scholarly journals How Influenza A Virus NS1 Deals with the Ubiquitin System to Evade Innate Immunity

Viruses ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2309
Author(s):  
Laurie-Anne Lamotte ◽  
Lionel Tafforeau
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Influenza A Virus ◽  
Virulence Factors ◽  
Influenza A ◽  
Innate Immune ◽  
Structural Protein ◽  
Post Translational Modification ◽  
Cellular Processes ◽  
Ubiquitin System

Ubiquitination is a post-translational modification regulating critical cellular processes such as protein degradation, trafficking and signaling pathways, including activation of the innate immune response. Therefore, viruses, and particularly influenza A virus (IAV), have evolved different mechanisms to counteract this system to perform proper infection. Among IAV proteins, the non-structural protein NS1 is shown to be one of the main virulence factors involved in these viral hijackings. NS1 is notably able to inhibit the host’s antiviral response through the perturbation of ubiquitination in different ways, as discussed in this review.

scholarly journals The PB1 protein of influenza A virus inhibits the innate immune response by targeting MAVS for NBR1-mediated selective autophagic degradation

2021 ◽  
Vol 17 (2) ◽  
pp. e1009300
Author(s):  
Yan Zeng ◽  
Shuai Xu ◽  
Yanli Wei ◽  
Xuegang Zhang ◽  
Qian Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza A Virus ◽  
Innate Immune Response ◽  
Influenza A ◽  
Innate Immune ◽  
Negative Regulator ◽  
Poly I:C ◽  
H7n9 Virus ◽  
Autophagic Degradation ◽  
Negative Regulatory Mechanism

Influenza A virus (IAV) has evolved various strategies to counteract the innate immune response using different viral proteins. However, the mechanism is not fully elucidated. In this study, we identified the PB1 protein of H7N9 virus as a new negative regulator of virus- or poly(I:C)-stimulated IFN induction and specifically interacted with and destabilized MAVS. A subsequent study revealed that PB1 promoted E3 ligase RNF5 to catalyze K27-linked polyubiquitination of MAVS at Lys362 and Lys461. Moreover, we found that PB1 preferentially associated with a selective autophagic receptor neighbor of BRCA1 (NBR1) that recognizes ubiquitinated MAVS and delivers it to autophagosomes for degradation. The degradation cascade mediated by PB1 facilitates H7N9 virus infection by blocking the RIG-I-MAVS-mediated innate signaling pathway. Taken together, these data uncover a negative regulatory mechanism involving the PB1-RNF5-MAVS-NBR1 axis and provide insights into an evasion strategy employed by influenza virus that involves selective autophagy and innate signaling pathways.

scholarly journals Influenza A virus-encoded NS1 virulence factor protein inhibits innate immune response by targeting IKK

2012 ◽  
Vol 14 (12) ◽  
pp. 1849-1866 ◽  
Author(s):  
Shijuan Gao ◽  
Liping Song ◽  
Jiandong Li ◽  
Zhenzhu Zhang ◽  
Haiyan Peng ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza A Virus ◽  
Innate Immune Response ◽  
Virulence Factor ◽  
Influenza A ◽  
Innate Immune

scholarly journals The amazing innate immune response to influenza A virus infection

2013 ◽  
Vol 21 (1) ◽  
pp. 73-98 ◽  
Author(s):  
Shweta Tripathi ◽  
Mitchell R White ◽  
Kevan L Hartshorn
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Innate Immune Response ◽  
Influenza A ◽  
Innate Immune ◽  
Influenza A Virus Infection
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