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Depiction of the molecular interactions in the ganglia showing the inverse relationship between LATs and lytic proteins. Vaccine and Infectious Diseases Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA. Herpesviruses encode proteins that help them to evade detection by pattern recognition receptors (PRRs). This journal is a member of and subscribes to the principles of the Committee on Publication Ethics.


Activation comprises active transcription of viral RNA and high lytic protein expression accompanied by low LAT production. For example, the herpes simplex virus type 1 (HSV-1) proteins ICP34.5 and virion host shut-off protein (Vhs) prevent the recognition of viral nucleic acids by inhibiting autophagy and degrading viral RNA, respectively.
Purified RVLPs from (a–d) Vero 2-2 cells, (e,f) HeLa cells, and (g,h) Hek293 cells infected with HSV-1 amplicon vectors (MOI 1). Two days postinfection, RVLPs were purified over a sucrose cushion and the concentrated particles were analyzed by electron microscopy.


There are also more general mechanisms that target all PRRs; for example, human herpesvirus 8 (HHV8) ORF45 protein interacts with IFN regulatory factor 7 (IRF7) and inhibits its phosphorylation and nuclear translocation. This prevents the interaction of these transcription factors with DNA, and the assembly of functional transcriptional complexes.



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