MAVS and MyD88 are essential for innate immunity but not cytotoxic T lymphocyte response against respiratory syncytial virus

Bhoj, Vijay; Sun, Qing; Bhoj, Elizabeth; Somers, Cynthia; Chen, Xiang; Torres, Juan Pablo; Mejías, Asunción; Gómez, Ana M.; Jafri, Hasan S.; Ramilo, Octavio; Chen, Zhijian J.

doi:10.1073/pnas.0804717105

Cited by 138 publications

(159 citation statements)

References 33 publications

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“…MAVS is not critical in inducing type I IFN and inflammatory cytokines in response to lymphocytoid choriomeningitis virus (Jung et al, 2008), and only partially responsible for the induction of type I IFN by influenza virus (Koyama et al, 2007). The role of MAVS in controlling chemokine/cytokine induction in respiratory syncytial virus infection is similar to what we found in hMPV infection (Bhoj et al, 2008). Therefore, these data suggest the need to investigate the role of MAVS in host immunity in a pathogen-specific manner.…”

Section: Discussionsupporting

confidence: 67%

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

Deng

Chen

Liu

et al. 2015

Journal of General Virology

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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.

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Section: Discussionsupporting

confidence: 67%

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

Deng

Chen

Liu

et al. 2015

Journal of General Virology

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“…Overexpression of RIG-I and MAVS activates piratory syncytial virus also increases to higher levels in MAVS-deficient mice (4,36).…”

Section: Discussionmentioning

confidence: 93%

The Interferon Stimulator Mitochondrial Antiviral Signaling Protein Facilitates Cell Death by Disrupting the Mitochondrial Membrane Potential and by Activating Caspases

Chiang

Chang

et al. 2010

J Virol

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“…it is likely to affect IL15 gene expression). Thus, while the association is weak, due to the limitations of power of the original study, there is inferential evidence of a genetic association with RSV susceptibility and IL15 expression [29]. Finally, absence of PBMC IL-15 upregulation in severe bronchiolitis may reflect a viral pathogenic effect.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-15 is associated with disease severity in viral bronchiolitis

et al. 2015

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Disease severity in viral bronchiolitis in infancy is difficult to predict and has been linked to host innate immunity. The study aimed to investigate the innate cytokine interleukin-15 (IL-15) as a marker of disease severity.A prospective single-centre observational study was conducted in a university-affiliated paediatric teaching hospital, comparing children (0-18 months) hospitalised for viral bronchiolitis, those admitted to the paediatric intensive care unit with severe disease and healthy age-matched controls. IL-15-related parameters were compared between groups. PCR and microRNA (miRNA) sequencing was undertaken on natural killer (NK) cells collected from study participants.Samples from 88 children with viral bronchiolitis and 43 controls enrolled between 2009 and 2012 were analysed. Peripheral blood mononuclear cell (PBMC) IL-15 mRNA expression was significantly higher in those with moderate severity bronchiolitis compared with controls and those with severe disease. Serum IL-15 levels correlated with disease severity. The relative frequency of NK cells in peripheral blood was significantly reduced in participants with bronchiolitis. The NK cell miRNA transcriptome in bronchiolitis was distinct. Targets of de-regulated miRNA were differentially expressed in bronchiolitis, including JAK3, STAT5A and NFKB1 on the IL-15 signalling pathway.IL-15 is associated with disease severity in children hospitalised with viral bronchiolitis.@ERSpublications Interleukin-15 influences the host innate response and is associated with disease severity in viral bronchiolitis

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MAVS and MyD88 are essential for innate immunity but not cytotoxic T lymphocyte response against respiratory syncytial virus

Cited by 138 publications

References 33 publications

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

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

The Interferon Stimulator Mitochondrial Antiviral Signaling Protein Facilitates Cell Death by Disrupting the Mitochondrial Membrane Potential and by Activating Caspases

Interleukin-15 is associated with disease severity in viral bronchiolitis

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