Innate Immune Components that Regulate the Pathogenesis and Resolution of hRSV and hMPV Infections

Viruses. 2020 Jun 12;12(6):637. doi: 10.3390/v12060637.

Abstract

The human respiratory syncytial virus (hRSV) and human Metapneumovirus (hMPV) are two of the leading etiological agents of acute lower respiratory tract infections, which constitute the main cause of mortality in infants. However, there are currently approved vaccines for neither hRSV nor hMPV. Moreover, despite the similarity between the pathology caused by both viruses, the immune response elicited by the host is different in each case. In this review, we discuss how dendritic cells, alveolar macrophages, neutrophils, eosinophils, natural killer cells, innate lymphoid cells, and the complement system regulate both pathogenesis and the resolution of hRSV and hMPV infections. The roles that these cells play during infections by either of these viruses will help us to better understand the illnesses they cause. We also discuss several controversial findings, relative to some of these innate immune components. To better understand the inflammation in the lungs, the role of the respiratory epithelium in the recruitment of innate immune cells is briefly discussed. Finally, we review the main prophylactic strategies and current vaccine candidates against both hRSV and hMPV.

Keywords: hMPV; hRSV; immunotherapy; innate immune response; vaccines.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Immunity, Innate
  • Killer Cells, Natural / immunology
  • Metapneumovirus / genetics
  • Metapneumovirus / physiology*
  • Neutrophils / immunology
  • Paramyxoviridae Infections / genetics
  • Paramyxoviridae Infections / immunology*
  • Paramyxoviridae Infections / virology
  • Respiratory Syncytial Virus Infections / genetics
  • Respiratory Syncytial Virus Infections / immunology*
  • Respiratory Syncytial Virus Infections / virology
  • Respiratory Syncytial Virus, Human / genetics
  • Respiratory Syncytial Virus, Human / physiology*