title: Human Respiratory Syncytial Virus: Role of Innate Immunity in Clearance and Disease Progression.
abstract: Human respiratory syncytial virus (HRSV) infections have worldwide records. The virus is responsible for bronchiolitis, pneumonia, and asthma in humans of different age groups. Premature infants, young children, and immunocompromised individuals are prone to severe HRSV infection that may lead to death. Based on worldwide estimations, millions of cases were reported in both developed and developing countries. In fact, HRSV symptoms develop mainly as a result of host immune response. Due to inability to establish long lasting adaptive immunity, HRSV infection is recurrent and hence impairs vaccine development. Once HRSV attached to the airway epithelia, interaction with the host innate immune components starts. HRSV interaction with pulmonary innate defenses is crucial in determining the disease outcome. Infection of alveolar epithelial cells triggers a cascade of events that lead to recruitment and activation of leukocyte populations. HRSV clearance is mediated by a number of innate leukocytes, including macrophages, natural killer cells, eosinophils, dendritic cells, and neutrophils. Regulation of these cells is mediated by cytokines, chemokines, and other immune mediators. Although the innate immune system helps to clear HRSV infection, it participates in disease progression such as bronchiolitis and asthma. Resolving the mechanisms by which HRSV induces pathogenesis, different possible interactions between the virus and immune components, and immune cells interplay are essential for developing new effective vaccines. Therefore, the current review focuses on how the pulmonary innate defenses mediate HRSV clearance and to what extent they participate in disease progression. In addition, immune responses associated with HRSV vaccines will be discussed.
authors.affiliation: Department of Botany and Microbiology, King Saud University , Riyadh, Saudi Arabia .
authors.forename: Mohamed A
authors.initials: MA
authors.lastname: Farrag
authors.affiliation: Department of Botany and Microbiology, King Saud University , Riyadh, Saudi Arabia .
authors.forename: Fahad N
authors.initials: FN
authors.lastname: Almajhdi
mesh_terms: D000914:Antibodies, Viral / Q000276:immunology; D001249:Asthma / Q000276:immunology* / Q000821:virology; D001988:Bronchiolitis / Q000276:immunology* / Q000821:virology; D002648:Child; D016207:Cytokines / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D018450:Disease Progression; D004804:Eosinophils / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007223:Infant; D007694:Killer Cells, Natural / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000821:virology; D022261:Respiratory Syncytial Virus Vaccines / Q000276:immunology; D018113:Respiratory Syncytial Virus, Human / Q000276:immunology*
chemical_list: D000914:Antibodies, Viral; D016207:Cytokines; D022261:Respiratory Syncytial Virus Vaccines