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      Viral and Bacterial Interactions in the Upper Respiratory Tract

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          Abstract

          Respiratory infectious diseases are mainly caused by viruses or bacteria that often interact with one another. Although their presence is a prerequisite for subsequent infections, viruses and bacteria may be present in the nasopharynx without causing any respiratory symptoms. The upper respiratory tract hosts a vast range of commensals and potential pathogenic bacteria, which form a complex microbial community. This community is assumed to be constantly subject to synergistic and competitive interspecies interactions. Disturbances in the equilibrium, for instance due to the acquisition of new bacteria or viruses, may lead to overgrowth and invasion. A better understanding of the dynamics between commensals and pathogens in the upper respiratory tract may provide better insight into the pathogenesis of respiratory diseases. Here we review the current knowledge regarding specific bacterial–bacterial and viral–bacterial interactions that occur in the upper respiratory niche, and discuss mechanisms by which these interactions might be mediated. Finally, we propose a theoretical model to summarize and illustrate these mechanisms.

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          Most cited references96

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          Defensins: antimicrobial peptides of innate immunity.

          Tomas Ganz (2003)
          The production of natural antibiotic peptides has emerged as an important mechanism of innate immunity in plants and animals. Defensins are diverse members of a large family of antimicrobial peptides, contributing to the antimicrobial action of granulocytes, mucosal host defence in the small intestine and epithelial host defence in the skin and elsewhere. This review, inspired by a spate of recent studies of defensins in human diseases and animal models, focuses on the biological function of defensins.
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            What are the consequences of the disappearing human microbiota?

            Humans and our ancestors have evolved since the most ancient times with a commensal microbiota. The conservation of indicator species in a niche-specific manner across all of the studied human population groups suggests that the microbiota confer conserved benefits on humans. Nevertheless, certain of these organisms have pathogenic properties and, through medical practices and lifestyle changes, their prevalence in human populations is changing, often to an extreme degree. In this Essay, we propose that the disappearance of these ancestral indigenous organisms, which are intimately involved in human physiology, is not entirely beneficial and has consequences that might include post-modern conditions such as obesity and asthma.
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              Insights into the interaction between influenza virus and pneumococcus.

              Bacterial infections following influenza are an important cause of morbidity and mortality worldwide. Based on the historical importance of pneumonia as a cause of death during pandemic influenza, the increasingly likely possibility that highly pathogenic avian influenza viruses will trigger the next worldwide pandemic underscores the need to understand the multiple mechanisms underlying the interaction between influenza virus and bacterial pathogens such as Streptococcus pneumoniae. There is ample evidence to support the historical view that influenza virus alters the lungs in a way that predisposes to adherence, invasion, and induction of disease by pneumococcus. Access to receptors is a key factor and may be facilitated by the virus through epithelial damage, by exposure or up-regulation of receptors, or by provoking the epithelial regeneration response to cytotoxic damage. More recent data indicate that alteration of the immune response by diminishing the ability of the host to clear pneumococcus or by amplification of the inflammatory cascade is another key factor. Identification and exploration of the underlying mechanisms responsible for this synergism will provide targets for prevention and treatment using drugs and vaccines.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS Pathog
                PLoS Pathog
                plos
                plospath
                PLoS Pathogens
                Public Library of Science (San Francisco, USA )
                1553-7366
                1553-7374
                January 2013
                January 2013
                10 January 2013
                : 9
                : 1
                : e1003057
                Affiliations
                [1]Department of Pediatric Immunology and Infectious Diseases, University Medical Center-Wilhelmina Children's Hospital, Utrecht, The Netherlands
                University of Alberta, Canada
                Author notes

                DB and KT declare to have received consulting fees from Pfizer. EAMS declares to have received unrestricted research support from Pfizer and Baxter, consulting fees from Pfizer and GlaxoSmithKline, lecturing fees from Pfizer, and grant support for vaccine studies from Pfizer and GlaxoSmithKline. None of the fees or grants listed here were received for the research described in this paper. For all other authors no conflicts of interest were declared. This does not alter our adherence to all PLOS Pathogens policies on sharing data and materials.

                Article
                PPATHOGENS-D-12-01710
                10.1371/journal.ppat.1003057
                3542149
                23326226
                4d4dc09c-5927-4a54-adc0-3070ebe8b4ca
                Copyright @ 2013

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Page count
                Pages: 11
                Funding
                This work was supported by the Netherlands Organization for Scientific Research through NWO-VENI Grant 91610121 and ZonMW Grant 91209010. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Review
                Biology
                Ecology
                Community Ecology
                Community Assembly
                Community Structure
                Species Interactions
                Species Extinction
                Medicine
                Epidemiology
                Infectious Disease Epidemiology
                Pediatric Epidemiology
                Infectious Diseases
                Viral Diseases
                Human Bocavirus Infection
                Human Metapneumovirus Infection
                Human Parainfluenza Virus Infection
                Influenza
                Respiratory Syncytial Virus Infection
                Viral Pneumonia
                Bacterial Diseases
                Infectious Disease Control
                Infectious Disease Modeling
                Public Health
                Child Health
                Health Screening

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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