Human immunodeficiency virus type 1 Vpu modifies viral cytopathic effect through augmented virus release.

Iwatani, Yoshinori; Song, Seong Kyu; Wang, Liqiang; Planas, Josè M.; Sakai, Hiroyuki; Ishimoto, Akinori; Cloyd, Miles W.

doi:10.1099/0022-1317-78-4-841

Cited by 13 publications

(4 citation statements)

References 20 publications

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“…In later stages, the envelope precursor gp160 traps the newly-synthetized CD4 molecules within the endoplasmatic reticulum. Moreover, Vpu induces the degradation of these CD4 molecules and releases the gp160 molecules allowing their maturation and trafficking (Willey et al, 1992;Schubert et al, 1996bSchubert et al, , 1996aIwatani et al, 1997). In addition, Vpu also forms ion conductive pores reported to enhance virus release (Ewart et al, 1996;Schubert et al, 1996c;Bour et al, 1999).…”

Section: Replication Of Hiv-1mentioning

confidence: 94%

Basics of the virology of HIV-1 and its replication

Sierra

Kupfer

Kaiser

2005

Journal of Clinical Virology

126

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Section: Replication Of Hiv-1mentioning

confidence: 94%

Basics of the virology of HIV-1 and its replication

Sierra

Kupfer

Kaiser

2005

Journal of Clinical Virology

126

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“…The evolutionary distances were computed using the Tamura-Nei method [ 31 ] and the rate variation among sites was modeled with a gamma distribution (shape parameter =1). The corresponding sequence regions from the standard laboratory HIV strains, such as HIV NL4–3 [ 32 ], HIV 213 [ 33 ], HIV JRCSF [ 26 ], HIV C1P [ 25 ], were included in the outgroup. The bootstrap test (1000 replicates) was performed [ 34 ] and the values are shown next to the branches.…”

Section: Methodsmentioning

confidence: 99%

Prolonged persistence of a novel replication-defective HIV-1 variant in plasma of a patient on suppressive therapy

Rassler

Ramírez

Khoury

et al. 2016

Virol J

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BackgroundCell-free residual HIV-1 virions (RVs) persist in plasma below 20–50 vRNA copies/ml in most patients on suppressive antiretroviral therapy (ART). How RVs are produced in the body during therapy is not fully clear. In this study, we have attempted to characterize these viruses of an ART-treated patient in vitro in order to gain insights into the mechanism of their production in vivo.MethodsWe have reconstructed almost the entire genomes of RVs as DNA forms using the patient’s residual plasma vRNA by an overlapping RT-nested PCR method, and then sequence-analyzed the cloned genomes and tested them for their biological activities in vitro.ResultsWe found that the reconstructed molecular clones of RVs lacked antiretroviral drug-resistant mutations, as well as G-to-A hypermutations. The vDNA clones, when transfected into TZM-bl cells, released HIV-p24 into the culture media at extremely low levels. This low-level virus production was found to be due to the presence of a unique mutation (GU-to-GC) in the conserved 5′-major splice donor (MSD) motif of the corresponding vRNAs. We found that the incorporation of this point mutation by itself could cause defects in the replication of a standard HIV strain (JRCSF) in vitro. However, this novel viral variant was intermittently detected at 5 of 7 time-points in the patient’s plasma over a period of 39 months during therapy.ConclusionsThis is the first identification of a natural point mutation (GU-to-GC) in the conserved 5′-MSD motif of HIV genomic RNA. The intermittent but prolonged detection of this replication-defective HIV variant in the patient′s plasma among other viral populations strongly suggests that this variant is released from highly stable productively infected cells present in vivo during therapy. The potential implication of this observation is that the elimination of such productively infected cells that contribute to residual viremia during suppressive therapy could be an important first step towards achieving a cure for HIV.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-016-0617-0) contains supplementary material, which is available to authorized users.

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“…Σε αντίθεση με τη Nef, η οποία καταστρέφει CD4 υποδοχείς που βρίσκονται στην επιφάνεια του κυττάρου, η gp160 και η Vpu δρουν ενδοκυττάρια. H gp160 παγιδεύει CD4 μόρια στο ενδοπλασματικό δίκτυο, ενώ η Vpu καταστρέφει τις δεσμευμένες CD4 γλυκοπρωτεΐνες και απελευθερώνει τη gp160, επιτρέποντας την ωρίμανση και τη μεταφορά της (Willey 1992, Iwatani 1997, Sierra 2005, Costin 2007). Επιπρόσθετα, η Vpu προάγει την απελευθέρωση του HIV από το κύτταρο μέσω του σχηματισμού καναλιού ιόντων, το οποίο διαταράσσει το δυναμικό της κυτταρικής μεμβράνης και επιτρέπει την έξοδο του ιού (Sierra 2005, Costin 2007).…”

Section: δομή Hivunclassified

Ιογενής ηπατίτιδα β και hiv λοίμωξη στον ελληνικό πληθυσμό

Nikolopoulos¹

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Human immunodeficiency virus type 1 Vpu modifies viral cytopathic effect through augmented virus release.

Cited by 13 publications

References 20 publications

Basics of the virology of HIV-1 and its replication

Basics of the virology of HIV-1 and its replication

Prolonged persistence of a novel replication-defective HIV-1 variant in plasma of a patient on suppressive therapy

Ιογενής ηπατίτιδα β και hiv λοίμωξη στον ελληνικό πληθυσμό

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