ArticleFrontiers in microbiology2013
Macaques as model hosts for studies of HIV-1 infection.
Article in Frontiers in microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Advancing the preclinical study of comorbid neuroHIV and substance use disorders: Current perspectives and future directions.Brain, behavior, and immunity · 2023Review
- A Simian Immunodeficiency Virus-Infected Macaque Model ofAIDS research and human retroviruses · 2023Article
- Impact of human immunodeficiency virus on pulmonary vascular disease.Global cardiology science & practice · 2021Review
- Article
- African green monkeys avoid SIV disease progression by preventing intestinal dysfunction and maintaining mucosal barrier integrity.PLoS pathogens · 2020Article
- Commentary: Derivation of Simian Tropic HIV-1 Infectious Clone Reveals Virus Adaptation to a New Host.Frontiers in cellular and infection microbiology · 2020Article
- Toward a Macaque Model of HIV-1 Infection: Roadblocks, Progress, and Future Strategies.Frontiers in microbiology · 2020Review
- Cynomolgus macaque IL37 polymorphism and control of SIV infection.Scientific reports · 2019Article
- Characterization of major histocompatibility complex-related molecule 1 sequence variants in non-human primates.Immunogenetics · 2019Article
- The Many Faces of the Flavivirus NS5 Protein in Antagonism of Type I Interferon Signaling.Journal of virology · 2017Review
- Review
- Contrasted patterns of variation and evolutionary convergence at the antiviral OAS1 gene in old world primates.Immunogenetics · 2015Article
- MHC and KIR Polymorphisms in Rhesus Macaque SIV Infection.Frontiers in immunology · 2015Review
- Animal model studies on viral infections.Frontiers in microbiology · 2014Article
- Understanding restriction factors and intrinsic immunity: insights and lessons from the primate lentiviruses.Future virologyArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Increasing evidence indicates that the host range of primate lentiviruses is in part determined by their ability to counteract innate restriction factors that are effectors of the type 1 interferon (IFN-1) response. For human immunodeficiency virus type 1 (HIV-1), in vitro experiments have shown that its tropism may be narrow and limited to humans and chimpanzees because its replication in other non-human primate species is hindered by factors such as TRIM5α (tripartite motif 5 alpha), APOBEC3G (apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3), and tetherin. Based on these data, it has been hypothesized that primate lentiviruses will infect and replicate in a new species if they are able to counteract and evade suppression by the IFN-1 response. Several studies have tested whether engineering HIV-1 recombinants with minimal amounts of simian immunodeficiency virus sequences would enable replication in CD4(+) T cells of non-natural hosts such as Asian macaques and proposed that infection of these macaque species could be used to study transmission and pathogenesis. Indeed, infection of macaques with these viruses revealed that Vif-mediated counteraction of APOBEC3G function is central to cross-species tropism but that other IFN-induced factors may also play important roles in controlling replication. Further studies of these macaque models of infection with HIV-1 derivatives could provide valuable insights into the interaction of lentiviruses and the innate immune response and how lentiviruses adapt and cause disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.