Paradoxically, alphaherpesviruses, which otherwise are extremely lytic, establish reactivatable latent infections in their natural hosts; primarily, in nervous tissue. To accomplish this, lytic replication must not occur in neurons during the latent phase of infection, but is probably necessary for viral reactivation. Progress has been made in the last few years in describing molecular aspects of viral latency and reactivation. Restricted transcription of the viral genome is seen in latently infected neurons, with latency-associated transcription being antiparallel and overlapping viral immediate early genes. Results in animal latency systems using viral mutants containing deletions in this region of the genome indicate that latency-associated transcription has a significant role in viral latency, probably in establishment or reactivation of latent infection. The challenges, however, of understanding the complexities underlying conditional permissiveness of neurons for viral replication still lie ahead.
- Latency-associated transcripts
- Latent infection
- Viral reactivation
- Virus-neuron interaction
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