ArticlePathogens (Basel, Switzerland)2020
Human Metapneumovirus Induces Mucin 19 Which Contributes to Viral Pathogenesis.
Article in Pathogens (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- The intersection between human metapneumovirus and the respiratory microbiome.Virology journal · 2025Review
- hMPV co-infections: Distinct immunopathogenic mechanisms and clinical implications of viral and bacterial pathogenesis.Folia microbiologica · 2025Review
- MICBG406A polymorphism reduces risk of mechanical ventilation and death during viral acute lung injury.JCI insight · 2025Article
- Natural selection and adaptive traits in the Maniq, a nomadic hunter-gatherer society from Mainland Southeast Asia.Scientific reports · 2025Article
- METTL3 aggravates cell damage induced by Streptococcus pneumoniae via the NEAT1/CTCF/MUC19 axis.The Kaohsiung journal of medical sciences · 2024Article
- The potential role of ocular and otolaryngological mucus proteins in myalgic encephalomyelitis/chronic fatigue syndrome.Molecular medicine (Cambridge, Mass.) · 2024Article
- Abnormal Airway Mucus Secretion Induced by Virus Infection.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Human Metapneumovirus (HMPV) remains one of the most common viral infections causing acute respiratory tract infections, especially in young children, elderly, and immunocompromised populations. Clinical symptoms can range from mild respiratory symptoms to severe bronchiolitis and pneumonia. The production of mucus is a common feature during HMPV infection, but its contribution to HMPV-induced pathogenesis and immune response is largely unknown. Mucins are a major component of mucus and they could have an impact on how the host responds to infections. Using an in vitro system and a mouse model of infection, we identified that Mucin 19 is predominantly expressed in the respiratory tract upon HMPV infection. Moreover, the lack of Muc19 led to an improved disease, lower lung viral titers and a decrease in the number of CD4+ T cells. These data indicate that mucin 19 contributes to the activation of the immune response to HMPV and to HMPV-induced pathogenesis.
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Registered trials
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