Influence of cell cycle on HIV-1 expression differs among various models of chronic infection.
Because of an inherent dependence on host cell second and third messenger signaling pathways for activation of HIV-1 expression, a potential exists for a relationship between the induction of latent HIV-1 and cell-cycle-related events. To investigate this potential relationship, cellular models of latent HIV-1 infection (OM-10.1 promyelocytes, ACH-2 T-lymphocytes, and U1 promonocytes) were chemically treated or gamma-irradiated to synchronize cultures at each cell cycle stage and then examined for constitutive and TNF-alpha-induced HIV-1 expression. Cell cycle synchronization alone had no effect on HIV-1 expression in OM-10.1 and U1 cultures; whereas enhanced constitutive HIV-1 expression was observed in ACH-2 cultures at G2 + M. A 2 hour TNF-alpha treatment of all synchronized OM-10.1 cultures activated HIV-1 expression to a similar extent as unsynchronized cultures. In contrast, the extent of TNF-alpha-induced HIV-1 expression in ACH-2 S and G2 + M cultures and in the U1 G0/G1 culture was greater than that in unsynchronized control cultures. However, no delay in the initial response was observed. Thus, the influence of cell cycle on constitutive and induced HIV-1 expression varied in each cellular model and, therefore, may further relate to the different molecular mechanisms maintaining viral latency.
Roberts
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Retrovirus Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Fang
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Butera
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D002453:Cell Cycle; D002460:Cell Line; D016655:HIV Core Protein p24 / Q000032:analysis; D015497:HIV-1 / Q000235:genetics / Q000502:physiology*; D018922:HL-60 Cells; D006801:Humans; D012367:RNA, Viral; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014775:Virus Activation; D017735:Virus Latency; D014779:Virus Replication
D016655:HIV Core Protein p24; D012367:RNA, Viral; D014409:Tumor Necrosis Factor-alpha