Poster abstracts

Poster number 71 submitted by Amanda Claggett

Disruption of Glucocorticoid Receptor (GR) function by Respiratory Syncytial Virus

Amanda M. Claggett (1Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Internal Medicine, 2Institute of Behavioral Medicine Research), Ian C. Davis (Department of Veterinary Biosciences, School of Veterinary Medicine), Jeanette I. Webster Marketon (1Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Internal Medicine, 2Institute of Behavioral Medicine Research)

Abstract:
We have previously shown that the anthrax lethal toxin represses glucocorticoid receptor (GR) activity in vitro and in vivo. The effect of a viral infection, Respiratory Syncyctial Virus (RSV), on GR function is investigated in this study. RSV infects more people over 65 (3-7% of the population) than influenza A virus. In addition, RSV causes bronchiolitis and is responsible for the hospitalization of 2-3% of infants under 1 year old. Infection in both these groups causes serious illness. GR is a nuclear hormone receptor that is important in the modulation of immune responses. We have shown that RSV infection represses GR transactivation of the MMTV promoter in transient transfections in A549 cells. However, no change in GR number between infected and uninfected cells was observed. The molecular mechanism of the observed effect of RSV on GR signaling is under further investigation. This work will determine a role for the use of glucocorticoids during an on-going RSV infection and suggests a common connection between both bacterial and viral infections and GR signaling.
Funding provided by NIH T32 AI55411.

Keywords: RSV, glucocorticoid receptor, asthma