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Immune Netw.  2013 Oct;13(5):163-167. 10.4110/in.2013.13.5.163.

Respiratory Syncytial Virus (RSV) Modulation at the Virus-Host Interface Affects Immune Outcome and Disease Pathogenesis

Affiliations
  • 1Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens GA 30602, USA. ratripp@uga.edu

Abstract

The dynamics of the virus-host interface in the response to respiratory virus infection is not well-understood; however, it is at this juncture that host immunity to infection evolves. Respiratory viruses have been shown to modulate the host response to gain a replication advantage through a variety of mechanisms. Viruses are parasites and must co-opt host genes for replication, and must interface with host cellular machinery to achieve an optimal balance between viral and cellular gene expression. Host cells have numerous strategies to resist infection, replication and virus spread, and only recently are we beginning to understand the network and pathways affected. The following is a short review article covering some of the studies associated with the Tripp laboratory that have addressed how respiratory syncytial virus (RSV) operates at the virus-host interface to affects immune outcome and disease pathogenesis.

Keyword

RSV; Virus-host interface; Disease intervention

MeSH Terms

Gene Expression
Imidazoles
Nitro Compounds
Parasites
Respiratory Syncytial Viruses*
Viruses
Imidazoles
Nitro Compounds
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