Respiratory syncytial virus persistence in macrophages alters the profile of cellular gene expression

Abstract

Viruses can persistently infect differentiated cells through regulation of expression of both their own genes and those of the host cell, thereby evading detection by the host’s immune system and achieving residence in a non-lytic state. Models in vitro with cell lines are useful tools in understanding the mechanisms associated with the establishment of viral persistence. In particular, a model to study respiratory syncytial virus (RSV) persistence in a murine macrophage-like cell line has been established. Compared to non-infected macrophages, macrophages persistently infected with RSV show altered expression both of genes coding for cytokines and trans-membrane proteins associated with antigen uptake and of genes related to cell survival. The biological changes associated with altered gene expression in macrophages as a consequence of persistent RSV infection are summarized.

Figure 1

Changes in respiratory syncytial virus (RSV) and macrophages by persistent infection. RSV persistence in macrophages leads to genotypic changes, at least in the viral membrane fusion protein F and in the profile of cellular gene expression. Arrows indicate increase or decrease in biological activities or molecule expression.