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Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies
Published on: January 7, 2019
Human immunodeficiency virus persistence and production in T-cell development.
Kevin B Gurney1, Christel H Uittenbogaart
1Department of Microbiology, Immunology, and Molecular Genetics, UCLA School of Medicine, Los Angeles, CA 90095-1747, USA.
Clinical and Vaccine Immunology : CVI
|September 22, 2006
Summary
Human immunodeficiency virus type 1 (HIV-1) infection targets specific thymocyte subsets based on their developmental stage. R5 HIV-1 primarily infects mature cells, while X4 HIV-1 targets immature cells, impacting HIV pathogenesis.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- HIV-1 replication is influenced by host cell activation and coreceptor expression.
- Thymocyte development involves distinct stages with varying cellular characteristics.
Purpose of the Study:
- To investigate how thymocyte activation stage impacts HIV-1 life cycle.
- To determine the tropism of R5 and X4 HIV-1 in different thymocyte subsets.
Main Methods:
- Analysis of R5 and X4 HIV-1 entry, reverse transcription, and expression.
- Investigation in discrete thymocyte subsets across T-cell development stages.
Main Results:
- R5 HIV-1 preferentially entered and replicated in mature CD3(+/hi) CD27(+) thymocytes.
- X4 HIV-1 expression and replication were mainly observed in immature CD3(-/+/low) CD27(-) CD69(-) thymocytes.
- HIV-1 proviral burden correlated with coreceptor expression; full reverse transcription occurred in all subsets.
Conclusions:
- HIV-1 tropism in thymocytes is linked to developmental stage and coreceptor expression.
- R5 HIV-1 targets mature thymocytes crucial for immune response, influencing HIV pathogenesis.
- Latent HIV-1 DNA can be established early in T-cell development within immature thymocytes.
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