Herpes Simplex Virus Triggers and Then Disarms a Host Antiviral Response

Abstract

Virus infection induces an antiviral response that is predominantly associated with the synthesis and secretion of soluble interferon. Here, we report that herpes simplex virus type 1 virions induce an interferonindependent antiviral state in human embryonic lung cells that prevents plaquing of a variety of viruses. Microarray analysis of 19,000 human expressed sequence tags revealed induction of a limited set of host genes, the majority of which are also induced by interferon. Genes implicated in controlling the intracellular spread of virus and eliminating virally infected cells were among those induced. Induction of the cellular response occurred in the absence of de novo cellular protein synthesis and required viral penetration. In addition, this response was only seen when viral gene expression was inhibited, suggesting that a newly synthesized viral protein(s) may function as an inhibitor of this response.

Herpes simplex virus type-1 infection upregulates cellular promoters and telomerase activity in both tumor and nontumor human cells

“…In addition, the above mutants also showed significantly lower levels of ICP0 comparing to ICP0+/ICP4+ mutants (Fig.4b), which further emphasizes the role of ICP0 in regulating cellular promoter activity. On the other hand, ICP0 may enhance certain cellular gene expression but inhibits the others as shown by recent studies using cDNA arrays on infected cells 34,62,63 It is interesting to note that ICP27-mutant 5d1.2 showed significantly higher level of tyrosinase promoter activity than the wild-type KOS, which suggest that ICP27 may repress the ICP0 caused effect.…”

The Plant Virus Tomato Spotted Wilt Tospovirus Activates the Immune System of Its Main Insect Vector, Frankliniella occidentalis

“…Other studies, involving genomic-scale approaches to evaluate immune responses against viral infections, have used mostly cDNA microarrays (11,16,18,34,46,54). The method used here, which combined subtracted cDNA libraries and DNA macroarrays, is simple, practical, and less expensive than microarrays.…”

The major tegument structural protein VP22 targets areas of dispersed nucleolin and marginalized chromatin during productive herpes simplex virus 1 infection

“…This implies that neither incoming virion factors nor the induction of cellular antiviral responders (Mossman et al, 2001;Nicholl et al, 2000) are responsible for the effect. Although HSV-1 infection in the presence of CHX results in apoptosis (Aubert and Blaho, 1999;Koyama and Adachi, 1997) in tumor cells (Nguyen et al, 2007), Vero cells require protein facilitator(s) to stimulate this cell death response (Nguyen et al, 2005).…”