Mitochondrial antiviral-signalling protein plays an essential role in host immunity against human metapneumovirus

Junfang Deng, Yu Chen, Guangliang Liu, Junping Ren, Caroline Go, Teodora Ivanciuc, Kolli Deepthi, Antonella Casola, Roberto P. Garofalo, Xiaoyong Bao

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Human metapneumovirus (hMPV) is a common cause of respiratory tract infection in the paediatrics population. Recently, we and others have shown that retinoic acid-inducible gene 1 (RIG-I)-like receptors (RLRs) are essential for hMPV-induced cellular antiviral signalling. However, the contribution of those receptors to host immunity against pulmonary hMPV infection is largely unexplored. In this study, mice deficient in mitochondrial antiviral-signalling protein (MAVS), an adaptor of RLRs, were used to investigate the role(s) of these receptors in pulmonary immune responses to hMPV infection. MAVS deletion significantly impaired the induction of antiviral and pro-inflammatory cytokines and the recruitment of immune cells to the bronchoalveolar lavage fluid by hMPV. Compared with WT mice, mice lacking MAVS demonstrated decreased abilities to activate pulmonary dendritic cells (DCs) and abnormal primary T-cell responses to hMPV infection. In addition, mice deficient in MAVS had a higher peak of viral load at day 5 post-infection (p.i.) than WT mice, but were able to clear hMPV by day 7 p.i. similarly to WT mice. Taken together, our data indicate a role of MAVS-mediated pathways in the pulmonary immune responses to hMPV infection and the early control of hMPV replication.

Original languageEnglish (US)
Pages (from-to)2104-2113
Number of pages10
JournalJournal of General Virology
Issue number8
StatePublished - Aug 1 2015

ASJC Scopus subject areas

  • Virology


Dive into the research topics of 'Mitochondrial antiviral-signalling protein plays an essential role in host immunity against human metapneumovirus'. Together they form a unique fingerprint.

Cite this