Respiratory syncytial virus persistence in macrophages upregulates Fcgamma receptors expression

Area of Science:

• Immunology
• Virology
• Cell Biology

Background:

• Viruses can establish persistent infections in host cells like macrophages, altering cell function without causing cell death.
• Previous studies showed increased Fc gamma receptor (FcgR)-mediated phagocytosis and FcgRIIB/RIII expression in early passages of RSV-infected macrophages (MfP).

Purpose of the Study:

• To investigate the underlying mechanisms responsible for increased FcgR expression and phagocytosis in RSV-infected macrophages.
• To determine if these changes are stable over extended periods of viral persistence.

Main Methods:

• Analysis of FcgR isoform expression at both mRNA and protein levels in persistently RSV-infected macrophages (MfP) and mock-infected macrophages (MfN).
• Assessment of FcgR-mediated phagocytosis and FcgR expression after prolonged RSV infection (over 87 passages).
• Investigation of potential roles for soluble factors (cytokines) or viral products in mediating FcgR changes.

Main Results:

• Increased FcgR expression and FcgR-mediated phagocytosis were maintained in MfP cultures after more than 87 passages.
• RSV persistence distinctly altered the expression of specific FcgR isoforms at both mRNA and protein levels.
• The observed increase in FcgRs expression was not due to soluble factors, released viral products, or increased FcgR internalization.

Conclusions:

• RSV persistence in macrophages induces intracellular effects that modulate FcgR gene expression at the mRNA and protein levels.
• The observed alterations in FcgR expression and function are stable characteristics of RSV persistence in macrophages over extended periods.