Abstract

Respiratory syncytial virus (RSV) is the leading cause of severe respiratory infection in young children. Nearly all individuals become infected in their early childhood, and reinfections with RSV are common throughout life. Primary infection with RSV is usually involved in the symptom of bronchiolitis and pneumonia in the lower respiratory tract, which accounts for over 3 million hospitalizations and approximately 66,000 deaths annually worldwide. Despite the widespread prevalence and high morbidity and lethality rates of diseases caused by RSV infection, there is currently no licensed RSV vaccine. During RSV infection, innate immunity plays the first line of defense to suppress RSV infection and replication. However, RSV has evolved multiple mechanisms to evade the host’s innate immune responses to gain a window of opportunity for efficient viral replication. This review discusses the comprehensive interaction between RSV infection and the host antiviral innate immunity and updates recent findings on how RSV modulates the host innate immune response for survival, which may provide novel insights to find potent drug targets and vaccines against RSV.

Highlights

  • Respiratory syncytial virus (RSV) is an enveloped virus belonging to the Pneumovirus genus in the Paramyxoviridae family

  • The further structure–activity studies demonstrated that the C-terminal 20 residues of NS1 were required to decrease IKKε (Swedan et al, 2009). These results suggest that NS1 can block the IFN-I signaling by reducing the presence of adaptors downstream RLRs

  • While the deletion of the CX3CL1 motif in G protein results in increased levels of IFN-I/III, indicating that the interruption of CX3CCX3CR1 interaction by G protein greatly benefits RSV to evade IFN-I/III-mediated innate immune response (Chirkova et al, 2013). It is more than 60 years since human RSV was first discovered in 1957 (Chanock et al, 1957), and RSV has become one of the most important pathogens causing respiratory disease worldwide, especially in young children

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Summary

Innate Immune Evasion by Human Respiratory Syncytial Virus

Yan Ouyang 1†, Hongqun Liao 1,2†, Yan Hu 3†, Kaiyuan Luo 1, Shaowen Hu 4 and Huifang Zhu 1,2,4,5*. Immune Evasion by Human Respiratory Syncytial Virus. Respiratory syncytial virus (RSV) is the leading cause of severe respiratory infection in young children. Despite the widespread prevalence and high morbidity and lethality rates of diseases caused by RSV infection, there is currently no licensed RSV vaccine. During RSV infection, innate immunity plays the first line of defense to suppress RSV infection and replication. RSV has evolved multiple mechanisms to evade the host’s innate immune responses to gain a window of opportunity for efficient viral replication. This review discusses the comprehensive interaction between RSV infection and the host antiviral innate immunity and updates recent findings on how RSV modulates the host innate immune response for survival, which may provide novel insights to find potent drug targets and vaccines against RSV

INTRODUCTION
RSV Evades the Innate Immunity
INNATE IMMUNE RESPONSE AGAINST RSV INFECTION
RSV Infection Triggers TLRs Pathway
RSV Infection Triggers the RLRs Pathway
RSV Infection Triggers the NLRs Pathway
EVASION OF INNATE IMMUNE RESPONSE BY RSV
RSV Impedes the RLRs Signaling Pathway
RSV Subverts the TLRs Signaling Pathway
Findings
CONCLUDING REMARKS
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