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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Mitochondrial antiviral-signalling protein plays an essential role in host immunity against human metapneumovirus
Junfang Deng1,2, Yu Chen1,3, Guangliang Liu1,4
1Department of Pediatrics, University of Texas Medical Branch, Galveston, TX, USA.
Abstract:
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.
Insights
Mice lacking mitochondrial antiviral-signalling protein (MAVS) showed impaired immune responses to human metapneumovirus (hMPV) lung infection. These findings highlight MAVS-mediated pathways in controlling early hMPV replication and host immunity.
Area of Science:
- Immunology
- Virology
- Respiratory Medicine
Background:
- Human metapneumovirus (hMPV) causes respiratory infections, particularly in children.
- Retinoic acid-inducible gene 1 (RIG-I)-like receptors (RLRs) are crucial for cellular antiviral responses to hMPV.
- The role of RLRs in host immunity against pulmonary hMPV infection remains largely unknown.
Purpose of the Study:
- To investigate the function of RLR adaptor protein MAVS in pulmonary immune responses to hMPV.
- To determine the impact of MAVS deficiency on antiviral signaling and immune cell activation during hMPV infection.
Main Methods:
- Utilized MAVS-deficient mice to study pulmonary immune responses to hMPV.
- Assessed induction of antiviral/pro-inflammatory cytokines and immune cell recruitment.
- Evaluated dendritic cell activation and T-cell responses.
- Quantified viral loads post-infection.
Main Results:
- MAVS deficiency significantly reduced antiviral cytokine induction and immune cell infiltration in the lungs.
- Mice lacking MAVS exhibited impaired pulmonary dendritic cell activation and abnormal T-cell responses.
- While viral loads peaked later in MAVS-deficient mice, viral clearance was similar to wild-type mice by day 7.
Conclusions:
- MAVS-mediated pathways are critical for effective pulmonary immune responses against hMPV.
- MAVS plays a significant role in the early control of hMPV replication in the lungs.
- These findings elucidate the importance of the MAVS-dependent signaling pathway in hMPV pathogenesis.
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