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Evolution of gag and gp41 in Patients Receiving Ritonavir-Boosted Protease Inhibitors
Division of Infectious Diseases, Department of Medicine Stanford University, Stanford, CA, USA.
Division of Infectious Diseases, Department of Medicine Stanford University, Stanford, CA, USA.
Department of Biology, Temple University, Philadelphia, PA, USA.
Division of Infectious Diseases, Department of Medicine Stanford University, Stanford, CA, USA.
Vise andre og tillknytning
2017 (engelsk)Inngår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, nr 1, artikkel-id 11559Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Several groups have proposed that genotypic determinants in gag and the gp41 cytoplasmic domain (gp41-CD) reduce protease inhibitor (PI) susceptibility without PI-resistance mutations in protease. However, no gag and gp41-CD mutations definitively responsible for reduced PI susceptibility have been identified in individuals with virological failure (VF) while receiving a boosted PI (PI/r)-containing regimen. To identify gag and gp41 mutations under selective PI pressure, we sequenced gag and/or gp41 in 61 individuals with VF on a PI/r (n = 40) or NNRTI (n = 20) containing regimen. We quantified nonsynonymous and synonymous changes in both genes and identified sites exhibiting signal for directional or diversifying selection. We also used published gag and gp41 polymorphism data to highlight mutations displaying a high selection index, defined as changing from a conserved to an uncommon amino acid. Many amino acid mutations developed in gag and in gp41-CD in both the PI- and NNRTI-treated groups. However, in neither gene, were there discernable differences between the two groups in overall numbers of mutations, mutations displaying evidence of diversifying or directional selection, or mutations with a high selection index. If gag and/or gp41 encode PI-resistance mutations, they may not be confined to consistent mutations at a few sites. © 2017 The Author(s).

sted, utgiver, år, opplag, sider
London: Nature Publishing Group, 2017. Vol. 7, nr 1, artikkel-id 11559
Emneord [en]
Antivirals, Retrovirus, Viral evolution
HSV kategori
Identifikatorer
URN: urn:nbn:se:hh:diva-35120DOI: 10.1038/s41598-017-11893-8ISI: 000410739000057PubMedID: 28912582Scopus ID: 2-s2.0-85029527838OAI: oai:DiVA.org:hh-35120DiVA, id: diva2:1146394
Merknad

Funding: R.W.S., V.V., P.T., and S.Y.R. were supported in part by the N.I.H. grant AI0168581. D.A.K. and E.W. were supported in part by the N.I.H. grant AI102792. J.M. received support from the Stanford SPARK program and the Fogarty Global Health Equity Scholars Fellowship (NIAID R25 TW009338).

Tilgjengelig fra: 2017-10-02 Laget: 2017-10-02 Sist oppdatert: 2018-04-25bibliografisk kontrollert

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