Molecular basis of latency in pathogenic human viruses.
Several human viruses are able to latently infect specific target cell populations in vivo. Analysis of the replication cycles of herpes simplex virus, Epstein-Barr virus, and human immunodeficiency virus suggests that the latent infections established by these human pathogens primarily result from a lack of host factors critical for the expression of viral early gene products. The subsequent activation of specific cellular transcription factors in response to extracellular stimuli can induce the expression of these viral regulatory proteins and lead to a burst of lytic viral replication. Latency in these eukaryotic viruses therefore contrasts with latency in bacteriophage, which is maintained primarily by the expression of virally encoded repressors of lytic replication.
Garcia-Blanco
M A
MA
Section of Cell Growth, Regulation, and Oncogenesis, Duke University Medical Center, Durham, NC 27710.
Cullen
B R
BR
D015497:HIV-1 / Q000472:pathogenicity / Q000502:physiology; D004854:Herpesvirus 4, Human / Q000472:pathogenicity / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D018139:Simplexvirus / Q000472:pathogenicity / Q000502:physiology; D018406:Virus Physiological Phenomena; D014780:Viruses / Q000472:pathogenicity