Restricted expression of herpes simplex virus lytic genes during establishment of latent infection by thymidine kinase-negative mutant viruses.
Infection of cells by herpes simplex virus (HSV) can lead to either lytic, productive infection or nonlytic, latent infection. The factors influencing this infection pathway decision are largely unknown. Thymidine kinase-negative mutant viruses can establish latent infection in neurons of mouse trigeminal ganglia but do not replicate productively in these cells. We show that during the early stages of establishment of latency by these mutants, expression of viral lytic genes is drastically reduced or undetectable as assayed by in situ hybridization. Thus, establishment of latent infection by HSV can occur despite severely restricted levels of lytic gene expression. This suggests that the block to productive replication during establishment of latent infection by HSV occurs before or early during the expression of alpha genes.
Kosz-Vnenchak
M
M
Department of Microbiology, Harvard Medical School, Boston, Massachusetts 02115.
Coen
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DM
Knipe
D M
DM
D000818:Animals; D003315:Cornea / Q000382:microbiology; D015967:Gene Expression Regulation, Viral; D005814:Genes, Viral; D006561:Herpes Simplex / Q000235:genetics*; D066298:In Vitro Techniques; D051379:Mice; D009154:Mutation; D009693:Nucleic Acid Hybridization; D012367:RNA, Viral / Q000235:genetics; D018139:Simplexvirus / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity*; D013937:Thymidine Kinase / Q000235:genetics; D014158:Transcription, Genetic; D012668:Trigeminal Ganglion / Q000382:microbiology; D015678:Viral Structural Proteins / Q000235:genetics
D012367:RNA, Viral; D015678:Viral Structural Proteins; D013937:Thymidine Kinase