Abstract
Respiratory syncytial virus (RSV) is a major cause of severe respiratory disease in infants and the elderly. The socioeconomic burden of RSV infection is substantial because it leads to serious respiratory problems, subsequent hospitalization, and mortality. Despite its clinical significance, a safe and effective vaccine is not yet available to prevent RSV infection. Upon RSV infection, lung dendritic cells (DCs) detecting pathogens migrate to the lymph nodes and activate the adaptive immune response. Therefore, RSV has evolved various immunomodulatory strategies to inhibit DC function. Due to the capacity of RSV to modulate defense mechanisms in hosts, RSV infection results in inappropriate activation of immune responses resulting in immunopathology and frequent reinfection throughout life. This review discusses how DCs recognize invading RSV and induce adaptive immune responses, as well as the regulatory mechanisms mediated by RSV to disrupt DC functions and ultimately avoid host defenses.
Highlights
Respiratory syncytial virus (RSV) is an enveloped, single-stranded RNA virus that belongs to the Pneumoviridae family [1]
Upon RSV infection, TLR2/6, TLR3, TLR4, TLR7, retinoic acid-inducible gene-I (RIG-I), and NOD2 become important for recognizing RSV pathogen-associated molecular patterns (PAMPs) (Figure 2)
Toll-like receptors (TLRs) are essential for activation of innate immune responses by recognizing PAMPs derived from various pathogens
Summary
Respiratory syncytial virus (RSV) is an enveloped, single-stranded RNA virus that belongs to the Pneumoviridae family [1]. CCA was renamed RSV, and has been reported as the major cause of respiratory illness and morbidity in infants and children. No vaccine exists today because candidates failed to induce persistent immune responses against RSV antigen without causing vaccine-associated disease enhancement [8]. Dendritic cells (DCs), which participate in innate immunity, are professional antigen-presenting cells that play an essential role in activating adaptive immune responses. CDC1s are generally considered as the primary subset that cross-presents antigens to CD8+ T cells, while cDC2s mediate CD4+ T cell priming, and pDCs are well known as producers of type I interferon (type I IFN) [14]. We discuss how DCs recognize RSV infection and mediate anti-RSV immune responses, as well as the immunomodulatory strategies that RSV utilizes to avoid host defense mechanisms via DC regulation
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