Key result
Expression of exogenous Tas initiates a switch from latent to lytic replication, while Bet functions as a negative regulator of basal internal promoter activity, limiting PMA-induced activation.
The Bet protein functions as a negative regulator of basal internal promoter activity in foamy viruses, controlling the switch from latent to lytic replication.
No immediate clinical implications in humans; leaves open Bet as a regulatory target for foamy virus latency in future studies.
Spumaviruses, commonly called foamy viruses (FV), are complex retroviruses that establish lifelong persistent infections without any accompanying pathologies. In tissue culture, cells can be either lytically or latently infected, depending on cell type. Regulation of FV replication is controlled by two promoters: the LTR and a second promoter within the env gene termed the internal promoter (IP). The IP directs expression of the transcriptional activator, Tas, and a second accessory protein, Bet, whose function has been elusive. In this study, we report that expression of exogenous Tas is sufficient to initiate a switch from latent to lytic replication. We also show that treatment with the phorbol ester phorbol 12-myristate 13-acetate (PMA) can lead to an increase in transcription from the IP, and that Bet protein expression abrogates this effect. Finally, we demonstrate that Bet expression severely limits the ability of PMA to activate transcription of latent FV genomes, and that replication of a Bet(-) virus is more easily activated than wild-type FV. Taken together, these data suggest that viral transcription is regulated by a sensitive switch, and that Bet functions as a negative regulator of basal IP activity.
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Meiering et al. (2002) studied Spumavirus (foamy virus) infection. Exogenous Tas expression and Bet protein expression vs. Wild-type FV / Latent infection was evaluated on Viral transcription and replication switch from latent to lytic. Expression of exogenous Tas initiates a switch from latent to lytic replication, while Bet functions as a negative regulator of basal internal promoter activity, limiting PMA-induced activation.
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