AI Article Synopsis
- Previous studies suggest that latent herpesvirus infections may help protect against other infections and worsen chronic inflammatory diseases.
- Researchers found over 500 genes that were differently expressed in the spleens, livers, and brains of mice infected with gammaherpesvirus 68, with unique gene patterns for each organ.
- Key genes linked to the virus's latency were identified, indicating that chronic herpesvirus infections can significantly change how genes are expressed in host organs, potentially affecting overall health and immune response.
Article Abstract
Previous studies identified a role for latent herpesvirus infection in cross-protection against infection and exacerbation of chronic inflammatory diseases. Here, we identified more than 500 genes differentially expressed in spleens, livers, or brains of mice latently infected with gammaherpesvirus 68 and found that distinct sets of genes linked to different pathways were altered in the spleen compared to those in the liver. Several of the most differentially expressed latency-specific genes (e.g., the gamma interferon [IFN-γ], Cxcl9, and Ccl5 genes) are associated with known latency-specific phenotypes. Chronic herpesvirus infection, therefore, significantly alters the transcriptional status of host organs. We speculate that such changes may influence host physiology, the status of the immune system, and disease susceptibility.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3911696 | PMC |
| http://dx.doi.org/10.1128/JVI.02708-13 | DOI Listing |
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