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  1. Article ; Online: Effects of COVID-19 and Social Distancing on Rhinovirus Infections and Asthma Exacerbations.

    Kreger, Jordan E / Hershenson, Marc B

    Viruses

    2022  Volume 14, Issue 11

    Abstract: Since their discovery in the 1950s, rhinoviruses (RVs) have been recognized as a major causative agent of the "common cold" and cold-like illnesses, accounting for more than 50% of upper respiratory tract infections. However, more than that, respiratory ... ...

    Abstract Since their discovery in the 1950s, rhinoviruses (RVs) have been recognized as a major causative agent of the "common cold" and cold-like illnesses, accounting for more than 50% of upper respiratory tract infections. However, more than that, respiratory viral infections are responsible for approximately 50% of asthma exacerbations in adults and 80% in children. In addition to causing exacerbations of asthma, COPD and other chronic lung diseases, RVs have also been implicated in the pathogenesis of lower respiratory tract infections including bronchiolitis and community acquired pneumonia. Finally, early life respiratory viral infections with RV have been associated with asthma development in children. Due to the vast genetic diversity of RVs (approximately 160 known serotypes), recurrent infection is common. RV infections are generally acquired in the community with transmission occurring via inhalation of aerosols, respiratory droplets or fomites. Following the outbreak of coronavirus disease 2019 (COVID-19), exposure to RV and other respiratory viruses was significantly reduced due to social-distancing, restrictions on social gatherings, and increased hygiene protocols. In the present review, we summarize the impact of COVID-19 preventative measures on the incidence of RV infection and its sequelae.
    MeSH term(s) Child ; Adult ; Humans ; Rhinovirus/genetics ; COVID-19/prevention & control ; Physical Distancing ; Asthma/complications ; Respiratory Tract Infections/epidemiology ; Respiratory Tract Infections/prevention & control ; Respiratory Tract Infections/complications ; Communicable Diseases ; Picornaviridae Infections/epidemiology ; Picornaviridae Infections/prevention & control ; Picornaviridae Infections/complications
    Language English
    Publishing date 2022-10-25
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v14112340
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Tuft cells are required for a rhinovirus-induced asthma phenotype in immature mice.

    Li, Yiran / Han, Mingyuan / Singh, Shilpi / Breckenridge, Haley A / Kreger, Jordan E / Stroupe, Claudia C / Sawicky, Daniel A / Kuo, Shiuhyang / Goldsmith, Adam M / Ke, Fang / Shenoy, Anukul T / Bentley, J Kelley / Matsumoto, Ichiro / Hershenson, Marc B

    JCI insight

    2024  Volume 9, Issue 2

    Abstract: Infection of immature mice with rhinovirus (RV) induces an asthma-like phenotype consisting of type 2 inflammation, mucous metaplasia, eosinophilic inflammation, and airway hyperresponsiveness that is dependent on IL-25 and type 2 innate lymphoid cells ( ... ...

    Abstract Infection of immature mice with rhinovirus (RV) induces an asthma-like phenotype consisting of type 2 inflammation, mucous metaplasia, eosinophilic inflammation, and airway hyperresponsiveness that is dependent on IL-25 and type 2 innate lymphoid cells (ILC2s). Doublecortin-like kinase 1-positive (DCLK1+) tuft cells are a major source of IL-25. We sought to determine the requirement of tuft cells for the RV-induced asthma phenotype in wild-type mice and mice deficient in Pou2f3, a transcription factor required for tuft cell development. C57BL/6J mice infected with RV-A1B on day 6 of life and RV-A2 on day 13 of life showed increased DCLK1+ tuft cells in the large airways. Compared with wild-type mice, RV-infected Pou2f3-/- mice showed reductions in IL-25 mRNA and protein expression, ILC2 expansion, type 2 cytokine expression, mucous metaplasia, lung eosinophils, and airway methacholine responsiveness. We conclude that airway tuft cells are required for the asthma phenotype observed in immature mice undergoing repeated RV infections. Furthermore, RV-induced tuft cell development provides a mechanism by which early-life viral infections could potentiate type 2 inflammatory responses to future infections.
    MeSH term(s) Animals ; Mice ; Immunity, Innate ; Rhinovirus ; Tuft Cells ; Lymphocytes/metabolism ; Mice, Inbred C57BL ; Asthma/metabolism ; Enterovirus Infections ; Inflammation ; Phenotype ; Metaplasia
    Language English
    Publishing date 2024-01-23
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.166136
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: M2 Macrophages promote IL-33 expression, ILC2 expansion and mucous metaplasia in response to early life rhinovirus infections.

    Han, Mingyuan / Breckenridge, Haley A / Kuo, Shiuhyang / Singh, Shilpi / Goldsmith, Adam G / Li, Yiran / Kreger, Jordan E / Bentley, J Kelley / Hershenson, Marc B

    Frontiers in immunology

    2022  Volume 13, Page(s) 952509

    Abstract: Wheezing-associated rhinovirus (RV) infections are associated with asthma development. We have shown that infection of immature mice with RV induces type 2 cytokine production and mucous metaplasia which is dependent on IL-33 and type 2 innate lymphoid ... ...

    Abstract Wheezing-associated rhinovirus (RV) infections are associated with asthma development. We have shown that infection of immature mice with RV induces type 2 cytokine production and mucous metaplasia which is dependent on IL-33 and type 2 innate lymphoid cells (ILC2s) and intensified by a second heterologous RV infection. We hypothesize that M2a macrophages are required for the exaggerated inflammation and mucous metaplasia in response to heterologous RV infection. Wild-type C57Bl/6J mice and LysM
    Conclusion: Early-life RV infection alters the macrophage response to subsequent heterologous infection, permitting enhanced IL-33 expression, ILC2 expansion and intensified airway inflammation and mucous metaplasia.
    MeSH term(s) Animals ; Immunity, Innate ; Inflammation ; Interleukin-33 ; Lymphocytes ; Macrophages ; Metaplasia ; Mice ; RNA, Messenger ; Rhinovirus
    Chemical Substances Interleukin-33 ; RNA, Messenger
    Language English
    Publishing date 2022-08-12
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.952509
    Database MEDical Literature Analysis and Retrieval System OnLINE

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