GB virus C

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GB virus C
Virus classification
Group: Group IV ((+)ssRNA)
Order: Unassigned
Family: Flaviviridae
Genus: Unassigned
Species: GB virus C

GB virus C (GBV-C) is a species of virus in the Flaviviridae family which has not yet been assigned to a genus, is known to infect humans, but is not known to cause human disease. There have been reports that HIV patients coinfected with GBV-C can survive longer than those without GBV-C, but the patients may be different in other ways. There is current active research into the virus' effects on the immune system in patients coinfected with GBV-C and HIV.[1][2]

Contents

[edit] History

Hepatitis G virus and GB virus C (GBV-C) are RNA viruses that were independently identified in 1995, and were subsequently found to be two isolates of the same virus.[3][4][5][6] Although GBV-C was initially thought to be associated with chronic hepatitis, extensive investigation failed to identify any association between this virus and any clinical illness.[7]

[edit] Taxonomy

GBV-C is a member of the Flaviviridae family and is phylogenetically related to hepatitis C virus but appears to replicate primarily in lymphocytes, and poorly if at all in hepatocytes.[8][9] GBV-A and GBV-B are probably Tamarin viruses, while GBV-C infects humans.[10]

[edit] Human infection

The majority of immune-competent individuals appear to clear GBV-C viraemia within the first few years following infection and although the time interval between GBV-C infection and clearance of viraemia (detection of GBV-C RNA in plasma) is not known, infection may persist for decades in some individuals.

Approximately 2% of healthy US blood donors are viraemic with GBV-C, and up to 13% of blood donors have antibodies to E2 protein, indicating prior infection.

Parenteral, sexual and vertical transmission of GBV-C have all been documented, and because of shared modes of transmission, individuals infected with HIV are commonly co-infected with GBV-C. Among people with HIV infection, the prevalence of GBV-C viraemia ranges from 14 to 43%.[11]

Some studies have suggested that co-infection with GBV-C will actually slow the progression of HIV disease.[12]

[edit] References

  1. ^ Mosam A, Sathar MA, Dawood H, Cassol E, Esterhuizen TM, Coovadia HM (2007). "Effect of GB virus C co-infection on response to generic HAART in African patients with HIV-1 clade C infection". AIDS 21 (10): 1377–1379. doi:10.1097/QAD.0b013e3281532cb8. PMID 17545721. 
  2. ^ Jung S, Eichenmüller M, Donhauser N, et al. (2007). "HIV entry inhibition by the envelope 2 glycoprotein of GB virus C". AIDS 21 (5): 645–7. doi:10.1097/QAD.0b013e32803277c7. PMID 17314528. 
  3. ^ Simons JN, Pilot-Matias TJ, Leary TP, et al. (April 1995). "Identification of two flavivirus-like genomes in the GB hepatitis agent". Proc. Natl. Acad. Sci. U.S.A. 92 (8): 3401–5. doi:10.1073/pnas.92.8.3401. PMID 7724574. 
  4. ^ Simons JN, Leary TP, Dawson GJ, et al. (June 1995). "Isolation of novel virus-like sequences associated with human hepatitis". Nat. Med. 1 (6): 564–9. doi:10.1038/nm0695-564. PMID 7585124. 
  5. ^ Yoshiba M, Okamoto H, Mishiro S (October 1995). "Detection of the GBV-C hepatitis virus genome in serum from patients with fulminant hepatitis of unknown aetiology". Lancet 346 (8983): 1131–2. doi:10.1016/S0140-6736(95)91802-7. PMID 7475605. 
  6. ^ Birkenmeyer LG, Desai SM, Muerhoff AS, Leary TP, Simons JN, Montes CC, Mushahwar IK (1998). "Isolation of a GB virus-related genome from a chimpanzee". J. Med. Virol. 56 (1): 44–51. doi:10.1002/(SICI)1096-9071(199809)56:1<44::AID-JMV8>3.0.CO;2-N. PMID 9700632. 
  7. ^ Alter HJ (June 1996). "The cloning and clinical implications of HGV and HGBV-C". N. Engl. J. Med. 334 (23): 1536–7. doi:10.1056/NEJM199606063342310. PMID 8618611. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8618611&promo=ONFLNS19. 
  8. ^ Leary TP, Muerhoff AS, Simons JN, Pilot-Matias TJ, Erker JC, Chalmers ML, Schlauder GG, Dawson GJ, Desai SM, Mushahwar IK (1996). "Sequence and genomic organization of GBV-C: a novel member of the flaviviridae associated with human non-A-E hepatitis". J. Med. Virol. 48 (1): 60–7. doi:10.1002/(SICI)1096-9071(199601)48:1<60::AID-JMV10>3.0.CO;2-A. PMID 8825712. 
  9. ^ Thurner C, Witwer C, Hofacker IL, Stadler PF (May 2004). "Conserved RNA secondary structures in Flaviviridae genomes". J. Gen. Virol. 85 (Pt 5): 1113–24. doi:10.1099/vir.0.19462-0. PMID 15105528. http://vir.sgmjournals.org/cgi/pmidlookup?view=long&pmid=15105528. 
  10. ^ Simons JN, Desai SM, Schultz DE, Lemon SM, Mushahwar IK (1996). "Translation initiation in GB viruses A and C: evidence for internal ribosome entry and implications for genome organization". J. Virol. 70 (9): 6126–35. PMID 8709237. 
  11. ^ George SL, Varmaz D, Stapleton JT (2006). "GB virus C replicates in primary T and B lymphocytes". J. Infect. Dis. 193 (3): 451–4. doi:10.1086/499435. PMID 16388494. 
  12. ^ Zhang W, Chaloner K, Tillmann HL, Williams CF, Stapleton JT (2006). "Effect of early and late GB virus C viraemia on survival of HIV-infected individuals: a meta-analysis". HIV Med. 7 (3): 173–80. doi:10.1111/j.1468-1293.2006.00366.x. PMID 16494631. http://www.blackwell-synergy.com/openurl?genre=article&sid=nlm:pubmed&issn=1464-2662&date=2006&volume=7&issue=3&spage=173. 

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