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- W2321344171 abstract "The only successful HIV cure was produced by allogeneic stem cell bone marrow transplantation (BMT) using a [INCREMENT]32 CCR5 homozygous donor. Other HIV patients with lymphoma, treated with BMT and HAART, had significant decreases in HIV reservoirs. One possible explanation for BMT's effect on HIV reservoirs is that BMT conditioning regimens helped deplete the reservoirs. Recently, we showed that host cell apoptosis initiates an alternative replication program in latent herpesviruses. We postulated that although HIV is taxonomically distinct from herpesviruses, apoptosis may also trigger HIV replication. To explore whether apoptosis induces HIV replication, we studied the HIV latently infected cell lines ACH2 and U1. We treated these cells with apoptosis inducing drugs commonly used in BMT conditioning regimens: etoposide, fludarabine, doxorubicin, or vincristine. We found that drug induced apoptosis elicited HIV reactivation and treatment with the pan-caspase inhibitor (zVAD-fmk) before inducing apoptosis, inhibited HIV reactivation. Overexpression of activated caspase-3 and caspase-8 also induced apoptosis-mediated HIV reactivation, suggesting the involvement of caspase activation in HIV reactivation. We conclude that HIV can sense host cell apoptosis and replicate in response. Our findings provide new insight into the reduction in HIV reservoirs observed in patients treated with BMT. Understanding the mechanisms through which apoptosis activates HIV may lead to the development of new ways to attack and deplete the HIV latent reservoir." @default.
- W2321344171 created "2016-06-24" @default.
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- W2321344171 date "2014-11-01" @default.
- W2321344171 modified "2023-09-23" @default.
- W2321344171 title "P-B1 Apoptosis-mediated HIV reactivation" @default.
- W2321344171 doi "https://doi.org/10.1097/01.qai.0000456181.73981.7b" @default.
- W2321344171 hasPublicationYear "2014" @default.
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