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      Respiratory syncytial virus (RSV) and its propensity for causing bronchiolitis

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          Abstract

          Infants and young children with acute onset of wheezing and reduced respiratory airflows are often diagnosed with obstruction and inflammation of the small bronchiolar airways, ie bronchiolitis. The most common aetological agents causing bronchiolitis in young children are the respiratory viruses, and of the commonly encountered respiratory viruses, respiratory syncytial virus ( RSV) has a propensity for causing bronchiolitis. Indeed, RSV bronchiolitis remains the major reason why previously healthy infants are admitted to hospital. Why RSV infection is such a predominant cause of bronchiolitis is the subject of this review. By reviewing the available histopathology of RSV bronchiolitis, both in humans and relevant animal models, we identify hallmark features of RSV infection of the distal airways and focus attention on the consequences of columnar cell cytopathology occurring in the bronchioles, which directly impacts the development of bronchiolar obstruction, inflammation and disease. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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          Most cited references61

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          Respiratory syncytial virus and parainfluenza virus.

          C Hall (2001)
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            Bronchiolitis-associated hospitalizations among US children, 1980-1996.

            Respiratory syncytial virus (RSV) causes more lower respiratory tract infections, often manifested as bronchiolitis, among young children than any other pathogen. Few national estimates exist of the hospitalizations attributable to RSV, and recent advances in prophylaxis warrant an update of these estimates. To describe rates of bronchiolitis-associated hospitalizations and to estimate current hospitalizations associated with RSV infection. Descriptive analysis of US National Hospital Discharge Survey data from 1980 through 1996. Children younger than 5 years who were hospitalized in short-stay, non-federal hospitals for bronchiolitis. Bronchiolitis-associated hospitalization rates by age and year. During the 17-year study period, an estimated 1.65 million hospitalizations for bronchiolitis occurred among children younger than 5 years, accounting for 7.0 million inpatient days. Fifty-seven percent of these hospitalizations occurred among children younger than 6 months and 81 % among those younger than 1 year. Among children younger than 1 year, annual bronchiolitis hospitalization rates increased 2.4-fold, from 12.9 per 1000 in 1980 to 31.2 per 1000 in 1996. During 1988-1996, infant hospitalization rates for bronchiolitis increased significantly (P for trend <.001), while hospitalization rates for lower respiratory tract diseases excluding bronchiolitis did not vary significantly (P for trend = .20). The proportion of hospitalizations for lower respiratory tract illnesses among children younger than 1 year associated with bronchiolitis increased from 22.2% in 1980 to 47.4% in 1996; among total hospitalizations, this proportion increased from 5.4% to 16.4%. Averaging bronchiolitis hospitalizations during 1994-1996 and assuming that RSV was the etiologic agent in 50% to 80% of November through April hospitalizations, an estimated 51, 240 to 81, 985 annual bronchiolitis hospitalizations among children younger than 1 year were related to RSV infection. During 1980-1996, rates of hospitalization of infants with bronchiolitis increased substantially, as did the proportion of total and lower respiratory tract hospitalizations associated with bronchiolitis. Annual bronchiolitis hospitalizations associated with RSV infection among infants may be greater than previous estimates for RSV bronchiolitis and pneumonia hospitalizations combined.
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              Human and avian influenza viruses target different cell types in cultures of human airway epithelium.

              The recent human infections caused by H5N1, H9N2, and H7N7 avian influenza viruses highlighted the continuous threat of new pathogenic influenza viruses emerging from a natural reservoir in birds. It is generally believed that replication of avian influenza viruses in humans is restricted by a poor fit of these viruses to cellular receptors and extracellular inhibitors in the human respiratory tract. However, detailed mechanisms of this restriction remain obscure. Here, using cultures of differentiated human airway epithelial cells, we demonstrated that influenza viruses enter the airway epithelium through specific target cells and that there were striking differences in this respect between human and avian viruses. During the course of a single-cycle infection, human viruses preferentially infected nonciliated cells, whereas avian viruses as well as the egg-adapted human virus variant with an avian virus-like receptor specificity mainly infected ciliated cells. This pattern correlated with the predominant localization of receptors for human viruses (2-6-linked sialic acids) on nonciliated cells and of receptors for avian viruses (2-3-linked sialic acids) on ciliated cells. These findings suggest that although avian influenza viruses can infect human airway epithelium, their replication may be limited by a nonoptimal cellular tropism. Our data throw light on the mechanisms of generation of pandemic viruses from their avian progenitors and open avenues for cell level-oriented studies on the replication and pathogenicity of influenza virus in humans.
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                Author and article information

                Journal
                J Pathol
                J. Pathol
                10.1002/(ISSN)1096-9896
                PATH
                The Journal of Pathology
                John Wiley & Sons, Ltd (Chichester, UK )
                0022-3417
                1096-9896
                January 2015
                11 December 2014
                : 235
                : 2 , Viruses and Disease ( doiID: 10.1002/path.2015.235.issue-2 )
                : 266-276
                Affiliations
                [ 1 ] Department of Microbiology and Immunology University of North Carolina Chapel Hill NC USA
                [ 2 ] Department of Paediatrics, Microbiology, Immunology and Biochemistry, Division of Infectious Diseases University of Tennessee School of Medicine, and Molecular Diagnostics and Virology Laboratories, Le Bonheur Children's Hospital Memphis TN USA
                Author notes
                [*] [* ]Correspondence to: RJ Pickles, Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, 7021 Thurston Bowles, Chapel Hill, NC 27599‐7248, USA. E‐mail: branston@ 123456med.unc.edu
                Article
                PATH4462
                10.1002/path.4462
                5638117
                25302625
                4663eaa2-ef4b-499f-a606-29dd81286856
                Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd

                This article is being made freely available through PubMed Central as part of the COVID-19 public health emergency response. It can be used for unrestricted research re-use and analysis in any form or by any means with acknowledgement of the original source, for the duration of the public health emergency.

                History
                : 24 September 2014
                : 24 September 2014
                : 05 October 2014
                Page count
                Pages: 11
                Categories
                Invited Review
                Invited Reviews
                Custom metadata
                2.0
                January 2015
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.0 mode:remove_FC converted:15.04.2020

                Pathology
                respiratory syncytial virus,airway obstruction,bronchiolitis,acute lung disease
                Pathology
                respiratory syncytial virus, airway obstruction, bronchiolitis, acute lung disease

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