AI Article Synopsis
- HIV-1 primarily establishes latency by infecting activated CD4+ T cells, which then turn into lasting memory cells.
- This latency helps the virus evade the immune system and survive even when patients are on antiretroviral therapy, creating challenges for treatment.
- The text describes both original and simplified models of HIV-1 latency, which utilize replication-competent viruses to generate many latently infected CD4+ T cells for studying the underlying mechanisms of HIV latency and reactivation.
Article Abstract
HIV-1 establishes latency primarily by infecting activated CD4+ T cells that later return to quiescence as memory cells. Latency allows HIV-1 to evade immune responses and to persist during antiretroviral therapy, which represents an important problem in clinical practice. Here we describe both the original and a simplified version of HIV-1 latency models that mimics this process using replication competent viruses. Our model allows generation of large numbers of latently infected CD4+ T cell to dissect molecular mechanisms of HIV latency and reactivation.
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| http://dx.doi.org/10.1007/978-1-0716-1871-4_3 | DOI Listing |
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