Lv1 Inhibition of Human Immunodeficiency Virus Type 1 Is Counteracted by Factors That Stimulate Synthesis or Nuclear Translocation of Viral cDNA

Berthoux, Lionel; Sebastian, Sarah; Sokolskaja, Elena; Luban, Jeremy

doi:10.1128/jvi.78.21.11739-11750.2004

Cited by 77 publications

(95 citation statements)

References 50 publications

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“…Disruption of the CA-CypA interaction frees HIV-1 from Lv1 restriction in macaque and owl monkey cells (7,33,50) and renders HIV-1 susceptible to Ref1 restriction in human cells (43,50). In contrast to what was reported with the previous studies, virion-associated CypA was not important for these effects, suggesting that only target cell CypA is relevant for the CA-specific effects on HIV-1 infectivity.…”

contrasting

confidence: 56%

Target Cell Cyclophilin A Modulates Human Immunodeficiency Virus Type 1 Infectivity

Sokolskaja

Sayah²,

Luban

2004

J Virol

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211

244

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contrasting

confidence: 56%

Target Cell Cyclophilin A Modulates Human Immunodeficiency Virus Type 1 Infectivity

Sokolskaja

Sayah²,

Luban

2004

J Virol

Self Cite

211

244

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“…64 pNL4-3, pNL-GFP, pMD-G, pCIG3N, pCIG3B, pCNCG, pDR8.9, pTRIP CMVÀGFP , pCL-Eco, pROD NefÀGFP , pSIV macÀGFP , pONY3.1 and pONY8.0 have all been extensively described before 44,[65][66][67][68][69][70][71][72] …”

Section: Cells and Plasmids Dnasmentioning

confidence: 99%

Generation of human TRIM5α mutants with high HIV-1 restriction activity

et al. 2010

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“…Several reports suggest that As 2 O 3 inhibits TRIM5␣-mediated restriction, at least in some cell types (3,4,18,27,29,30,36). To seek a contribution of TRIM5␣ to the restriction of HIV infection of iDC and its suppression by As 2 O 3 , we measured the levels of TRIM5␣ in iDC by Western blotting.…”

Section: Several Model Systems Have Indicated That a Key Event In Thementioning

confidence: 99%

Identification of an Arsenic-Sensitive Block to Primate Lentiviral Infection of Human Dendritic Cells

Pion

Stalder

Corrêa

et al. 2007

J Virol

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Dendritic cells are central to the early events of human immunodeficiency virus type 1 (HIV-1) transmission, but HIV-1 infects dendritic cells inefficiently in vitro compared to activated CD4؉ T cells. There is a strong postentry restriction of HIV-1 infection in dendritic cells, partly mediated by the cellular restriction factor APOBEC3G. Here, we reveal that arsenic trioxide markedly increases HIV infection of immature and mature dendritic cells as well as blood-derived myeloid dendritic cells in an APOBEC3G-and TRIM5␣-independent way. Our data suggest the presence of powerful, arsenic-sensitive antiviral activities in primary human immune cells of the dendritic cell lineage.Several model systems have indicated that a key event in the early transmission of human immunodeficiency virus (HIV) is the transfer of virus from dendritic cells (DC) to CD4 ϩ T cells, as reviewed in references 19, 33, and 38. However, high doses of HIV are required to infect DC in vitro (9, 16), as reviewed in reference 24. In the absence of viral replication, DC, including Langerhans cells, can capture and transfer HIV type 1 (HIV-1) to CD4 ϩ T cells via an infectious synapse, which results in high levels of infection (1,13,20,37). There is an early block to HIV-1 entry into DC (6, 9, 25), as well as a strong postentry block to infection (26). The TRIM5 and APOBEC families have recently been shown to be able to block retroviral infection in primate cells (31,35), as reviewed in references 5, 23, and 32. Specifically, TRIM5␣ or APOBEC3G (A3G) can operate, at least in some circumstances, after viral entry and prior to viral integration (7,35). Human TRIM5␣ restricts HIV-1 only weakly (12, 35) and is not thought to have a strong impact on HIV-1 infection or pathogenesis in vivo (15, 28) The restriction factors A3G and, to a lesser extent, APOBEC3F can restrict HIV-1 infection in DC (26). The mechanism of A3G-mediated restriction correlates with the presence of an active form of A3G in lowmolecular-mass (LMM) complexes in resting CD4 ϩ T cells (7) and in DC (26, 34).Arsenic trioxide (As 2 O 3 ) has been shown to increase retroviral infectivity in some cases of restricted infection, but the mechanisms by which it does this are not well understood. In some cases, arsenic has been shown to have an inhibitory effect on TRIM5 (2,4,17,18,27,30). Here, we show that As 2 O 3 treatment restores HIV-1 infectivity in immature DC (iDC) but not in the more permissive CD4 ϩ T cells. The effect of arsenic on DC is specific to primate lentiviruses HIV-1 and HIV-2 and simian immunodeficiency virus from rhesus macaques (SIVmac) but not to the equine lentivirus equine infectious anemia virus (EIAV). Furthermore, it occurs independently of TRIM5␣ and A3G. First, we assayed whether As 2 O 3 affects HIV-1 replication in human iDC. iDC were generated by 6-day culture of monocytes in a mixture of granulocyte-macrophage colony-stimulating factor and interleukin-4 as described previously (8,26). The iDC were then pretreated with As 2 O 3 (2 M) for 18 h, and groups ...

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Lv1 Inhibition of Human Immunodeficiency Virus Type 1 Is Counteracted by Factors That Stimulate Synthesis or Nuclear Translocation of Viral cDNA

Cited by 77 publications

References 50 publications

Target Cell Cyclophilin A Modulates Human Immunodeficiency Virus Type 1 Infectivity

Target Cell Cyclophilin A Modulates Human Immunodeficiency Virus Type 1 Infectivity

Generation of human TRIM5α mutants with high HIV-1 restriction activity

Identification of an Arsenic-Sensitive Block to Primate Lentiviral Infection of Human Dendritic Cells

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