences were analyzed in DNA extracted from 33 frozen medulloblastoma and PNET samples using quantitative polymerase chain reaction. (biomedcentral.com)
  • JC virus T-Ag DNA sequences were found in 77% of CRCs and are associated with promoter methylation of multiple genes. (beds.ac.uk)
  • BK virus (BKV), together with JC virus and simian virus 40, are members of the genus polyomavirus (Polyomaviridae family). (thefreedictionary.com)
  • hepatitis viruses B and C are associated with hepatocellular carcinoma (Monto and Wright 2001 ), Simian virus 40 has been linked to mesothelioma (Rizzo et al. (beds.ac.uk)
  • 2011. Comparisons between murine polyomavirus and Simian virus 40 show significant differences in small t antigen function. (springer.com)
  • 2010. Multiple DNA damage signaling and repair pathways deregulated by Simian virus 40 large T antigen. (springer.com)
  • 1994. T-antigen kinase inhibits simian virus 40 DNA replication by phospho-rylation of intact T antigen on serines 120 and 123. (springer.com)
  • 2003. Simian virus 40 infection of humans. (springer.com)
  • 2013. Replication stress and mitotic dysfunction in cells expressing simian virus 40 large T antigen. (springer.com)
  • PCR detection of JC virus DNA in the brain tissue of a 9-year-old child with pleomorphic xanthoastrocytoma. (thefreedictionary.com)
  • Detection of JC virus DNA in peripheral blood cell subpopulations of HIV-1-infected individuals. (rush.edu)
  • Comparison of JC virus antibody status in serum versus JC virus DNA status in urine. (nih.gov)
  • People excrete the virus in their urine, and there can be traces of it in sewage, so there is speculation that it gets transmitted through contaminated water, but that has not been established either, says Cortese. (everydayhealth.com)
  • You can usually see JC in urine. (quizlet.com)
  • JC virus in saliva, oropharyngeal flui bloo and urine samples obtained from. (ket-rt.ru)
  • JC virus is spread via the urine-oral route. (kartalozelders.com)
  • BK virus (BKV) belongs to the human Polyomaviridae, initially isolated from urine sample of a 29-year-old male patient with renal blockage and failure at 1971. (kartalozelders.com)
  • One report applied a homemade nucleic acid probe with PCR amplification to urine of JC virus patients and obtained an excellent detection rate. (med-life.net)
  • JC polyomavirus (JCV) is ubiquitous in humans, persisting in renal tissue and excreting progeny in urine. (microbiologyresearch.org)
  • Skin infections: Rash site and, depending on the virus, serum and urine b. (issuu.com)
  • We investigated whether the presence of infectious agents in urine might be associated with LUTS by combining next-generation DNA sequencing for virus discovery, microbiome analysis for characterization of bacterial communities, and mass spectrometry-based metabolomics. (elsevier.com)
  • Reactivation of the JC virus can cause progressive multifocal. (ket-rt.ru)
  • Progressive Multifocal Leukoencephalopthy (PML) is an often-fatal demyelinating disease of the central nervous system that is caused by the JC polyomavirus (JCV). (tufts.edu)
  • Multiple Sclerosis Trust: "JC virus. (webmd.com)
  • Nearly one-half of Brazilian patients with multiple sclerosis using natalizumab are DNA-JC virus positive. (bvsalud.org)
  • JCV is a ubiquitous small DNA virus that leads to persistent infection of humans with no clinical consequences. (uzh.ch)
  • The level of combinatorial diversity in TCR- and HLA-peptide interactions used by brain-infiltrating, JCV-specific CD4(+) T cells has not, to our knowledge, been reported before in humans for other viral infections and confirms the exceptional plasticity that characterizes virus-specific immune responses. (uzh.ch)
  • Since most humans are infected with JCV and BKV, these data indicate that the ingestion of contaminated water or food could represent a possible portal of entrance of these viruses or polyomavirus DNA into the human population. (kartalozelders.com)
  • Merkel cell virus was discovered in 2008 in a rare skin cancer in humans. (umsl.edu)
  • The virus is harmless to macaques or may cause only a herpetic rash in macaques, but in humans it often produces fatal infections of the brain and meninges. (tabers.com)
  • Natalizumab, to the best of my knowledge, does not affect the humoral or antibody responses to viruses. (blogspot.com)
  • JC virus (JCV) is ubiquitous among the general population. (nih.gov)
  • The ubiquitous human polyomavirus JC (JCV) is a small double-stranded DNA virus that establishes a persistent infection, and it is often transmitted from parents to children. (ed.ac.uk)
  • JC virus is a small ubiquitous human DNA polyomavirus that causes asymptomatic primary infection in up to 86% of the general population. (kartalozelders.com)
  • Prevalence of polyomavirus BK and JC infection and replication in 400 healthy blood donors. (semanticscholar.org)
  • Because these properties are shared by certain bacteria ( rickettsiae , chlamydiae ), viruses are now characterized by their simple organization and their unique mode of replication. (thefreedictionary.com)
  • In the context of antirejection treatment, viral replication and progression toward disease are related to patient, virus, and graft determinants. (hindawi.com)
  • Presence of nucleic acid or antigen in semen does not represent the presence of replication-competent or infection-competent virus, which can generally only be demonstrated by isolation and culture of virus. (cdc.gov)
  • Furthermore, we reported that G144 cells support robust levels of JCV DNA replication and infection by JC virus. (tufts.edu)
  • Viruses are obligate intracellular parasites that subvert cellular metabolism and pathways to mediate their own replication-normally at the expense of the host cell. (springer.com)
  • A definition of the term "papovavirus," which refers to any of a group of viruses, many of which are encogenic, that are important in viral carcinogenesis, is presented. (ebscohost.com)
  • The Jc Virus Antibody Positivity reagent is RUO (Research Use Only) to test human serum or cell culture lab samples. (crossfirebeilstein.com)
  • Because of its capacity to cause demyelination in the central nervous system and multiply chiefly in human glial cells in culture, JCV was considered strictly a neurotropic virus. (asm.org)
  • It has been postulated that for the JC virus to preferentially infect granule cell neurons instead of glial cells, there must be a mutation, typically involving the C terminus of the VP1 gene, that triggers this change 6 . (radiopaedia.org)
  • To investigate whether chromatin structure controls glial cell-specific expression of JC virus early genes, glial and nonglial cells were transfected with a reporter plasmid containing the JC virus early promoter and then treated with the histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate. (elsevier.com)
  • TSA and butyrate induced 20- to 30-fold activation of the JC virus promoter in nonglial cells, whereas less than 2-fold induction was observed in glial cells. (elsevier.com)
  • A definition of the term "polyomavirus" which refers to a double-stranded deoxyribonucleic acid (DNA) virus causing kidney, nerve and lymphoid disease in people is presented. (ebscohost.com)
  • Granule cell neuronopathy (GCN) is a rare disease caused by the JC virus, leading to degeneration of cerebellar granule cell neurons. (biomedcentral.com)
  • Granule cell neuronopathy (GCN) is a rare disease caused by the JC virus that is characterized by lytic infection of cerebellar granule cell neurons. (biomedcentral.com)
  • JC virus granule cell neuronopathy is secondary to progressive infection of granule cell neurons in the cerebellum due to the reactivation of the JC virus 1-4 . (radiopaedia.org)
  • There is derangement of the normal laminar cellular organization of cerebellum, with the hallmark histological feature of JC virus granule cell neuronopathy being infection and loss of granule cell neurons in the internal granule cell layer, with sparing of the molecular and Perkinje layers 1,3 . (radiopaedia.org)
  • There is currently (as of March 2019) no disease-specific therapy available for JC virus granule cell neuronopathy, and management is therefore supportive. (radiopaedia.org)
  • Heterogeneous imaging characteristics of JC virus granule cell neuronopathy (GCN): a case series and review of the literature. (radiopaedia.org)
  • 2. Henry C, Jouan F, De Broucker T. JC virus granule cell neuronopathy: A cause of infectious cerebellar degeneration. (radiopaedia.org)
  • JC polyomavirus granule cell neuronopathy in a patient treated with rituximab. (radiopaedia.org)
  • In situ hybridization with biotinylated JC virus probe may be useful in the diagnosis of PML on brain biopsy specimens. (elsevier.com)
  • Diagnosis by in situ hybridization with a biotinylated JC virus DNA probe using an automated Histomatic Code-On slide stainer. (duke.edu)
  • Previous studies by other authors have established that in situ hybridization with a biotinylated JC virus DNA probe can be a valuable diagnostic adjunct because it identifies the virally infected cells with great specificity and does not depend on the larger specimen, which may be necessary for a firm histological diagnosis. (duke.edu)
  • [14] This syndrome, called JCV granule cell layer neuronopathy (JCV GCN), is characterized by a productive and lytic infection by a JC variant with a mutation in the VP1 coding region. (wikipedia.org)
  • [2] The virus causes PML and other diseases only in cases of immunodeficiency , as in AIDS or during treatment with drugs intended to induce a state of immunosuppression (e.g. organ transplant patients). (wikipedia.org)
  • The JCV virus may also be a causative agent of aseptic meningitis (JCVM), as JCV was the only pathogen identified in the CSF of certain patients with meningitis. (wikipedia.org)
  • Sequence rearrangement in JC virus DNAs molecularly cloned from immunosuppressed renal transplant patients. (asm.org)
  • However, JCV infection has also been described in lymphoid cells of PML patients ( 21 ), in peripheral blood lymphocytes from patients with and without PML ( 5 , 36 ), and in peripheral blood lymphocytes from human immunodeficiency virus-infected patients ( 13 ) and from immunocompetent individuals ( 12 ). (asm.org)
  • Polyomavirus belongs to Papovaviridae, among which, BC virus (BCV) and JC virus (JCV) can induce diseases.1,2 It has been reported that,3 patients who undergo renal transplant usually have weak immune function, which improves possibility of polyomavirus infection. (thefreedictionary.com)
  • Richard Frisque , professor of molecular virology and the lead investigator on the grant, is studying the connections between these treatments and the development of JC virus-induced PML: "We are investigating why this one particular disease caused by this one particular virus is suddenly being activated in patients receiving therapies for unrelated illnesses. (psu.edu)
  • In HIV-positive patients without PML, however, JC virus DNA was detected. (ket-rt.ru)
  • Here, we describe the clinical and pathologic findings in 7 patients with biopsy-proven JC-PVN. (elsevier.com)
  • Two early presenting patients were treated for acute rejection just before acquiring JC-PVN. (elsevier.com)
  • We use positvie or negative JCV serostatus to assess whether or not our patients are infected with the virus. (blogspot.com)
  • The JCV + -cell subpopulations in HIV + patients included B, T, NK and NKT cells, with a JC viral load ranging from 2-1080 copies/ug DNA, while HIV - patients had JCV in the same subpopulations, as well as PMN and monocytes, with a viral load ranging from 2-250 copies/ug DNA. (beds.ac.uk)
  • The study will review clinical information from patients and analyze genetic factors from both patients and control subjects to investigate genes associated with AIDS and JC virus infection. (clinicaltrials.gov)
  • JC virus is one of many opportunistic infections that arise in AIDS patients. (clinicaltrials.gov)
  • These observations unravel a new pathway for the molecular interaction of these two viruses in biologically relevant cells in the brains of AIDS/PML patients. (nntc.org)
  • To confirm and extend these findings, we have used a commercially available biotinylated JC virus DNA probe to demonstrate the presence of viral DNA in formalin-fixed, paraffin-embedded tissues from four open biopsies, four needle biopsies, and two autopsies of patients with PML. (duke.edu)
  • Genotypes of JC virus in East, Central and Southwest Europe. (semanticscholar.org)
  • Distinctive genotypes of JC virus have been described for the major continental landmasses. (semanticscholar.org)
  • Four geographically distinct genotypes of JC virus are prevalent in China and Mongolia: implications for the racial composition of modern China. (microbiologyresearch.org)
  • Five major genotypes of JC virus (JCV) have been defined based on nucleotide differences in the VP1 gene of the DNA sequence. (nih.gov)
  • The virus was first discovered in 1971, when a doctor found it in the brain of a man with Hodgkin's lymphoma and named the virus after him. (webmd.com)
  • This development occurs when the immune system is suppressed and JC virus can cause an opportunistic infection , Cortese explains. (everydayhealth.com)
  • In people who are treated with Tysabri for two years who are antibody positive to JC virus and have a history of prior immune suppression treatments, the risk is now 1 in 75. (everydayhealth.com)
  • Infections are usually asymptomatic, with most people unaware they have the virus unless their immune system is compromised by a disease or disease treatment. (psu.edu)
  • The JC virus can be activated when a person's immune system is compromised because of disease or immunosuppressive medication. (ket-rt.ru)
  • JC virus enters these kidney cells and starts replicating, but the cytotoxic CD8+ T cells of our immune system keep the virus in check by killing any cell that has replicating JV virus. (osmosis.org)
  • It is caused by the JC virus , which is normally present and kept under control by the immune system. (wikipedia.org)
  • The JC virus is harmless except in cases of weakened immune systems. (wikipedia.org)
  • The virus causes disease only when the immune system has been severely weakened. (wikipedia.org)
  • Some people who are JCV seropositive may not be infected with the virus, i.e. their immune systems have cleared the JC virus, and therefore may not be at risk of developing PML in the future. (blogspot.com)
  • On the other hand in people with a high index, or an increasing index, or in those who become seropositive with a high index, the virus must be stimulating their immune systems to produce antibody. (blogspot.com)
  • If you go onto treatments that interfere with the immune system, particularly immunosuppressive drugs, then the immune response to the JC virus cannot be used to assess risk. (blogspot.com)
  • This complex interaction is modulated by the net balance of immunosuppression and its impact on virus-specific immune response. (hindawi.com)
  • The virus only becomes active in people who have compromised immune systems, such as those undergoing immune suppressive chemotherapy for cancer and those with damaged immune systems due to HIV. (clinicaltrials.gov)
  • Viruses with lipid envelopes have a greater ability to adhere to cell membranes and to avoid destruction by the immune system. (tabers.com)
  • Induction of Siglec-G by RNA viruses inhibits the innate immune response by promoting RIG-I degradation. (nature.com)
  • When a complete virus particle ( virion ) comes in contact with a host cell, only the viral nucleic acid and, in some viruses, a few enzymes are injected into the host cell. (thefreedictionary.com)
  • 5. The classification of viruses is based on nucleic acid type, size and shape of virion, and presence or absence of an envelope. (issuu.com)
  • These results indicate that the JC virus early promoter might be highly suppressed in nonglial cells by hypoacetylated chromatin and activated by hyperacetylation. (elsevier.com)
  • The cause of PML is a type of polyomavirus called the JC virus (JCV), after the initials of the person from whose tissue the virus was first successfully cultured. (wikipedia.org)
  • PML is caused by a polyomavirus called the JC virus. (clinicaltrials.gov)
  • The "tumor antigen" (T antigen), a nonstructural protein expressed by the viruses, is responsible for cell transformation in animal models. (aacrjournals.org)
  • No JC virus was identified in the embryonal brain tumor samples, while an endogenous human retrovirus (ERV-3) was readily detected. (biomedcentral.com)
  • It is thought that these differences in promoter sequence contribute to the fitness of the virus in the CNS and thus to the development of PML. (wikipedia.org)
  • The complete DNA sequence of the human JC virus, which was found to consist of 5,130 nucleotide pairs, is presented. (semanticscholar.org)
  • MS Drug Tied to Rising JC Virus Antibody Levels. (ket-rt.ru)
  • The sensitivity of the system was 25 copies of JC plasmid per 10 microliters of digested tissue. (ox.ac.uk)
  • Understanding the underlying mechanisms that lead a normally harmless virus to morph into an opportunistic pathogen capable of killing its host represents an initial step in combating PML. (psu.edu)
  • [8] JC viral DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue. (wikipedia.org)
  • American Journal of Neuroradiology: "JC Virus Infection of the Brain. (webmd.com)
  • Recently his doctor discovered his right brain has shadow and think it's JC virus (or disease:PML). (thebody.com)
  • For the JC virus to reach the brain and lead to PML, it likely requires a multistep process, Cortese says, adding that it's likely some genetic rearrangements occur that allow the virus to gain access to the central nervous system. (everydayhealth.com)
  • Although the JC virus can be detected by PCR in CSF, the definitive diagnosis should be made by detecting JC virus DNA or antigens in a brain biopsy. (thefreedictionary.com)
  • The virus may break down the protective coating of nerve cells, damaging the white matter of the brain. (kartalozelders.com)
  • Detection of reactivation and size variation in the regulatory region of JC virus in brain tissue. (ox.ac.uk)
  • CONCLUSIONS: Variation in the regulatory region of JC virus can be specifically and sensitively detected from routinely processed, paraffin wax embedded brain tissue. (ox.ac.uk)
  • Moreover, a possible association between JC virus and human brain and non-central system tumors has also been reported. (tufts.edu)
  • Immunohistochemical analysis of brain tissue from subjects with AIDS/PML revealed colocalization of the human immunodeficiency virus type 1 (HIV-1) transactivator, Tat, and JCV agnoprotein in nucleus and cytoplasm of "bizarre" astrocytes. (nntc.org)
  • Once inside living cells, viruses induce the host cell to synthesize virus particles. (issuu.com)
  • Like other viruses, chronic infection with JCV may induce CRC by different mechanisms which should be further investigated. (beds.ac.uk)
  • The mechanisms responsible for the malignant transformation in cases of long-lasting viral infection differ according to the particular virus and cancer and have been extensively studied. (beds.ac.uk)
  • Quantification of JC virus DNA is based upon real-time PCR amplification and detection of JCV genomic DNA. (specialtylabs.com)
  • However, JC virus infection is not responsible for increased levels of p53 protein. (biomedcentral.com)
  • A virus consists of genetic material, which may be either DNA or RNA, and is surrounded by a protein coat and, in some viruses, by a membranous envelope. (thefreedictionary.com)
  • ABBR: AAV A genus in the parvovirus family whose members cannot replicate without the presence of another virus. (tabers.com)
  • [12] Several studies since 2000 have suggested that the virus is also linked to colorectal cancer , as JCV has been found in malignant colon tumors, but these findings are still controversial. (wikipedia.org)
  • Some studies have linked the virus to human colorectal cancer, but this concept remains controversial. (hopkinsguides.com)
  • The association of these viruses with colorectal cancers remains controversial. (exeley.com)
  • This test is intended to be used as an aid to the diagnosis of infections caused by JC virus. (labcorp.com)
  • A serological investigation of BK virus and JC virus infections in recipients of renal allografts. (thefreedictionary.com)
  • Hemorrhagic cystitis results from damage to the bladder's transitional epithelium and blood vessels by toxins, viruses, radiation, drugs (in particular, chemotherapeutic drugs), bacterial infections, or other disease processes. (medscape.com)
  • American Association for Clinical Chemistry: "JC Virus: What Is It, and How Should I Test for It? (webmd.com)
  • Clinical Laboratory News // All CLN Articles // JC Virus: What Is It, and How Should I Test for IT? (aacc.org)
  • We performed next-generation sequencing to gain single-nucleotide resolution and relative copy number of JC virus (JCV) clinical standards. (physiciansweekly.com)
  • The herpes simplex virus and enterovirus by polymerase chain reaction (PCR) testing were also negative. (redorbit.com)
  • AIMS: To develop a sensitive and specific polymerase chain reaction (PCR) based system for detecting genomic variation in JC virus. (ox.ac.uk)
  • For indications for PCR testing for JC polyomavirus, see CPB 0650 - Polymerase Chain Reaction - Selected Indications . (aetna.com)

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