Ihmisen pegivius HPgV, myös kutsuttu hepatiitti G virukseksi joskus , pinttynyt virus

J Gen Virol. 2014 Jun;95(Pt 6):1307-19. doi: 10.1099/vir.0.063016-0. Epub 2014 Mar 25. Human pegivirus RNA is found in multiple blood mononuclear cells in vivo and serum-derived viral RNA-containing particles are infectious in vitro.

Chivero ET¹, Bhattarai N¹, Rydze RT², Winters MA³, Holodniy M³, Stapleton JT⁴.

Abstract

Human pegivirus (HPgV; previously called GB virus C/hepatitis G virus) has limited pathogenicity, despite causing persistent infection, and is associated with prolonged survival in human immunodeficiency virus-infected individuals. Although HPgV RNA is found in and produced by T- and B-lymphocytes, the primary permissive cell type(s) are unknown. We quantified HPgV RNA in highly purified CD4(+) and CD8(+) T-cells, including naïve, central memory and effector memory populations, and in B-cells (CD19(+)), NK cells (CD56(+)) and monocytes (CD14(+)) using real-time reverse transcription-PCR. Single-genome sequencing was performed on viruses within individual cell types to estimate genetic diversity among cell populations. HPgV RNA was present in CD4(+) and CD8(+) T-lymphocytes (nine of nine subjects), B-lymphocytes (seven of ten subjects), NK cells and monocytes (both four of five). HPgV RNA levels were higher in naïve (CD45RA(+)) CD4(+) cells than in central memory and effector memory cells (P<0 .01="" 0.006-0.010="" 0.07="" 0.58-0.14="" a="" among="" and="" apparent="" b-lymphocytes="" broad="" by="" carboxyfluorescein="" cells="" class="highlight" commercial="" conserved="" contribute="" csfe="" delivered="" delivery="" ester="" evidence="" exosome="" explaining="" highly="" hpgv="" in="" including="" isolation="" labelled="" low="" may="" microvesicles="" monocytes="" nk="" non-synonymous="" of="" particles="" pbmcs="" per="" persistent="" precipitated="" pressure.="" range="" ratio="" reagent="" replication.="" rna-containing="" rna="" selective="" sequences="" serum="" site="" span="" subjects="" subsequent="" substitution="" substitutions="" succinimidyl="" suggesting="" synonymous="" t-="" the="" this="" thus="" to="" transferred="" tropism="" uninfected="" virus="" vivo="" was="" were="" with="" within="">human

RNA virus.PMID:24668525[PubMed - indexed for MEDLINE]PMCID:PMC4027039[Available on 2015/6/1]

Ihmisen pegivirus HPgV

Virology. 2014 May;456-457:300-9. doi: 10.1016/j.virol.2014.03.018. Epub 2014 Apr 24.Human pegivirus (GB virus C) NS3 protease activity inhibits induction of the type I interferon response and is not inhibited by HCV NS3 protease inhibitors.Chowdhury AY¹, Tavis JE², George SL³.

Abstract

We previously found that human pegivirus (HPgV; formerly GBV-C) NS3 protease activity inhibits Human Immunodeficiency Virus (HIV) replication in a CD4+ T cell line.
 Given the protease׳s similarity to the Hepatitis C virus (HCV) NS3 protease, we characterized HPgV protease activity and asked whether it affects the type I interferon response or is inhibited by HCV protease antagonists.
We characterized the activity of proteases with mutations in the catalytic triad and demonstrated that the HCV protease inhibitors Telaprevir, Boceprevir, and Danoprevir do not affect HPgV protease activity. HPgV NS3 protease cleaved MAVS but not TRIF, and it inhibited interferon responses sufficiently to enhance growth of an interferon-sensitive virus. Therefore, HPgV׳s inhibition of the interferon response could help promote HPgV persistence, which is associated with clinical benefits in HIV-infected patients. Our results also imply that HCV protease inhibitors should not interfere with the beneficial effects of HPgV in HPgV/HCV/HIV infected patients.
Published by Elsevier Inc.

KEYWORDS: GB Virus-C; Hepatitis C virus; Human pegivirus; MAVS; Protease inhibitors; Serine protease; TRIF; Type I interferon