Functional Analysis of Vif Protein Shows Less Restriction of Human Immunodeficiency Virus Type 2 by APOBEC3G

Ribeiro, Ana Clara; Silva, Alexandra Maia e; Santa‐Marta, Mariana; Pombo, Ana; Moniz-Pereira, José; Gonçalves, João; Barahona, Isabel

doi:10.1128/jvi.79.2.823-833.2005

Cited by 42 publications

(24 citation statements)

References 56 publications

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“…Therefore, it appears that HIV-2 Vif is functionally similar to HIV-1 Vif. Surprisingly, however, it has also been reported that an HIV-2 proviral clone lacking a functional vif gene can replicate effectively in a human T-cell line, termed H9, that expresses hA3G mRNA and that is nonpermissive for Vif-deficient HIV-1 (44). In contrast, primary CD4…”

Section: Other Exogenous Viruses and The Apobec3 Proteinsmentioning

confidence: 95%

Role and Mechanism of Action of the APOBEC3 Family of Antiretroviral Resistance Factors

Cullen

2006

J Virol

254

264

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Metazoan organisms are subject to invasion by a wide range of microbial pathogens and have, as a result, evolved a range of defensive measures. While scientific attention historically has focused on adaptive immune responses, such as antibodies and cytotoxic T cells, it has of late become increasingly apparent that innate immunity also plays a key role in shielding animals from infection (62). Unlike adaptive immunity, innate immunity acts immediately and thus can prevent an infection from getting started. Innate immunity may be particularly effective at shielding animals from infection by opportunistic or zoonotic pathogens. However, because innate immune responses are largely invariant, microorganisms that are common pathogens of a given animal species will frequently have evolved mechanisms that confer resistance to relevant innate immune responses in that species. Indeed, comparative analyses of a host innate immune response and the microbial countermeasures to that response can provide key insights into the biological mechanisms underlying these antagonistic processes.A wide range of innate immune responses have been identified; many of these rely on the recognition of a "pathogenassociated molecular pattern" (PAMP) that is characteristic of a given type of pathogen (62). In this paper, I will review our current understanding of one protein family, the apolipoprotein B mRNA editing enzyme catalytic polypeptide 3 (APO BEC3) proteins, which can confer innate immunity to a wide range of exogenous retroviruses. Moreover, individual APO BEC3 family members can also block the replication of hepatitis B virus, a distant relative of retroviruses, and inhibit the replication of retrotransposons, endogenous transposable elements related to retroviruses that can disrupt the integrity of host cell genomes. APOBEC3 PROTEIN FAMILYThe genomes of humans and other primates encode at least five, and possibly up to seven, APOBEC3 proteins, all of which are encoded by a single gene cluster on chromosome 22 (20). This gene cluster appears to be unique to primates, as the genomes of several other mammalian species, such as mice, cats, and cows, encode only a single APOBEC3 protein (31,36). The fact that the single APOBEC3 gene found in these other vertebrates is at the syntenic chromosomal location relative to the primate APOBEC3 gene cluster (66) indicates that the primate APOBEC3 gene family appeared relatively recently in vertebrate evolution due to gene duplication. This finding, together with the observation that the rate of nonsynonymous nucleotide substitutions has been significantly higher than the rate of synonymous substitutions during the evolution of several members of the APOBEC3 gene family, suggests that primate APOBEC3 genes have been under significant selective pressure (47a, 75). As discussed below, it seems possible that the evolutionary pressure for amplification and diversification of the primate APOBEC3 genes arose from the appearance of viral mechanisms that are able to neutralize the APOBEC3-mediated inhi...

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Section: Other Exogenous Viruses and The Apobec3 Proteinsmentioning

confidence: 95%

Role and Mechanism of Action of the APOBEC3 Family of Antiretroviral Resistance Factors

Cullen

2006

J Virol

254

264

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“…The antiretroviral activity of APOBEC3-subfamily proteins extends well beyond HIV-1 and has been shown to inhibit various lentiviruses such as HIV-2, SIVmac, SIVagm, and EIAV [114,122,128,129]. There is also evidence that some APOBEC proteins can target a variety of retroviral substrates, such as various oncoviruses and spumaviruses.…”

Section: Apobec3mentioning

confidence: 96%

Current Topics in Prevention of Human T-Cell Leukemia Virus Type I Infection: NF-κ B Inhibitors and APOBEC3

Ohsugi

Koito

2008

International Reviews of Immunology

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Human T-cell leukemia virus type I (HTLV-I) is the first human retrovirus and causes adult T-cell leukemia/lymphoma (ATL). Constitutive activation of nuclear factor-kappa B (NF-kappa B) in the leukemic cells is essential for their growth and survival. Thus, NF-kappa B inhibitors have been attracting attention as a potential strategy to treat ATL. Recently, the field of retrovirus research has been stimulated by the discovery of an innate host defense factor, APOBEC3, against the retroviruses. HTLV-I is relatively resistant to the antiviral effects of APOBEC3. To clarify the resistance of HTLV-I against APOBEC3 might contribute to the design of effective therapeutic approaches.

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“…One such factor is APOBEC3G, which was shown to antagonize the activity of HIV-1 Vif; its expression was postulated to underlie the difference among some target cells lines in their susceptibility to Vif-negative HIV-1 (29). Curiously, although HIV-2 Vif can complement Vif-negative HIV-1 (30), it is poorly antagonized by APOBEC3G, and cell lines expressing APOBEC3G can be susceptible to Vif-negative HIV-2 but not to Vif-negative HIV-1 (31). Different species-specific host restriction factors have been proposed to interact with the CypA-binding domain of CA during early phases of HIV-1 infection of certain nonpermissive simian cells (21,32,33).…”

Section: Discussionmentioning

confidence: 99%

Novel Activities of Cyclophilin A and Cyclosporin A during HIV-1 Infection of Primary Lymphocytes and Macrophages

Saini

Potash

2006

The Journal of Immunology

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Studies conducted in cell lines indicate that cyclophilin A (CypA) is a component of HIV type 1 (HIV-1) virions, and that when CypA incorporation into virions is inhibited by treatment of infected cells with the immunosuppressive agent cyclosporin A (CsA), HIV-1 infection also is inhibited. Because HIV-1 particles assemble along a different pathway and incorporate different host proteins in macrophages than in other cell types, we investigated CypA and CsA activities in HIV-1-infected primary human macrophages, compared with primary human lymphocytes. We tested virus protein production, virion composition and infectivity, and progress through the virus life cycle under perturbation by drug treatment or mutagenesis in infected cells from multiple donors. Our findings from both primary cell types are different from that previously reported in transformed cells and show that the amount of CypA incorporated into virions is variable and that CsA inhibits HIV-1 infection at both early and late phases of virus replication, the stage affected is determined by the sequence of HIV-1 Gag. Because the cell type infected determines the identity of host proteins active in HIV-1 replication and can influence the activity of some viral inhibitors, infection of transformed cells may not recapitulate infection of the native targets of HIV-1.

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Functional Analysis of Vif Protein Shows Less Restriction of Human Immunodeficiency Virus Type 2 by APOBEC3G

Abstract: Viral infectivity factor (Vif) is one of the human immunodeficiency virus (HIV) accessory proteins and is

Cited by 42 publications

References 56 publications

Role and Mechanism of Action of the APOBEC3 Family of Antiretroviral Resistance Factors

Role and Mechanism of Action of the APOBEC3 Family of Antiretroviral Resistance Factors

Current Topics in Prevention of Human T-Cell Leukemia Virus Type I Infection: NF-κ B Inhibitors and APOBEC3

Novel Activities of Cyclophilin A and Cyclosporin A during HIV-1 Infection of Primary Lymphocytes and Macrophages

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