Acetylsalicylic acid reduces viral shedding induced by thermal stress

Acetylsalicylic acid reduces viral shedding induced by thermal stress

Acetylsalicylic acid reduces viral shedding induced by thermal stress
The stress-induced host cell factors initiating the expression of the herpes simplex virus lytic cycle from the latent viral genome are not known. Vhs mutants display a host range phenotype: translation of viral true late mRNAs is severely impaired and stress granules accumulate in HeLa cells, while translation proceeds normally in Vero cells. Distinct phases were identified including the native state of the virus, an intermediate phase that could represent gradual swelling and/or shedding of the viral envelope, and a highly disrupted, aggregated phase. Without FS, CY significantly decreased survival and body weight gain, splenic leukocyte numbers, in vivo serum cytokine level and in vitro splenocyte cytokine production during HSV-1infection. Furthermore, this model has the potential to advance our understanding of how HS initiates the HSV-1 productive cycle from a cryptic viral genome. The suppression of IFN-gamma-induced, macrophage-mediated lysis of HSV-infected cells occurred concomitantly with a marked increase in macrophage intracellular cyclic AMP levels. Acetylsalicylic acid inhibited heat stress–induced shedding of virus in the tears and reduced the numbers of corneal and trigeminal ganglion homogenates containing virus.

In contrast, infectious virus was detected in the ganglia of mice latently infected with the parental strain but not with ICP0 null mutant dl1403 or FXE. Our results demonstrate that PKR is essential for stress granule formation in the absence of vhs, but plays at best a secondary role in suppressing translation of viral mRNAs. The results indicate that a cyclooxygenase inhibitor such as acetylsalicylic acid can reduce recurrent viral infection in mice. These findings may implicate prostaglandins as agents in the viral reactivation process and suggest that therapy to suppress viral reactivation using nontoxic inhibitors of prostaglandin synthesis may be effective in humans.

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