ArticleRetrovirology2013
Heterogeneous susceptibility of circulating SIV isolate capsids to HIV-interacting factors.
Article in Retrovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
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- Cyclophilin A facilitates HIV-1 integration.Journal of virology · 2024Article
- A new class of capsid-targeting inhibitors that specifically block HIV-1 nuclear import.EMBO molecular medicine · 2024Article
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- Defining the HIV Capsid Binding Site of Nucleoporin 153.mSphere · 2022Article
- The SARS-CoV-2 S1 Spike Protein Promotes MAPK and NF-kB Activation in Human Lung Cells and Inflammatory Cytokine Production in Human Lung and Intestinal Epithelial Cells.Microorganisms · 2022Article
- Multiple expansions of globally uncommon SARS-CoV-2 lineages in Nigeria.Nature communications · 2022Article
- HIV-1 capsid variability: viral exploitation and evasion of capsid-binding molecules.Retrovirology · 2021Review
- Coincident rapid expansion of two SARS-CoV-2 lineages with enhanced infectivity in Nigeria.medRxiv : the preprint server for health sciences · 2021Article
- Cell Type-Dependent Escape of Capsid Inhibitors by Simian Immunodeficiency Virus SIVcpz.Journal of virology · 2020Article
- Characterization of HIV-1 uncoating in human microglial cell lines.Virology journal · 2020Article
- Multiple Pathways To Avoid Beta Interferon Sensitivity of HIV-1 by Mutations in Capsid.Journal of virology · 2019Article
- Species-specific vulnerability of RanBP2 shaped the evolution of SIV as it transmitted in African apes.PLoS pathogens · 2018Article
- Early cytoplasmic uncoating is associated with infectivity of HIV-1.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Cyclophilins and nucleoporins are required for infection mediated by capsids from circulating HIV-2 primary isolates.Scientific reports · 2017Article
- Capsid-CPSF6 Interaction Is Dispensable for HIV-1 Replication in Primary Cells but Is Selected during Virus Passage In Vivo.Journal of virology · 2016Article
- Nonhuman Primates and Humanized Mice for Studies of HIV-1 Integrase Inhibitors: A Review.Pathogens & immunity · 2016Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMany species of non-human primates in Africa are naturally infected by simian immunodeficiency viruses (SIV) and humans stand at the forefront of exposure to these viruses in Sub-Saharan Africa. Cross-species transmission and adaptation of SIV to humans have given rise to human immunodeficiency viruses (HIV-1 and HIV-2) on twelve accountable, independent occasions. However, the determinants contributing to a simian-to-human lasting transmission are not fully understood. Following entry, viral cores are released into the cytoplasm and become the principal target of host cellular factors. Here, we evaluated cellular factors likely to be involved in potential new SIV cross-species transmissions. We investigated the interactions of capsids from naturally circulating SIV isolates with both HIV-1 restricting (i.e. TRIM5 proteins) and facilitating (i.e. cyclophilin A and nucleopore-associated Nup358/RanBP2 and Nup153) factors in single-round infectivity assays that reproduce early stages of the viral life-cycle.
resultsWe show that human TRIM5α is unlikely to prevent cross-species transmission of any SIV we tested and observed that the SIV CA-CypA interaction is a widespread but not a universal feature. Moreover, entry in the nucleus of different SIV appeared to follow pathways that do not necessarily recruit Nup358/RanBP2 or Nup153, and this regardless of their interaction with CypA. Nevertheless, we found that, like HIV-1, human-adapted HIV-2 infection was dependent on Nup358/RanBP2 and Nup153 interactions for optimal infection. Furthermore, we found that, unlike HIV CA, SIV CA did not require a direct interaction with the Cyp-like domain of Nup358/RanBP2 to carry out successful infection.
conclusionsCirculating SIV present a variety of phenotypes with regard to CA-interacting restricting or facilitating factors. Altogether, we unveiled unidentified pathways for SIV CA, which could also be exploited by HIV in different cellular contexts, to drive entry into the nucleus. Our findings warrant a closer evaluation of other potential defenses against circulating SIV.
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