ArticlePloS one2015
Effective Apical Infection of Differentiated Human Bronchial Epithelial Cells and Induction of Proinflammatory Chemokines by the Highly Pneumotropic Human Adenovirus Type 14p1.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Pooled it
- Tropism, replication competence, and cellular responses of HAdV-14p1 in human airway organoids.iScience · 2026Article
- Molecular signaling in coinfection: howFrontiers in immunology · 2026Review
- Human Adenovirus Type 26 Induced IL-6 Gene Expression in an αvβ3 Integrin- and NF-κB-Dependent Manner.Viruses · 2022Article
- The FDA-Approved Drug Nelfinavir Inhibits Lytic Cell-Free but Not Cell-Associated Nonlytic Transmission of Human Adenovirus.Antimicrobial agents and chemotherapy · 2020Article
- Article
- Severe acute respiratory distress syndrome (ARDS) induced by human adenovirus B21: Report on 2 cases and literature review.Journal of critical care · 2019Review
- Post-transplant Replication of Torque Teno Virus in Granulocytes.Frontiers in microbiology · 2018Article
- Mechanisms of pathogenesis of emerging adenoviruses.F1000Research · 2017Review
- Characterization of Nipah virus infection in a model of human airway epithelial cells cultured at an air-liquid interface.The Journal of general virology · 2016Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOnly a few pneumotropic types of the human adenoviruses (e.g. type B14p1) cause severe lower respiratory tract infections like pneumonia and acute respiratory distress syndrome (ARDS) even in immunocompetent patients. By contrast, many other human adenovirus (HAdV) types (e.g. HAdV-C5) are associated mainly with upper respiratory tract infections. This is in accordance with a highly physiological cell culture system consisting of differentiated primary human bronchial epithelial cells which are little susceptible for apical HAdV-C5 infections. OBJECTIVE AND
methodsWe hypothesized that a pneumotropic and highly pathogenic HAdV type infects differentiated human bronchial epithelial cells efficiently from the apical surface and also induces proinflammatory cytokines in order to establish ARDS and pneumonia. Therefore, the apical infection of differentiated primary human bronchial epithelial cells with the pneumotropic and virulent type HAdV-B14p1 was investigated in comparison to the less pneumotropic HAdV-C5 as a control.
resultsBinding of HAdV-B14p1 to the apical surface of differentiated human bronchial epithelial cells and subsequent internalization of HAdV DNA was 10 fold higher (p<0.01) compared to the less-pneumotropic HAdV-C5 one hour after infection. Overall, the replication cycle of HAdV-B14p1 following apical infection and including apical release of infectious virus progeny was about 1000-fold more effective compared to the non-pneumotropic HAdV-C5 (p<0.001). HAdV-B14p1 infected cells expressed desmoglein 2 (DSG2), which has been described as potential receptor for HAdV-B14p1. Moreover, HAdV-B14p1 induced proinflammatory chemokines IP-10 and I-Tac as potential virulence factors. Interestingly, IP-10 has already been described as a marker for severe respiratory infections e.g. by influenza virus A H5N1.
conclusionsThe efficient "apical to apical" replication cycle of HAdV-B14p1 can promote endobronchial dissemination of the infection from the upper to the lower respiratory tract. Simultaneous induction of proinflammatory cytokines probably contributes to the high virulence of HAdV-B14p1.
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