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Human herpesvirus 6 (HHV-6A and HHV-6B) can cause primary infection or reactivate from latency in liver transplant recipients, which can result in a variety of clinical syndromes, including fever, hepatitis, encephalitis and higher rates of graft dysfunction as well as indirect effects including increased risks of mortality, CMV disease, hepatitis C progression and greater fibrosis scores. Although HHV-6 infection is currently diagnosed by quantifying viral DNA in plasma or blood, biopsy to demonstrate histopathological effects of HHV-6 remains the gold standard for diagnosis of end-organ disease. HHV-6 reactivation may be restricted to the infected organ with no evidence of active infection in the blood. Read More ...
In conclusion, owls eyes and humans eyes are both mainly the same except for some differences such as owls not having good binocular vision and that human eyes and owl eyes are not shaped the same. However, similarities such as the layout of the inside of both eyes being the same and that humans and owls both have binocular vision. All in all, humans and owls eyes are mostly the same, except for some little differences ...
The various methods used for the diagnosis of HHV-6 include PCR, serology, viral culture, in situ hybridization, and immunohistochemistry. Since HHV-6 has the ability to persist and establish latency, the problem arises that diagnostic tests must be able to distinguish active viral replication from latent infection. Reverse transcription-PCR assays have been developed to detect the presence of viral mRNA, which constitutes a marker for active infection (44). The detection of immunoglobulin M or immunoglobulin G antibodies to HHV-6 in serum or CSF does not discriminate between active infection and latent/chronic persistent infection. The same is true for the detection of HHV-6 DNA by PCR in peripheral blood mononuclear cells (PBMCs), the site where the virus establishes latency. In these cases, HHV-6 DNA can be detected by PCR in PBMCs at low levels (9). Viral culture is a difficult and time-consuming process and is not routinely used in clinical laboratories to detect virus in CSF specimens. ...
Human herpesvirus 6B (HHV-6B) is a DNA virus that infects most children within the first few years of life. After primary infection, HHV-6B persists as a chronic, latent infection in many cell types. Additionally, HHV-6B can integrate into germ line chromosomes, resulting in individuals with viral DNA in every nucleated cell. Given that PCR to detect viral DNA is the mainstay for diagnosing HHV-6B infection, the characteristics of HHV-... ...
Researchers from Childrens National Medical Center have found that an alternate, escape replication process triggered by apoptosis-the process of cell death or cell suicide-appears to be common in human herpesviruses ...
Got my latest test results back and, after 2 months on 1800 mg valcyte per day, my hhv-6 titer is the same, 1:320. So, anyone got any ideas? I just...
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Read "Genetic content of a 20.9 kb segment of human herpesvirus 6B strain Z29 spanning the homologs of human herpesvirus 6A genes U40-57 and containing the origin of DNA replication, Archives of Virology" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
Roseolovirus is a genus of viruses in the order Herpesvirales, in the family Herpesviridae, in the subfamily Betaherpesvirinae. Humans serve as natural hosts. There are currently three species in this genus including the type species Human herpesvirus 6A. Diseases associated with this genus include: HHV-6: sixth disease (roseola infantum, exanthem subitum); HHV-7: symptoms analog to the sixth disease. Viruses in Roseolovirus are enveloped, with icosahedral, spherical to pleomorphic, and round geometries, and T=16 symmetry. The diameter is around 150-200 nm. Genomes are linear and non-segmented, around 200kb in length. Viral replication is nuclear, and is lysogenic. Entry into the host cell is achieved by attachment of the viral glycoproteins to host receptors, which mediates endocytosis. Replication follows the dsDNA bidirectional replication model. DNA-templated transcription, with some alternative splicing mechanism, is the method of transcription. The virus exits the host cell by nuclear ...
TY - JOUR. T1 - Chromosomally integrated human herpesvirus 6 in the Japanese population. AU - Miura, Hiroki. AU - Kawamura, Yoshiki. AU - Hattori, Fumihiko. AU - Kozawa, Kei. AU - Ihira, Masaru. AU - Ohye, Tamae. AU - Kurahashi, Hiroki. AU - Yoshikawa, Tetsushi. PY - 2018/10. Y1 - 2018/10. N2 - The objectives of the work are to elucidate the incidence and virological findings of chromosomally integrated human herpesvirus 6 (ciHHV-6) in Japanese population and to analyze an association between ciHHV-6 and the clinical manifestation of exanthema subitum (ES). Real-time polymerase chain reaction was performed to determine HHV-6 DNA loads in 2347 cord blood samples from healthy neonates (cohort A), febrile children less than 5 years old (cohort B), and hematopoietic cell transplant recipients (cohort C). CiHHV-6 was confirmed by detection of high copy numbers of viral DNA in somatic cells. The integration site was determined by fluorescent in situ hybridization analysis. In the ciHHV-6 subjects of ...
Infections with human herpesvirus 6 (HHV-6), a ß-herpesvirus of which two variant groups (A and B) are recognized, is very common, approaching 100% in seroprevalence. Primary infection with HHV-6B causes roseola infantum or exanthem subitum, a common childhood disease that resolves spontaneously. After primary infection, the virus replicates in the salivary glands and is shed in saliva, the recognized route of transmission for variant B strains; it remains latent in lymphocytes and monocytes and persists at low levels in cells and tissues. Not usually associated with disease in the immunocompetent, HHV-6 infection is a major cause of opportunistic viral infections in the immunosuppressed, typically AIDS patients and transplant recipients, in whom HHV-6 infection/reactivation may culminate in rejection of transplanted organs and death. Other opportunistic viruses, human cytomegalovirus and HHV-7, also infect or reactivate in persons at risk. Another disease whose pathogenesis may be correlated with
Human herpesvirus (HHV) 6 and 7 are involved in the pathogenesis of pityriasis rosea (PR). Our aim was to evaluate the role of the innate immune response in PR through the detection of Toll-like receptors (TLR) 2, 3, 4, 7, 8, and 9 expression in the skin of affected patients and to detect the possibility of being induced by HHV-6 and/or HHV-7 viral coexistence in these patients. Twenty-four patients with PR and 24 healthy controls were included in this case-control study. Biopsy was obtained from the PR lesion and from the healthy skin of controls for detection of HHV-6 and 7 as well as TLRs 2, 3, 4, 7, 8, and 9 gene expression using real-time polymerase chain reaction (PCR ...
Human herpesvirus 6 (HHV-6) belongs to the subfamily Betaherpesvirinae (30), which is represented by Human cytomegalovirus (HCMV). Both HHV-6 and HCMV establish latency in the monocyte/macrophage lineage (9, 17-19, 25, 33, 38), and during latent infection HHV-6 and HCMV express latency-associated transcripts that show similar features: (i) both transcripts contain open reading frames (ORFs) encoding immediate-early proteins IE1 and IE2 (20, 21) and (ii) both transcripts are expressed in a small proportion of latently infected cells (19, 20, 32). The function and expression profile of these transcripts have been unknown (24, 39).. In the present study, we first developed a sensitive method to detect the latency-associated transcripts of HHV-6 (H6LTs). Because productive-phase IE1 and IE2 transcripts share their entire sequences with H6LTs (Fig. 1), we previously used the 5′ rapid amplification of cDNA ends (RACE) method to distinguish H6LTs from IE1 and IE2 transcripts (20). To increase the ...
Human herpesvirus 6 (HHV-6) was the sixth herpesvirus discovered. Isolated in 1986 during attempts to find novel viruses in patients with lymphoproliferative diseases, HHV-6 is now recognized as a T-cell lymphotropic virus with high affinity for CD4 lymphocytes.
ID L46634; SV 1; linear; genomic DNA; STD; VRL; 1272 BP. XX AC L46634; L46689; XX DT 06-NOV-1995 (Rel. 45, Created) DT 04-MAR-2000 (Rel. 63, Last updated, Version 3) XX DE Human herpesvirus 7 (clone ED1321.2) telomeric repeat region. XX KW telomeric repeat. XX OS Human herpesvirus 7 OC Viruses; dsDNA viruses, no RNA stage; Herpesvirales; Herpesviridae; OC Betaherpesvirinae; Roseolovirus. XX RN [1] RP 1-1272 RX PUBMED; 7494318. RA Secchiero P., Nicholas J., Deng H., Xiaopeng T., van Loon N., Ruvolo V.R., RA Berneman Z.N., Reitz M.S.Jr., Dewhurst S.; RT "Identification of human telomeric repeat motifs at the genome termini of RT human herpesvirus 7: structural analysis and heterogeneity"; RL J. Virol. 69(12):8041-8045(1995). XX FH Key Location/Qualifiers FH FT source 1..1272 FT /organism="Human herpesvirus 7" FT /strain="JI" FT /mol_type="genomic DNA" FT /clone="ED1321.2" FT /db_xref="taxon:10372" FT repeat_region 207..928 FT /note="long and complex repeat region composed of various FT direct ...
Herpesviruses 6, 7, and 8 are the most recently described members of the human herpesvirus family. Like other herpesviruses, they have the ability to establish a latent or persistent infection following primary infection, and reactivation may occur in healthy and immunocompromised people in response to different stimuli. A variety of methods are available or under development for the laboratory diagnosis of each virus, including viral isolation in cell culture, demonstration of viral antigens or nucleic acids in body fluids or tissues, and serology for detection of virus-specific antibodies. This chapter focuses on the immunologic and molecular diagnosis and monitoring of infections with human herpesvirus 6 (HHV-6), HHV-7, and HHV-8, and provides information on the unique features of the epidemiology and biological and clinical characteristics of these viruses.
Professional antigen presenting cells (APC), i.e., dendritic cells, monocytes/macrophages, and B lymphocytes, are critically important in the recognition of an invading pathogen and presentation of antigens to the T cell-mediated arm of immunity. Human herpesvirus 8 (HHV-8) is one of the few human viruses that primarily targets these APC for infection, altering their cytokine profiles, manipulating their surface expression of MHC molecules and altering their ability to activate HHV-8 specific T cells. This could be why T cell responses to HHV-8 antigens are not very robust. Of these APC, only B cells support complete, lytic HHV-8 infection. However, both complete and abortive virus replication cycles in APC could directly affect viral pathogenesis and progression to Kaposis sarcoma (KS) and HHV-8 associated B cell cancers. In this review, we discuss the effects of HHV-8 infection on professional APC and their relationship to the development of KS and B cell lymphomas.
Human herpesvirus 6 (HHV-6) was the sixth herpesvirus discovered. Isolated in 1986 during attempts to find novel viruses in patients with lymphoproliferative diseases, HHV-6 is now recognized as a T-cell lymphotropic virus with high affinity for CD4 lymphocytes.
Human herpesvirus 6 (HHV-6) has recently been identified as the agent associated with both pediatric and adult infections. Most children have been infected by age three. The acute infection in children is characterized clinically by an acute febrile il
Main description: This comprehensive account of the human herpesviruses provides an encyclopedic overview of their basic virology and clinical manifestations. This group of viruses includes human simplex type 1 and 2, Epstein-Barr virus, Kaposis Sarcoma-associated herpesvirus, cytomegalovirus, HHV6A, 6B and 7, and varicella-zoster virus. The viral diseases and cancers they cause are significant and often recurrent. Their prevalence in the developed world accounts for a major burden of disease, and as a result there is a great deal of research into the pathophysiology of infection and immunobiology. Another important area covered within this volume concerns antiviral therapy and the development of vaccines. All these aspects are covered in depth, both scientifically and in terms of clinical guidelines for patient care. The text is illustrated generously throughout and is fully referenced to the latest research and developments.. ...
Progressive multifocal leukoencephalopathy (PML), a fatal demyelinating disease caused by JC virus (JCV), occurs mainly in immunocompromised patients. While JCV DNA is detected in the cerebrospinal fluid (CSF) from a certain proportion of patients suspected of having PML, JCV-negative patients may also develop brain lesions due to other infectious agents. This study assessed the prevalence of six herpesviruses in the CSF from patients diagnosed with or suspected of PML. Two hundred and ninety-nine CSF specimens and clinical data were collected from 255 patients, including 31 confirmed PML cases. Quantitative PCR assays were carried out to detect the genomic DNA of JCV, herpes simplex virus (HSV), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus 6 (HHV-6). Herpesvirus DNAs were detected in the CSF specimens from 29 of 255 patients (11.4%). HSV-1 and CMV were detected in JCV-negative patients, whereas VZV and EBV were detected in both CSF JCV-positive
HHV-8 | Information on Human herpesvirus 8 (Kaposis sarcoma-associate herpes virus) incliuding symptoms, diagnosis, transmission, and treatment.
Integration of the complete human herpesvirus 6 (HHV-6) genome into the telomere of a chromosome has been reported in some individuals (inherited chromosomally integrated HHV-6; iciHHV-6). Since the proportion of iciHHV-6-positive individuals with integration in chromosome 22 is high in Japan, we hypothesized a founder effect. In this study, we sought to elucidate the reason for the high proportion of viral integrations into chromosome 22. We analyzed six cases of iciHHV-6A and two cases of iciHHV-6B, including one iciHHV-6A case with a matched sample from a father and one iciHHV-6B case with a matched sample from a mother. In iciHHV-6A, the same copy numbers of viral telomeric repeat sequences (TRS) and the same five microsatellite markers were detected in both the index case and paternal sample. Moreover, the same five microsatellite markers were demonstrated in four cases and the same copy numbers of viral TRS were demonstrated in two pairs of two cases. The present microsatellite analysis suggested
human herpesvirus 7 U21 glycoprotein: encodes an immunoevasin that binds to class I major histocompatibility complex molecules and diverts them to a lysosomal compartment
Human herpesvirus 3 ATCC ® VR-1367D™ Designation: DNA from VZV strain Ellen [ATCC ® VR-1367™] Application: It is appropriate for use in polymerase chain reaction (PCR) for viral gene products and other molecular virology applications.
Human herpesvirus 2 ATCC ® VR-734D™ Designation: DNA from HSV-2 strain G [ATCC ® VR-734™] Application: It is appropriate for use in polymerase chain reaction (PCR) for viral gene products and other molecular virology applications.
Human herpesvirus-6 is a lymphotropic virus which infectssusceptible individuals during the first year of life andusually causes life-long l
Human herpesvirus 1 UL9 protein: necessary for viral DNA synthesis; amino acid sequence has been determined; has helicase activity
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Transcriptional activator of immediate-early (IE) gene products (alpha genes). Acts as a key activator of lytic infection by initiating the lytic program through the assembly of the transcriptional regulatory VP16-induced complex composed of VP16 and two cellular factors, HCFC1 and POU2F 1. VP16-induced complex represents a regulatory switch: when it is on, it promotes IE-gene expression and thus lytic infection, and when it is off, it limits IE-gene transcription favoring latent infection.
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The HHV-6 Foundation in a non-profit entity founded to encourage scientific exchange between investigators and to provide pilot grants for promising scientific and clinical research on the under- appreciated viruses HHV-6A and HHV-6B.. The Foundation sponsors international conferences and supports scientists and clinicians seeking to clarify the role of the two HHV-6 viruses in disease. Since HHV-6A and HHV-6B can smolder in the brain and other organs without circulating in the peripheral blood or plasma, identifying chronic infection is a challenge.. Read More. ...
I have a client looking for small quantities of IgM antibody to Human Herpesvirus 6 (HHV-6). Client is will pay for material. Urgently needed for research project for HHV-6 immunoassay. Reply to: Eugene H. LaBrec E. H. LaBrec & Assoc. PO Box 5410 Rockville MD 20848 TEL: 301-871-3171 FAX: 310-871-5325 or elabrec at cpcug.org ...
Fatal myocarditis is a rare complication in immunosuppressed children. Recent reports have linked human herpesvirus 6 (HHV-6) infection, typically a benign infection in childhood, with myocarditis. HHV-6 can reactivate during periods of immunosuppression. Here, we report 2 cases in which children we …
of this study was to analyse the range of emerging mutations in herpesvirus by whole genome deep sequencing. We tested human herpesvirus 6 treatment with novel antiviral K21, where evidence indicated distinct effects on virus envelope proteins.. ...
Febrile convulsions are age dependent, with a peak age at 14-18 months, and are rare before 9 months and after 5 years of age. It is well known that viral infections of the upper respiratory tract, exanthem subitum, and acute otitis media are frequently associated with febrile convulsions.16 In our study, approximately 90% of patients with febrile convulsions had upper and lower respiratory tract infections or exanthem subitum. The age distribution of febrile convulsions ranged from 1 month to 77 months and the peak age was 1-2 years. Primary HHV-6 infection was found in 20% of patients with febrile convulsions and more than half of these patients were younger than 1 year. The median age of patients with primary HHV-6 infection was significantly lower than those without primary HHV-6 infection, which can be easily understood in view of the fact that in Japan more than 90% of infants are infected with the virus by 1 year of age.14 17 18 Three quarters of our patients were experiencing a first ...
Human herpesvirus 7 (HHV-7) is one of nine known members of the Herpesviridae family that infects humans. HHV-7 is a member of Betaherpesviridae, a subfamily of the Herpesviridae that also includes HHV-6 and cytomegalovirus (HHV-5 or HCMV). HHV-7 often acts together with HHV-6, and the viruses together are sometimes referred to by their genus, Roseolovirus. HHV-7 was first isolated in 1990 from CD4+ T cells taken from peripheral blood lymphocytes. Both HHV-6B and HHV-7, as well as other viruses, can cause a skin condition in infants known as exanthema subitum, although HHV-7 causes the disease less frequently than HHV-6B. HHV-7 infection also leads to or is associated with a number of other symptoms, including acute febrile respiratory disease, fever, rash, vomiting, diarrhea, low lymphocyte counts, and febrile seizures, though most often no symptoms present at all. There are indications that HHV-7 can contribute to the development of drug-induced hypersensitivity syndrome, encephalopathy, ...
The predominant types of dendritic cells (DC) in the skin and mucosa are Langerhans cells (LC) and interstitial dermal DC (iDDC). LC and iDDC process cutaneous antigens and migrate out of the skin and mucosa to the draining lymph nodes to present antigens to T and B cells. Because of the strategic location of LC and iDDC and the ability of these cells to capture and process pathogens, we hypothesized that they could be infected with human herpesvirus 8 (HHV-8) (Kaposis sarcoma [KS]-associated herpesvirus) and have an important role in the development of KS. We have previously shown that HHV-8 enters monocyte-derived dendritic cells (MDDC) through DC-SIGN, resulting in nonproductive infection. Here we show that LC and iDDC generated from pluripotent cord blood CD34(+) cell precursors support productive infection with HHV-8. Anti-DC-SIGN monoclonal antibody (MAb) inhibited HHV-8 infection of iDDC, as shown by low expression levels of viral proteins and DNA. In contrast, blocking of both langerin and the
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... Emerging Microbes &Infections 6, e45 (June 2017). doi:10.1038/emi.2017.32 Authors: Kuo-Chih Tseng, Ming-Nan Lin, Tang-Yuan Chu, Jen-Pi Tsai &Cheng-Chuan Su...
Peripheral blood mononuclear cells collected from 13 patients withchronic fatigue syndrome and 13 healthy controls were analyzedfor the pres
The HHV-6 Foundation in a non-profit entity founded to encourage scientific exchange between investigators and to provide pilot grants for promising scientific and clinical research on the under- appreciated viruses HHV-6A and HHV-6B.. The Foundation sponsors international conferences and supports scientists and clinicians seeking to clarify the role of the two HHV-6 viruses in disease. Since HHV-6A and HHV-6B can smolder in the brain and other organs without circulating in the peripheral blood or plasma, identifying chronic infection is a challenge.. Read More. ...
H G Guo, P Browning, J Nicholas, G S Hayward, E Tschachler, Y W Jiang, M Sadowska, M Raffeld, S Colombini, R C Gallo, M S Jr Reitz
FUNCTION:Involved in the presentation of foreign antigens to the immune system.,,SUBUNIT:Heterodimer of an alpha chain and a beta chain (beta-2- microglobulin). Interacts with human herpesvirus 8 MIR1 protein (By similarity).,,INTERACTION:P30457:HLA-A; NbExp=1; IntAct=EBI-1050524, EBI-1049899;,,SUBCELLULAR LOCATION:Membrane; Single-pass type I membrane protein.,,PTM:Polyubiquitinated in a post ER compartment by interaction with human herpesvirus 8 MIR1 protein. This targets the protein for rapid degradation via the ubiquitin system (By similarity).,,POLYMORPHISM:The following alleles of A-36 are known:A*36:01 and A*36:02. The sequence shown is that of A*36:01.,,SIMILARITY:Belongs to the MHC class I family.,,SIMILARITY:Contains 1 Ig-like C1-type (immunoglobulin-like) domain. ...
FUNCTION:Involved in the presentation of foreign antigens to the immune system.,,SUBUNIT:Heterodimer of an alpha chain and a beta chain (beta-2- microglobulin). Interacts with human herpesvirus 8 MIR1 protein (By similarity).,,INTERACTION:P30450:HLA-A; NbExp=1; IntAct=EBI-1044129, EBI-1042870; P30457:HLA-A; NbExp=1; IntAct=EBI-1044129, EBI-1049899;,,SUBCELLULAR LOCATION:Membrane; Single-pass type I membrane protein.,,PTM:Polyubiquitinated in a post ER compartment by interaction with human herpesvirus 8 MIR1 protein. This targets the protein for rapid degradation via the ubiquitin system (By similarity).,,POLYMORPHISM:The following alleles of A-30 are known:A*30:01 (A30.3), A*30:02, A*30:03, A*30:04 (A30W7), A*30:06, A*30:07 and A*30:08. The sequence shown is that of A*30:01.,,SIMILARITY:Belongs to the MHC class I family.,,SIMILARITY:Contains 1 Ig-like C1-type (immunoglobulin-like) domain. ...
Free, official coding info for 2018 ICD-10-CM B10.01 - includes detailed rules, notes, synonyms, ICD-9-CM conversion, index and annotation crosswalks, DRG grouping and more.
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