forumhiv.de • HIV reactivation by apoptosis

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The general picture input post congress presentation is now also available as regular publication in the journal Retrovirology. In addition to the already written summary we learn now tell you that the HI virus, which were produced in connection with the apoptosis of host cells were infectious, while the replication kinetics thereby different from the kinetics of which one or with conventional agents such as TNF-α PMA (12-o-tetradecanoylphorbol-13-acetate) was observed. Apoptosis can strongly actively dividing HIV both in itself, as well as activate in cells in the G1 phase of the cell cycle. Furthermore, the authors go on an analogy with herpesviruses, which have as HIV-1 on the one hand developed evolutionary mechanisms to prevent apoptosis of host cells. On the other hand herpesviruses such as HSV-1, KSHV. developed HHV6A, HHV6B, HHV7 and EBV but also alternative replication programs (ARP) ,, to be produced as an emergency escape mechanism even before the death of the cell new virions. From an evolutionary point of view, triggered by apoptosis ARP is useful because without ARP would the virus die with the cell to have produced no offspring. An ARP, which is triggered by apoptosis, therefore represents a useful strategy for survival in viruses which are capable of long-term latency. Although herpes viruses and retroviruses belong to completely different families, they seem by the long latent infection to be exposed to comparable evolutionary pressure, which resulted in similar adjustments to risk of apoptosis. It is unclear how exactly activated caspases enable replication of latent viruses such as HIV or herpes viruses. One hypothesis is that converted by the caspase cleavage of a viral or host factors, an inert protein into a potent transactivator and so the replication of the virus is activated. Abstract Background

Despite much work, safe and effective Approaches to attack and deplete the long-lived reservoir of cells latently infected with HIV-1 remain on elusive goal. Patients infected with HIV-1 Treated with cytotoxic agents or bone marrow transplantation can experience Decreases in the reservoir of HIV-1 latently infected cells. Other viruses capable of long-term latency,: such as herpesviruses, can sense host cell apoptosis and respond by initiating replication. These observations suggest did other viruses capable of long-term latency, like HIV-1, might also sense When its host cell is about to undergo apoptosis and respond by initiating replication. results Pro-monocytic (U1) and lymphoid (ACH-2) HIV-1 persistently infected cell lines were Treated with cytotoxic drugs – doxorubicin, etoposide, fludarabine phosphate, or vincristine – and activation of latent HIV-1 which Evaluated using assays for HIV 1 RNA and p24 production. Both cell lines Showed dose-dependent Increases in apoptosis and associated HIV-1 activation Following exposure to the cytotoxic agents. Pretreatment of the cells with the pan-caspase inhibitor Z-VAD-FMK prior to exposure to the cytotoxic agents inhibited apoptosis and viral activation. Direct exposure of the latently infected cell lines to activated caspases therefore induced viral replication. HIV-1 virions produced in association with host cell apoptosis were infectious. Conclusions The results indicate did latent HIV-1 can sense When its host cell is undergoing apoptosis and Responds by Completing its replication cycle. The results may help explain why patients Treated with cytotoxic regimens for bone marrow transplantation Showed Reductions in the reservoir of latently infected cells.

The results therefore suggest dass die mechanisms did HIV-1 uses to sense and respond to host cell apoptosis signal may represent new targets for helpful Approaches to attack and deplete the long-lived reservoir of cells latently infected with HIV-1. Apoptosis-induced activation of HIV-1 in latently infected cell lines: http://www. retrovirology. com/c . . . abstracts