JC Virus: 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.Leukoencephalopathy, Progressive Multifocal: 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)BK Virus: 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.Polyomavirus Infections: 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).Tumor Virus Infections: 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.Polyomavirus: 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.RNA Viruses: Viruses whose genetic material is RNA.Simian virus 40: A species of POLYOMAVIRUS originally isolated from Rhesus monkey kidney tissue. It produces malignancy in human and newborn hamster kidney cell cultures.Antigens, Viral, Tumor: 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.DNA, Viral: Deoxyribonucleic acid that makes up the genetic material of viruses.Virus Replication: 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.Vaccinia virus: 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.Receptors, 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.Virus Cultivation: Process of growing viruses in live animals, plants, or cultured cells.Virus Shedding: 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).Virus Activation: 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.Virus Diseases: A general term for diseases produced by viruses.Antigens, Polyomavirus Transforming: 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.Virus Assembly: The assembly of VIRAL STRUCTURAL PROTEINS and nucleic acid (VIRAL DNA or VIRAL RNA) to form a VIRUS PARTICLE.Polyomaviridae: A family of small, non-enveloped DNA viruses, infecting mainly MAMMALS, and containing a single genus: POLYOMAVIRUS.Neuroglia: 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.Plant Viruses: Viruses parasitic on plants higher than bacteria.Genes, Viral: The functional hereditary units of VIRUSES.DNA Viruses: Viruses whose nucleic acid is DNA.Gene Expression Regulation, Viral: Any of the processes by which cytoplasmic factors influence the differential control of gene action in viruses.Defective 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.Sindbis 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.Measles virus: The type species of MORBILLIVIRUS and the cause of the highly infectious human disease MEASLES, which affects mostly children.Influenza A Virus, H1N1 Subtype: 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.Capsid Proteins: Proteins that form the CAPSID of VIRUSES.Molecular Sequence Data: 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.Antigens, Viral: Substances elaborated by viruses that have antigenic activity.Rabies virus: 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.Influenza A Virus, H5N1 Subtype: 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.Viral Proteins: Proteins found in any species of virus.NFI Transcription Factors: 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.RNA, Viral: Ribonucleic acid that makes up the genetic material of viruses.Virus Latency: 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.Viral Regulatory and Accessory Proteins: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Influenza A Virus, H3N2 Subtype: 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.Hepatitis B virus: 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.Polymerase Chain Reaction: 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.West Nile virus: 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.Virion: 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.Respiratory Syncytial Viruses: 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.Urine: Liquid by-product of excretion produced in the kidneys, temporarily stored in the bladder until discharge through the URETHRA.Y-Box-Binding Protein 1: 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.Capsid: The outer protein protective shell of a virus, which protects the viral nucleic acid.Vesicular stomatitis Indiana virus: 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.Cerebrospinal Fluid: 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.Antiviral Agents: 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.Hemagglutinin Glycoproteins, Influenza Virus: 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.Phylogeny: The relationships of groups of organisms as reflected by their genetic makeup.Oncogenic Viruses: Viruses that produce tumors.Vero Cells: A CELL LINE derived from the kidney of the African green (vervet) monkey, (CERCOPITHECUS AETHIOPS) used primarily in virus replication studies and plaque assays.Simian immunodeficiency virus: 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.Cercopithecus aethiops: 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.Antibodies, Viral: Immunoglobulins produced in response to VIRAL ANTIGENS.Mumps virus: The type species of RUBULAVIRUS that causes an acute infectious disease in humans, affecting mainly children. Transmission occurs by droplet infection.Parainfluenza Virus 1, Human: A species of RESPIROVIRUS also called hemadsorption virus 2 (HA2), which causes laryngotracheitis in humans, especially children.Mosaic Viruses: 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)

  • 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)
  • 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)
  • The protein encoded by these early sequences, T-antigen, also plays a key role in viral proliferation, 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)
  • More than 500 diagnostic specimens derived from 16 different pediatric cancer entities including solid tumors, leukemias and lymphomas were screened by highly sensitive and specific real-time quantitative PCR assays targeting important viral domains such as the large T-antigen, small T-antigen and virus protein 1. (clinmedjournals.org)
  • The vast majority of tumors investigated revealed negative findings, with only anecdotal presence of JC virus large/small T-antigen in individual cases of acute myeloid leukemia (1/30) and oligodendroglioma (1/30). (clinmedjournals.org)
  • Here the application of a virus concentration method based on skimmed milk organic flocculation (SMF) using 10L of sewage collected in different seasons enabled the detection of many viruses. (readbyqxmd.com)
  • As opposed to viral persistence as a putative source of oncogenic hits, the frequent detection of SV40 in brain tumors and other malignancies like Wilms'tumor, Ewing sarcoma, osteosarcoma or lymphoma was generally linked to the use of virus-contaminated polio vaccines several decades ago [13- . (clinmedjournals.org)
  • The presence of BKV was documented in urothelial carcinoma, and the virus was suggested to play a contributory role in the pathogenesis of neuroblastoma [6, 9, . (clinmedjournals.org)
  • In this review, we will discuss the effects of the interaction between large T antigen and Rb proteins in JC virus-mediated oncogenesis. (unisi.it)
  • Further research is needed to determine the exact etiological role of T-antigen, but there seems to be a connection to the early initiation of the active virus from its archetypal dormant state. (wikipedia.org)
  • 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)
  • JC viral DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue. (wikipedia.org)
  • 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)
  • The brain apparently serves as a sanctuary for the persistence of different viruses including JCV, and several studies reported the presence of viral sequences in various brain tumors [7, 11, . (clinmedjournals.org)
  • In contrast to studies describing the presence of BKV, JCV or SV40 in various tumors, other reports did not reveal any evidence for these viruses in brain tumors, other solid tumors or hematologic malignancies [17- . (clinmedjournals.org)
  • 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)
  • 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 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)
  • Multiple Sclerosis Trust: "JC virus. (webmd.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)
  • JC viral DNA can be detected in both non-PML affected and PML-affected (see below) brain tissue. (wikipedia.org)
  • 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)
  • The protein encoded by these early sequences, T-antigen, also plays a key role in viral proliferation, 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)
  • 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)
  • 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)
  • JC viral sequences were analyzed in DNA extracted from 33 frozen medulloblastoma and PNET samples using quantitative polymerase chain reaction. (biomedcentral.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)
  • Within the host cell the genetic material of a DNA virus is replicated and transcribed into messenger RNA by host cell enzymes, and proteins coded for by viral genes are synthesized by host cell ribosomes. (thefreedictionary.com)
  • 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)
  • Because host cells do not have the ability to replicate "viral RNA" but are able to transcribe messenger RNA, RNA viruses must contain enzymes to produce genetic material for new virions. (thefreedictionary.com)
  • For certain viruses the RNA is replicated by a viral enzyme ( transcriptase ) contained in the virion, or produced by the host cell using the viral RNA as a messenger. (thefreedictionary.com)
  • In other viruses a reverse transcriptase contained in the virion transcribes the genetic message on the viral RNA into DNA, which is then replicated by the host cell. (thefreedictionary.com)
  • In viruses that have membranes, membrane-bound viral proteins are synthesized by the host cell and move, like host cell membrane proteins, to the cell surface. (thefreedictionary.com)
  • In the context of antirejection treatment, viral replication and progression toward disease are related to patient, virus, and graft determinants. (hindawi.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)
  • Recent viral studies indicate two major groups found in the Japanese population: a group with the CY genotype JC virus (JCV) and a group with the MY genotype JCV. (biomedcentral.com)
  • 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)
  • Viral architecture is very complex, but every virus contains at least a genome and a capsid. (tabers.com)
  • 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)
  • The interaction between early viral antigens and cell cycle regulators represents an important mechanism through which viruses deregulate cell cycle and lead to cell transformation. (unisi.it)
  • Each SV40 strain was derived from an independent isolate of the virus, and DNA sequence polymorphisms in genetically stable regions of the viral genome outside of the viral regulatory region were used to distinguish strains (7,8). (bioscience.org)
  • The cover image shows a JC virus-infected oligodendrocyte stained for oligodendrocyte marker O4 (red), phospho-p53 (Ser15) (green), and viral T antigen (blue). (jci.org)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Although BK and JC viruses are latent in the kidney and may become reactivated in immunosuppressed individuals, only JC virus has been shown to infect the central nervous system. (thefreedictionary.com)
  • The JC virus localizes to and remains latent in the kidney, from whence it occasionally may reactivate. (med-life.net)
  • 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)
  • Sequence rearrangement in JC virus DNAs molecularly cloned from immunosuppressed renal transplant patients. (asm.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)
  • three distinct viruses can be distinguished based on DNA sequence analysis and clinical studies, and these three viruses are designated BFDV 1 3 (10). (bioscience.org)
  • American Association for Clinical Chemistry: "JC Virus: What Is It, and How Should I Test for It? (webmd.com)
  • JC virus in experimental and clinical brain tumors. (thefreedictionary.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)
  • 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)
  • 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)
  • With the advent of commercially available JC virus DNA probes and an automated system for hybridization histochemistry, this technology for diagnosis of PML may enter the routine diagnostic surgical pathology laboratory. (duke.edu)
  • 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)
  • 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)
  • JC virus is found in tonsils, so at one time experts thought it used an oral route, but it is not generally found in saliva or respiratory secretions. (everydayhealth.com)
  • The common influenza viruses have antigens that mutate or combine readily, requiring new vaccines with each mutation. (tabers.com)