SIV adaption to human cells

Hirsch, Vanessa M.; Edmondson, Peter W.; Murphey‐Corb, Michael; Arbeille, B.; Johnson, Philip R.; Mullins, James I.

doi:10.1038/341573a0

Cited by 168 publications

(147 citation statements)

References 17 publications

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“…Apart from the co-expression of normal gpl60 in both CI-17 and CI-789-76 cell lines, these findings accord with those found using simian immunodeficiency virus (SIV) systems since it has been shown that prolonged passage of SIV in human cells leads to extensive deletions in the Env glycoprotein cytoplasmic tail whereas minimally passaged virus V. Zaides and others expresses full-length glycoprotein (Chakrabarti et al, 1989;Hirsch et al, 1989;Luciw et al, 1992;Marthas et al, 1989;Ritter et al, 1993). This led us to characterize more precisely our truncated Env products using the CI-17 line as a model.…”

Section: Expression Of Hiv Env Gene Products In the Different Cell Linessupporting

confidence: 80%

Extensive C-terminal Deletion in Human Immunodeficiency Virus Type 1 Env Glycoprotein Arising After Long-term Culture of Chronically Infected Cells

Zaides

Yagello²,

Veselovskaya

et al. 1994

Journal of General Virology

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Human immunodeficiency virus type 1 (HIV-1) chronically infected (CI) cell lines were established from HIV-1,~B/LA~-infected MT-4 cells that survived acute infection. The HIV env gene expressed in the two longterm cultured cell lines differed from that of the lines cultured for shorter periods, by coding for a glycoprotein gpl60 that had the C terminus deleted. One long-term cultured cell line, CI-17, was studied in detail. An insertion of a premature stop codon in the env gene caused about 90 % of gpl60 molecules to be truncated (gpl60x), lacking both cytoplasmic and transmembrane domains; these species were secreted into the cell medium, and could form oligomers with other truncated gpl60 molecules as well as with their normal counterparts. CI-17 cells constantly yielded high levels of viral protein and relatively low quantities of infectious virus, without cytopathicity. However, acute infection of fresh MT-4 cells with CI-17-derived virus led to cytopathicity, the rate of which as well as the Env glycoprotein pattern depended on multiplicity: (i) using an infection dose of 10 -4 IDs0/cell, cells died 7 to 8 days post-infection with normal gpl60 synthesis predominating; (ii) with l0 -2 IDs0, gpl60x was produced as early as 48 h postinfection and cell death was delayed. Predominant gpl60x formation occurred again when new CI cell lines were obtained with CI-17-derived virus. Thus, two human immunodeficiency virus variants, a normal and a defective one, are persistently expressed in CI-17 cells. The other long-term cultured CI cell line also expressed gpl60 with a similar (albeit slightly longer) deletion of a C-terminal region in most molecules, but the cell lines that were cultured for shorter periods did not. These results suggest that the emergence of HIV variants with a C-terminal deletion in the Env glycoprotein, which coexist with normal virus, may play a role in maintaining the long-term growth capacity and viability of CI ceils.

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Section: Expression Of Hiv Env Gene Products In the Different Cell Linessupporting

confidence: 80%

Extensive C-terminal Deletion in Human Immunodeficiency Virus Type 1 Env Glycoprotein Arising After Long-term Culture of Chronically Infected Cells

Zaides

Yagello²,

Veselovskaya

et al. 1994

Journal of General Virology

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“…Truncations of the cytoplasmic tail enhance infectivity, fusogenicity, and Env incorporation into virions and expand the host range (23,35,41,50). Although passage of SIVmac in human T-cell lines selects for variants with premature stop codons that truncate the cytoplasmic tail (25), truncated cytoplasmic tails rapidly revert to full-length tails during replication in infected macaques (21,25,31). These results indicate a selective advantage to SIV replication conferred by the full-length cytoplasmic tail in vivo.…”

mentioning

confidence: 63%

Effect of Extension of the Cytoplasmic Domain of Human Immunodeficiency Type 1 Virus Transmembrane Protein gp41 on Virus Replication

Chan

Wang

Lin

et al. 2004

J Virol

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The biological significance of the presence of a long cytoplasmic domain in the envelope (Env) transmembrane protein gp41 of human immunodeficiency virus type 1 (HIV-1) is still not fully understood. Here we examined the effects of cytoplasmic tail elongation on virus replication and characterized the role of the C-terminal cytoplasmic tail in interactions with the Gag protein. Extensions with six and nine His residues but not with fewer than six His residues were found to severely inhibit virus replication through decreased Env electrophoretic mobility and reduced Env incorporation compared to the wild-type virus. These two mutants also exhibited distinct N glycosylation and reduced cell surface expression. An extension of six other residues had no deleterious effect on infectivity, even though some mutants showed reduced Env incorporation into the virus and/or decreased cell surface expression. We further show that these elongated cytoplasmic tails in a format of the glutathione S-transferase fusion protein still interacted effectively with the Gag protein. In addition, the immediate C terminus of the cytoplasmic tail was not directly involved in interactions with Gag, but the region containing the last 13 to 43 residues from the C terminus was critical for Env-Gag interactions. Taken together, our results demonstrate that HIV-1 Env can tolerate extension at its C terminus to a certain degree without loss of virus infectivity and Env-Gag interactions. However, extended elongation in the cytoplasmic tail may impair virus infectivity, Env cell surface expression, and Env incorporation into the virus.

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“…However, if simian immunodeficiency viruses with this mutation are injected into monkeys, the mutation reverts. The simian immunodeficiency virus strains with a long envelope C terminus in gp4l would dominate in vivo, suggesting that the C terminus of gp4l is required for efficient viral replication in vivo (33). In this report, we demonstrate that the C terminus of gp4l in HIV-1 plays an important role in making the viral envelope permeable to dNTPs, which can assure intravirion RT and continuous utilization of dNTPs, in its physiological microenvironments.…”

Section: Methodsmentioning

confidence: 79%

Amphipathic domains in the C terminus of the transmembrane protein (gp41) permeabilize HIV-1 virions: a molecular mechanism underlying natural endogenous reverse transcription.

Zhang¹,

Dornadula²,

Alur³

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

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Reverse transcription of HIV-1, without detergent or amphipathic peptide-induced permeability of the viral envelope, has been demonstrated to occur in the intact HIV-1 virion. In this report, we demonstrate that the amphipathic domains in the C terminus of the transmembrane glycoprotein (gp4l) account for the natural permeability of the HIV-1 envelope to deoxyribonucleoside triphosphates, the substrates for DNA polymerization. In addition, nonphysiological deoxyribonucleoside triphosphates, such as 3'-azido-3'-deoxythymidine 5'-triphosphate and 3'-deoxythymidine 5'-triphosphate, can also penetrate the viral envelope, incorporate into, and irreversibly terminate reverse transcripts. As a result, viral infectivity is potently inhibited. Since the lentiviral envelope with these newly demonstrated characteristics can serve as a delivery pathway for anti-reverse transcription agents, we propose a unique strategy to prevent HIV-1 inter-

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SIV adaption to human cells

Cited by 168 publications

References 17 publications

Extensive C-terminal Deletion in Human Immunodeficiency Virus Type 1 Env Glycoprotein Arising After Long-term Culture of Chronically Infected Cells

Extensive C-terminal Deletion in Human Immunodeficiency Virus Type 1 Env Glycoprotein Arising After Long-term Culture of Chronically Infected Cells

Effect of Extension of the Cytoplasmic Domain of Human Immunodeficiency Type 1 Virus Transmembrane Protein gp41 on Virus Replication

Amphipathic domains in the C terminus of the transmembrane protein (gp41) permeabilize HIV-1 virions: a molecular mechanism underlying natural endogenous reverse transcription.

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