Abstract
The human Respiratory Syncytial Virus (hRSV) is the leading cause of severe acute lower respiratory tract infections (ALRTIs) in humans at all ages and is the main cause of hospitalization due to pneumonia, asthma, and bronchiolitis in infants. hRSV symptoms mainly develop due to an excessive host immune and inflammatory response in the respiratory tissue. hRSV infection during life is frequent and likely because of non-optimal immunological memory is developed against this virus. Vaccine development against this pathogen has been delayed after the detrimental effects produced in children by vaccination with a formalin-inactivated hRSV preparation (FI-hRSV), which caused enhanced disease upon natural viral infection. Since then, several studies have focused on understanding the mechanisms underlying such disease exacerbation. Along these lines, several studies have suggested that antibodies elicited by immunization with FI-hRSV show low neutralizing capacity and promote the formation of immune complexes containing hRSV (hRSV-ICs), which contribute to hRSV pathogenesis through the engagement of Fc gamma receptors (FcγRs) expressed on the surface of immune cells. Furthermore, a role for FcγRs is supported by studies evaluating the contribution of these molecules to hRSV-induced disease. These studies have shown that FcγRs can modulate viral clearance by the host and the inflammatory response triggered by hRSV infection. In addition, ICs can facilitate viral entry into host cells expressing FcγRs, thus extending hRSV infectivity. In this article, we discuss current knowledge relative to the contribution of hRSV-ICs and FcγRs to the pathogenesis caused by hRSV and their putative role in the exacerbation of the disease caused by this virus after FI-hRSV vaccination. A better understanding FcγRs involvement in the immune response against hRSV will contribute to the development of new prophylactic or therapeutic tools to promote virus clearance with limited inflammatory damage to the airways.
Highlights
The Human Respiratory Syncytial Virus is a singlestranded RNA enveloped virus belonging to the Pneumoviridae family (Amarasinghe et al, 2018)
It is possible that both, FcγRIII and FcγRIIb contribute to human Respiratory Syncytial Virus (hRSV) pathogenesis and re-infection by impairing the capacity of dendritic cells (DCs) to promote the production of IL-2 by CD4+ T cells
Several studies have focused on understanding the mechanisms that can contribute to hRSV induced pathology, and to elucidate the factors that contribute to re-infection episodes throughout life
Summary
The Human Respiratory Syncytial Virus (hRSV) is a singlestranded RNA enveloped virus belonging to the Pneumoviridae family (Amarasinghe et al, 2018). We review and discuss the current understanding on the contribution of FcγRs to infection and the modulation of the immune response against hRSV both, in vitro and in vivo and their impact on hRSV-induced pathology.
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