ArticleProceedings of the National Academy of Sciences of the United States of America2019
Derivation of simian tropic HIV-1 infectious clone reveals virus adaptation to a new host.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 17 citations in OpenAlex.
- CXCR4-tropic HIV-1 infection in an immunocompetent monkey model.Nature communications · 2026Article
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- Minimally Modified HIV-1 Infection of Macaques: Development, Utility, and Limitations of Current Models.Viruses · 2024Review
- Virus specificity and nucleoporin requirements for MX2 activity are affected by GTPase function and capsid-CypA interactions.PLoS pathogens · 2024Article
- Virus specificity and nucleoporin requirements for MX2 activity are affected by GTPase function and capsid-CypA interactions.bioRxiv : the preprint server for biology · 2023Article
- Genomic Evidence for the Nonpathogenic State in HIV-1-Infected Northern Pig-Tailed Macaques.Molecular biology and evolution · 2023Article
- A pigtailed macaque model of Kyasanur Forest disease virus and Alkhurma hemorrhagic disease virus pathogenesis.PLoS pathogens · 2021Article
- HIV-1 capsid variability: viral exploitation and evasion of capsid-binding molecules.Retrovirology · 2021Review
- Article
- Toward a Macaque Model of HIV-1 Infection: Roadblocks, Progress, and Future Strategies.Frontiers in microbiology · 2020Review
- Grand Challenge in Human/Animal Virology: Unseen, Smallest Replicative Entities Shape the Whole Globe.Frontiers in microbiology · 2020Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
To replicate in a new host, lentiviruses must adapt to exploit required host factors and evade species-specific antiviral proteins. Understanding how host protein variation drives lentivirus adaptation allowed us to expand the host range of HIV-1 to pigtail macaques. We have previously derived a viral swarm (in the blood of infected animals) that can cause AIDS in this new host. To further exploit this reagent, we generated infectious molecular clones (IMCs) from the viral swarm. We identified clones with high replicative capacity in pigtail peripheral blood mononuclear cells (PBMC) in vitro and used in vivo replication to select an individual IMC, named stHIV-A19 (for simian tropic HIV-1 clone A19), which recapitulated the phenotype obtained with the viral swarm. Adaptation of HIV-1 in macaques led to the acquisition of amino acid changes in viral proteins, such as capsid (CA), that are rarely seen in HIV-1-infected humans. Using stHIV-A19, we show that these CA changes confer a partial resistance to the host cell inhibitor Mx2 from pigtail macaques, but that complete resistance is associated with a fitness defect. Adaptation of HIV-1 to a new host will lead to a more accurate animal model and a better understanding of virus-host interactions.
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