Respiratory Syncytial Virus Persistence in Macrophages Upregulates Fcgamma Receptors Expression

Jorge Gaona,Beatriz Gómez,Enrique Ortega,Carlos Santiago-Olivares

doi:10.3390/v6020624

Jorge Gaona, Beatriz Gómez + Show 2 more

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https://doi.org/10.3390/v6020624

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Journal: Viruses	Publication Date: Feb 6, 2014
Citations: 58	License type: CC BY 4.0

Affiliation: Universidad Nacional Autónoma de México

Abstract

Viruses can persist in differentiated cells (i.e., macrophages) over long periods of time, altering host cells functions but not inducing their death. We had previously reported that, in early passages (14–40) of a murine macrophage-like cell line persistently infected with respiratory syncytial virus (RSV) (MɸP), FcγR-mediated phagocytosis and expression of FcγRIIB/RIII on the cell membrane were increased with respect to mock-infected macrophages (MɸN). In this work, we explored the mechanism underlying such effects. Increases in FcγR expression and FcγR-mediated phagocytosis are preserved after more than 87 passages of the persistently infected culture. We analyzed the expression of FcγR isoforms at both mRNA and protein levels, and found out that RSV persistence distinctly affects the expression of FcγR isoforms. We also observed that the increase in FcγRs expression results neither from soluble factors (cytokines) or viral products released by the infected cells, nor from an increase in the rate of FcγR internalization. Our results suggest that RSV persistence in macrophages induce intracellular effects that have an impact on FcγRs gene expression at both mRNA and protein levels, and that the characteristics of RSV persistence were preserved for over 87 passages.

Highlights

Viruses persisting in differentiated cells—i.e., macrophages (Mφs)—can regulate the expression of both their own genes and those of the host cell in order to achieve residence in a non-lytic state, besides selectively affecting functions of the infected cell without destroying it [1]
Changes in host cell-gene expression resulting from persistence of respiratory syncytial virus (RSV), another RNA virus, have been reported: in the human epithelial cell line HEp-2, viral persistence alters the expression of host genes involved in cell survival and chemokine production [6]
We have previously reported that persistent infection by RSV in a murine macrophage-like cell line (MφP) alters the expression of FcγRIIB/RIII on the cell membrane and FcγRs-mediated phagocytosis [8]

Summary

Introduction

Viruses persisting in differentiated cells—i.e., macrophages (Mφs)—can regulate the expression of both their own genes and those of the host cell in order to achieve residence in a non-lytic state, besides selectively affecting functions of the infected cell without destroying it [1]. Mφs play very important roles in innate and adaptive immune responses since they are involved in various processes, such as phagocytosis, antigen presentation, and cytokine production [2,3]. Mφs express on their membrane receptors for the Fc region of IgG antibodies (FcγRs). Alterations of FcγRs-mediated phagocytosis in vitro and in vivo have been reported in Mφs persistently infected with an RNA virus (HIV-1) This effect is caused by a decreased synthesis of the gamma chain of receptors, suggesting that viral persistence alters gene expression in the host cell [4,5]. We had previously shown that, in a macrophage-like murine cell line persistently infected with RSV (MφP) [7], FcγRs expression, FcγRs-mediated phagocytosis, and cytokines production are altered [8]

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