Respiratory syncytial virus attachment G and nonstructural proteins modulate the early antiviral host response to infection

Abstract

Respiratory syncytial virus (RSV) is an important cause of serious lower respiratory tract illness in infants and young children worldwide causing repeat infections throughout life with serious complications occurring in elderly and immune compromised populations. Little is understood about how RSV modulates the host immune response and currently there is no safe effective vaccine available. In the present study, we focused on the early antiviral host immune response to RSV infection, with emphasis on patterns of SOCS and interferon expression. Examination of mouse lung epithelial cells infected with wtRSV, RSVdelta G or RSV delta NS1/2revealed differential induction of SOCS and interferons respective of G/NS gene deletions. RSVdelta G infection upregulated secreted IFNbeta andISG15 while RSVdelta NS1/2 induced significant SOCS1 and interferon mRNA expression. These data provide additional information regarding the various roles of RSV proteins and highlights RSV G protein as a potent modulator of the early antiviral host response to RSV infection.