Controlling lentiviruses: Single amino acid changes can determine specificity

Kaiser, Shari M.; Emerman, Michael

doi:10.1073/pnas.0400929101

Cited by 6 publications

(2 citation statements)

References 24 publications

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“…The identification of an SIV vif cellular target, a member of the cytidine deaminase APOBEC family, has permitted a better understanding of species restrictions on the emergence of lentiviral infections. The cellular deaminase is incorporated into the lentiviral virion during reverse transcription to direct the deamination of cytidine to uridine on the minus strand of viral DNA (200). This deamination results in catastrophic G-to-A mutations in the viral genome, determining inactivation (157,215,237,411) and/or degradation (348) of the viral genome.…”

Section: Cytidine Deaminase and Vifmentioning

confidence: 99%

Going Wild: Lessons from Naturally Occurring T-Lymphotropic Lentiviruses

2006

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SUMMARY Over 40 nonhuman primate (NHP) species harbor species-specific simian immunodeficiency viruses (SIVs). Similarly, more than 20 species of nondomestic felids and African hyenids demonstrate seroreactivity against feline immunodeficiency virus (FIV) antigens. While it has been challenging to study the biological implications of nonfatal infections in natural populations, epidemiologic and clinical studies performed thus far have only rarely detected increased morbidity or impaired fecundity/survival of naturally infected SIV- or FIV-seropositive versus -seronegative animals. Cross-species transmissions of these agents are rare in nature but have been used to develop experimental systems to evaluate mechanisms of pathogenicity and to develop animal models of HIV/AIDS. Given that felids and primates are substantially evolutionarily removed yet demonstrate the same pattern of apparently nonpathogenic lentiviral infections, comparison of the biological behaviors of these viruses can yield important implications for host-lentiviral adaptation which are relevant to human HIV/AIDS infection. This review therefore evaluates similarities in epidemiology, lentiviral genotyping, pathogenicity, host immune responses, and cross-species transmission of FIVs and factors associated with the establishment of lentiviral infections in new species. This comparison of consistent patterns in lentivirus biology will expose new directions for scientific inquiry for understanding the basis for virulence versus avirulence.

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Section: Cytidine Deaminase and Vifmentioning

confidence: 99%

Going Wild: Lessons from Naturally Occurring T-Lymphotropic Lentiviruses

2006

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“…While the HIV-1 Vif accessory protein was found to inhibit APOBEC3G activity in human cells to allow productive virus replication, it fails to counteract APOBEC3G in monkey cells such as rhesus macaques and African monkeys [ 21 ]. A single amino acid change between human and macaque APOBOEC3G was shown to be responsible for the inability of HIV-1 Vif to counteract macaque APOBEC3G [ 22 , 23 , 24 ]. Other studies have further shown that TRIM5α, a cellular protein belonging to the tripartite motif-containing (TRIM) family of proteins, represses HIV-1 from infecting Old World monkey cells, in addition to other retroviruses in multiple species, by destabilizing capsid uncoating.…”

Section: Introductionmentioning

confidence: 99%

Productive Replication of HIV-1 but Not SIVmac in Small Ruminant Cells

et al. 2022

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Animal lentiviruses (LVs) have been proven to have the capacity to cross the species barrier, to adapt in the new hosts, and to increase their pathogenesis, therefore leading to the emergence of threatening diseases. However, their potential for widespread diffusion is limited by restrictive cellular factors that block viral replication in the cells of many species. In previous studies, we demonstrated that the restriction of CAEV infection of sheep choroid plexus cells was due to aberrant post-translation cleavage of the CAEV Env gp170 precursor. Later, we showed that the lack of specific receptor(s) for caprine encephalitis arthritis virus (CAEV) on the surface of human cells was the only barrier to their infection. Here, we examined whether small ruminant (SR) cells can support the replication of primate LVs. Three sheep and goat cell lines were inoculated with cell-free HIV-1 and SIVmac viral stocks or transfected with infectious molecular clone DNAs of these viruses. The two recombinant lentiviral clones contained the green fluorescent protein (GFP) reporter sequence. Infection was detected by GFP expression in target cells, and the infectious virus produced and released in the culture medium of treated cells was detected using the indicator TZM-bl cell line. Pseudotyped HIV-GFP and SIV-GFP with vesicular stomatitis virus G glycoprotein (VSV-G) allowed the cell receptors to be overcome for virus entry to further evaluate the viral replication/restriction in SR cells. As expected, neither HIV nor SIV viruses infected any of the SR cells. In contrast, the transfection of plasmid DNAs of the infectious molecular clones of both viruses in SR cells produced high titers of infectious viruses for human indicators, but not SR cell lines. Surprisingly, SR cells inoculated with HIV-GFP/VSV-G, but not SIV-GFP/VSV-G, expressed the GFP and produced a virus that efficiently infected the human indictor, but not the SR cells. Collectively, these data provide a demonstration of the lack of replication of the SIVmac genome in SR cells, while, in contrast, there was no restriction on the replication of the IV-1 genome in these cells. However, because of the lack of functional receptors to SIVmac and HIV-1 at the surface of SR cells, there is specific lentiviral entry.

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Lentiviruses in Their Natural Hosts

Voevodin¹,

Marx

2009

Simian Virology

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Controlling lentiviruses: Single amino acid changes can determine specificity

Cited by 6 publications

References 24 publications

Going Wild: Lessons from Naturally Occurring T-Lymphotropic Lentiviruses

Going Wild: Lessons from Naturally Occurring T-Lymphotropic Lentiviruses

Productive Replication of HIV-1 but Not SIVmac in Small Ruminant Cells

Lentiviruses in Their Natural Hosts

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