No Evidence of an Association between the<i>APOBEC3B</i>Deletion Polymorphism and Susceptibility to HIV Infection and AIDS in Japanese and Indian Populations

Itaya, Sakiko; Nakajima, Toshiaki; Kaur, Gurvinder; Takahashi, Hiroshi; Ohtani, Hideyuki; Mehra, N. K.; Kimura, Akinori

doi:10.1086/655227

Cited by 21 publications

(23 citation statements)

References 9 publications

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“…Also, no effects of HIV viral load and CD4+ T-cell count characterizing different stages of the disease severity were seen in association with the APOBEC3B polymorphism was in corroboration with our results [44].…”

Section: Resultssupporting

confidence: 92%

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

Kakkar¹,

Sharma²,

Rathore³

et al. 2017

J AIDS Clin Res

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Section: Resultssupporting

confidence: 92%

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

Kakkar¹,

Sharma²,

Rathore³

et al. 2017

J AIDS Clin Res

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“…The role of A3B in restricting HIV-1 in vivo is under debate; on one hand there is evidence that individuals who are homozygous deficient in A3B due to a naturally occurring deletion of the entire gene are more susceptible to HIV-1 infection and generally have a faster disease progression (3), while others find that the deletion has no consequences for HIV-1-induced disease (23). Similarly, the effect of A3B on HIV-1 infection in experimental settings varies significantly between different groups, from the 15% inhibition we observed to 50-fold restriction (5,14).…”

Section: Discussionmentioning

confidence: 99%

The Role of Amino-Terminal Sequences in Cellular Localization and Antiviral Activity of APOBEC3B

Pak

Heidecker

Pathak

et al. 2011

J Virol

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Human APOBEC3B (A3B) has been described as a potent inhibitor of retroviral infection and retrotransposition. However, we found that the predominantly nuclear A3B only weakly restricted infection by HIV-1, HIV-1⌬vif, and human T-cell leukemia virus type 1 (HTLV-1), while significantly inhibiting LINE-1 retrotransposition. The chimeric construct A3G/B, in which the first 60 amino acids of A3B were replaced with those of A3G, restricted HIV-1, HIV-1⌬vif, and HTLV-1 infection, as well as LINE-1 retrotransposition. In contrast to the exclusively cytoplasmic A3G, which is inactive against LINE-1 retrotransposition, the A3G/B protein, while localized mainly to the cytoplasm, was also present in the nucleus. Further mutational analysis revealed that residues 18, 19, 22, and 24 in A3B were the major determinants for nuclear versus cytoplasmic localization and antiretroviral activity. HIV-1⌬vif packages A3G, A3B, and A3G/B into particles with close-to-equal efficiencies. Mutation E68Q or E255Q in the active centers of A3G/B resulted in loss of the inhibitory activity against HIV-1⌬vif, while not affecting activity against LINE-1 retrotransposition. The low inhibition of HIV1⌬vif by A3B correlated with a low rate of G-to-A hypermutation. In contrast, viruses that had been exposed to A3G/B showed a high number of G-to-A transitions. The mutation pattern was similar to that previously reported for A3B, with a preference for the GA context. In summary, these observations suggest that changing 4 residues in the amino terminus of A3B not only retargets the protein from the nucleus to the cytoplasm but also enhances its ability to restrict HIV while retaining inhibition of retrotransposition.

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“…APOBEC3B (A3B), APOBEC3C (A3C), APOBEC3DE (A3DE), APOBEC3F (A3F), APOBEC3G (A3G), and some APOBEC3H haplotypes have been reported to inhibit HIV-1 in the absence of the accessory protein viral infectivity factor (Vif) (1)(2)(3)(4)(6)(7)(8)(9)(10)(11)(12)(13)(14). The antiviral activities of A3B (9,15), A3C (6), and A3DE (8,16) have been reported in a limited number of studies and in some cases have been controversial (16)(17)(18)(19)(20); overall, A3G and A3F have been consistently reported to have strong antiviral activity in transient-transfection assays by numerous investigators and are thought to be the primary restriction factors that inhibit HIV-1 replication (21,22).…”

mentioning

confidence: 99%

APOBEC3G Restricts HIV-1 to a Greater Extent than APOBEC3F and APOBEC3DE in Human Primary CD4 ⁺ T Cells and Macrophages

Chaipan

Smith

et al. 2013

J Virol

102

116

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؉ T cells and macrophages, and only the NL4-3 YRHHY>A5 mutant showed a 2-to 4-day delay in replication compared to the wild type. During the subsequent 27 days (round 2) of cultures initiated with peak virus obtained from round 1, the NL4-3 YRHHY>A5 mutant exhibited a longer, 8-to 10-day delay and the NL4-3 DRMR>A4 mutant exhibited a 2-to 6-day delay in replication compared to the wild type. The NL4-3 YRHHY>A5 and NL4-3 DRMR>A4 mutant proviruses displayed G-to-A hypermutations primarily in GG and GA dinucleotides as expected of A3G-and A3F-or A3DE-mediated deamination, respectively. We conclude that A3G exerts a greater restriction effect on HIV-1 than A3F and A3DE.

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No Evidence of an Association between theAPOBEC3BDeletion Polymorphism and Susceptibility to HIV Infection and AIDS in Japanese and Indian Populations

Cited by 21 publications

References 9 publications

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

The Role of Amino-Terminal Sequences in Cellular Localization and Antiviral Activity of APOBEC3B

APOBEC3G Restricts HIV-1 to a Greater Extent than APOBEC3F and APOBEC3DE in Human Primary CD4 ⁺ T Cells and Macrophages

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No Evidence of an Association between theAPOBEC3BDeletion Polymorphism and Susceptibility to HIV Infection and AIDS in Japanese and Indian Populations

Cited by 21 publications

References 9 publications

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

The Role of Amino-Terminal Sequences in Cellular Localization and Antiviral Activity of APOBEC3B

APOBEC3G Restricts HIV-1 to a Greater Extent than APOBEC3F and APOBEC3DE in Human Primary CD4 + T Cells and Macrophages

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APOBEC3G Restricts HIV-1 to a Greater Extent than APOBEC3F and APOBEC3DE in Human Primary CD4 ⁺ T Cells and Macrophages