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      Complement and viral pathogenesis

      review-article
      Author(s): a , b , c , a , b , *
      Publication date (Electronic):
      Journal: Virology
      Publisher: Elsevier Inc.
      Keywords: Complement, Virus, Pathogenesis

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The complement system functions as an immune surveillance system that rapidly responds to infection. Activation of the complement system by specific recognition pathways triggers a protease cascade, generating cleavage products that function to eliminate pathogens, regulate inflammatory responses, and shape adaptive immune responses. However, when dysregulated, these powerful functions can become destructive and the complement system has been implicated as a pathogenic effector in numerous diseases, including infectious diseases. This review highlights recent discoveries that have identified critical roles for the complement system in the pathogenesis of viral infection.

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          Global Spread and Persistence of Dengue

          Jennifer L. Kyle, Eva Harris (2008)
          Dengue is a spectrum of disease caused by four serotypes of the most prevalent arthropod-borne virus affecting humans today, and its incidence has increased dramatically in the past 50 years. Due in part to population growth and uncontrolled urbanization in tropical and subtropical countries, breeding sites for the mosquitoes that transmit dengue virus have proliferated, and successful vector control has proven problematic. Dengue viruses have evolved rapidly as they have spread worldwide, and genotypes associated with increased virulence have expanded from South and Southeast Asia into the Pacific and the Americas. This review explores the human, mosquito, and viral factors that contribute to the global spread and persistence of dengue, as well as the interaction between the three spheres, in the context of ecological and climate changes. What is known, as well as gaps in knowledge, is emphasized in light of future prospects for control and prevention of this pandemic disease.
          Article 0 comments Cited 279 times – based on 0 reviews     Review now
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            High circulating levels of the dengue virus nonstructural protein NS1 early in dengue illness correlate with the development of dengue hemorrhagic fever.

            Daniel H. Libraty, Paul R Young, Darren Pickering … (2002)
            Infection with any 1 of 4 dengue viruses produces a spectrum of clinical illness ranging from a mild undifferentiated febrile illness to dengue fever (DF) to dengue hemorrhagic fever (DHF), a potentially life-threatening disease. The morbidity and mortality of DHF can be reduced by early hospitalization and careful supportive care. To determine its usefulness as a predictor of DHF, plasma levels of the secreted dengue virus nonstructural protein NS1 (sNS1) were measured daily in 32 children with dengue-2 virus infections participating in a prospective, hospital-based study. Free sNS1 levels in plasma correlated with viremia levels and were higher in patients with DHF than in those with DF. An elevated free sNS1 level (> or =600 ng/mL) within 72 h of illness onset identified patients at risk for developing DHF.
            Article 0 comments Cited 213 times – based on 0 reviews     Review now
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              Virulence differences between monkeypox virus isolates from West Africa and the Congo basin

              Nanhai Chen, Guiyun Li, M. Kathryn Liszewski … (2005)
              Studies indicate that West African and Congo basin isolates of monkeypox virus (MPXV) are genetically distinct. Here, we show Congo basin MPXV-ZAI-V79 is more virulent for cynomolgus monkeys as compared to presumed West African MPXV-COP-58. This finding may explain the lack of case-fatalities in the U.S. 2003 monkeypox outbreak, which was caused by a West African virus. Virulence differences between West African and Congo basin MPXV are further supported by epidemiological analyses that observed a similar prevalence of antibodies in non-vaccinated humans in both regions, while >90% of reported cases occurred in the Congo basin, and no fatal cases were observed outside of this region. To determine the basis for this difference in virulence, we sequenced the genomes of one human West African isolate, and two presumed West African isolates and compared the sequences to Congo basin MPXV-ZAI-96-I-16. The analysis identified D10L, D14L, B10R, B14R, and B19R as possible virulence genes, with D14L (ortholog of vaccinia complement protein) as a leading candidate.
              Article 0 comments Cited 181 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Thomas E. Morrison
                Journal
                Journal ID (nlm-ta): Virology
                Journal ID (iso-abbrev): Virology
                Title: Virology
                Publisher: Elsevier Inc.
                ISSN (Print): 0042-6822
                ISSN (Electronic): 1096-0341
                Publication date PMC-release: 2 February 2011
                Publication date (Print): 15 March 2011
                Publication date (Electronic): 2 February 2011
                Volume: 411
                Issue: 2
                Pages: 362-373
                Affiliations
                [a ]Department of Microbiology, University of Colorado School of Medicine, Aurora, CO 80045, USA
                [b ]Department of Immunology, University of Colorado School of Medicine, Aurora, CO 80045, USA
                [c ]Graduate Program in Immunology, University of Colorado School of Medicine, Aurora, CO 80045, USA
                Author notes
                [* ]Corresponding author at: Department of Microbiology, University of Colorado School of Medicine, 12800 East 19th Avenue, Mail Stop 8333, Aurora, CO 80045, USA. Fax: +1 303 724 5226. thomas.morrison@ 123456ucdenver.edu
                Article
                Publisher ID: S0042-6822(10)00813-5
                DOI: 10.1016/j.virol.2010.12.045
                PMC ID: 3073741
                PubMed ID: 21292294
                SO-VID: 655c9498-0694-4347-913a-848b67b183cc
                Copyright © Copyright © 2010 Elsevier Inc. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 30 November 2010
                Date revision received : 14 December 2010
                Date accepted : 23 December 2010
                Categories
                Subject: Article

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: complement,virus,pathogenesis
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: complement, virus, pathogenesis

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