RIG-I Signaling via MAVS Is Dispensable for Survival in Lethal Influenza Infection In Vivo

• Main Authors: Wenxin Wu (Author), Xiaoqiu Wang (Author), Wei Zhang (Author), Lili Tian (Author), J. Leland Booth (Author), Elizabeth S. Duggan (Author), Sunil More (Author), Lin Liu (Author), Mikhail Dozmorov (Author), Jordan P. Metcalf (Author)
• Format: Book
• Published: Hindawi Limited, 2018-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

Retinoic acid-inducible gene I (RIG-I) is an important regulator of virus-induced antiviral interferons (IFNs) and proinflammatory cytokines. It requires interaction with an adaptor molecule, mitochondrial antiviral-signaling protein (MAVS), to activate downstream signaling pathways. To elucidate the mechanism(s) by which RIG-I-dependent recognition of IAV infection in vivo triggers innate immune responses, we infected mutant mice lacking RIG-I or MAVS with influenza A virus (IAV) and measured their innate immune responses. As has previously been demonstrated with isolated deletion of the virus recognition receptors TLR3, TLR7, and NOD2, RIG-I or MAVS knockout (KO) did not result in higher mortality and did not reduce IAV-induced cytokine responses in mice. Infected RIG-I KO animals displayed similar lung inflammation profiles as did WT mice, in terms of the protein concentration, total cell count, and inflammatory cell composition in the bronchoalveolar lavage fluid. RNA-Seq results demonstrated that all types of mice exhibited equivalent antiviral and inflammatory gene responses following IAV infection. Together, the results indicated that although RIG-I is important in innate cytokine responses in vitro, individual deletion of the genes encoding RIG-I or MAVS did not change survival or innate responses in vivo after IAV infection in mice.

Item Description

0962-9351
1466-1861
10.1155/2018/6808934