Current Understanding of the Pathogenesis of Dengue Virus Infection
The pathogenesis of dengue virus infection is attributed to complex interplay between virus, host genes and host immune response. Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major dete...
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Veröffentlicht in: | Current microbiology 2021-01, Vol.78 (1), p.17-32 |
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description | The pathogenesis of dengue virus infection is attributed to complex interplay between virus, host genes and host immune response. Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major determinants of disease susceptibility. NS1 protein and anti-DENV NS1 antibodies were believed to be responsible for pathogenesis of severe dengue. The cytokine response of cross-reactive CD4+ T cells might be altered by the sequential infection with different DENV serotypes, leading to further elevation of pro-inflammatory cytokines contributing a detrimental immune response. Fcγ receptor-mediated antibody-dependent enhancement (ADE) results in release of cytokines from immune cells leading to vascular endothelial cell dysfunction and increased vascular permeability. Genomic variation of dengue virus and subgenomic flavivirus RNA (sfRNA) suppressing host immune response are viral determinants of disease severity. Dengue infection can lead to the generation of autoantibodies against DENV NS1antigen, DENV prM, and E proteins, which can cross-react with several self-antigens such as plasminogen, integrin, and platelet cells. Apart from viral factors, several host genetic factors and gene polymorphisms also have a role to play in pathogenesis of DENV infection. This review article highlights the various factors responsible for the pathogenesis of dengue and also highlights the recent advances in the field related to biomarkers which can be used in future for predicting severe disease outcome. |
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Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major determinants of disease susceptibility. NS1 protein and anti-DENV NS1 antibodies were believed to be responsible for pathogenesis of severe dengue. The cytokine response of cross-reactive CD4+ T cells might be altered by the sequential infection with different DENV serotypes, leading to further elevation of pro-inflammatory cytokines contributing a detrimental immune response. Fcγ receptor-mediated antibody-dependent enhancement (ADE) results in release of cytokines from immune cells leading to vascular endothelial cell dysfunction and increased vascular permeability. Genomic variation of dengue virus and subgenomic flavivirus RNA (sfRNA) suppressing host immune response are viral determinants of disease severity. Dengue infection can lead to the generation of autoantibodies against DENV NS1antigen, DENV prM, and E proteins, which can cross-react with several self-antigens such as plasminogen, integrin, and platelet cells. Apart from viral factors, several host genetic factors and gene polymorphisms also have a role to play in pathogenesis of DENV infection. This review article highlights the various factors responsible for the pathogenesis of dengue and also highlights the recent advances in the field related to biomarkers which can be used in future for predicting severe disease outcome.</description><identifier>ISSN: 0343-8651</identifier><identifier>EISSN: 1432-0991</identifier><identifier>DOI: 10.1007/s00284-020-02284-w</identifier><identifier>PMID: 33231723</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antibodies ; Antibodies, Viral ; Antibody-Dependent Enhancement ; Antigens ; Autoantibodies ; Autoantigens ; Autoimmune diseases ; Autoimmunity ; Biomarkers ; Biomedical and Life Sciences ; Biotechnology ; CD4 antigen ; Cytokines ; Dengue ; Dengue fever ; Dengue hemorrhagic fever ; Dengue Virus ; Endothelial cells ; Gene polymorphism ; Genetic factors ; Genomics ; Humans ; Immune response ; Immune system ; Immunological memory ; Infections ; Inflammation ; Life Sciences ; Lymphocytes ; Lymphocytes T ; Memory cells ; Microbiology ; NS1 protein ; Pathogenesis ; Permeability ; Proteins ; Review ; Review Article ; Ribonucleic acid ; RNA ; RNA viruses ; Serotypes ; Vector-borne diseases ; Virus Diseases ; Viruses</subject><ispartof>Current microbiology, 2021-01, Vol.78 (1), p.17-32</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major determinants of disease susceptibility. NS1 protein and anti-DENV NS1 antibodies were believed to be responsible for pathogenesis of severe dengue. The cytokine response of cross-reactive CD4+ T cells might be altered by the sequential infection with different DENV serotypes, leading to further elevation of pro-inflammatory cytokines contributing a detrimental immune response. Fcγ receptor-mediated antibody-dependent enhancement (ADE) results in release of cytokines from immune cells leading to vascular endothelial cell dysfunction and increased vascular permeability. Genomic variation of dengue virus and subgenomic flavivirus RNA (sfRNA) suppressing host immune response are viral determinants of disease severity. Dengue infection can lead to the generation of autoantibodies against DENV NS1antigen, DENV prM, and E proteins, which can cross-react with several self-antigens such as plasminogen, integrin, and platelet cells. Apart from viral factors, several host genetic factors and gene polymorphisms also have a role to play in pathogenesis of DENV infection. This review article highlights the various factors responsible for the pathogenesis of dengue and also highlights the recent advances in the field related to biomarkers which can be used in future for predicting severe disease outcome.</description><subject>Antibodies</subject><subject>Antibodies, Viral</subject><subject>Antibody-Dependent Enhancement</subject><subject>Antigens</subject><subject>Autoantibodies</subject><subject>Autoantigens</subject><subject>Autoimmune diseases</subject><subject>Autoimmunity</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Biotechnology</subject><subject>CD4 antigen</subject><subject>Cytokines</subject><subject>Dengue</subject><subject>Dengue fever</subject><subject>Dengue hemorrhagic fever</subject><subject>Dengue Virus</subject><subject>Endothelial cells</subject><subject>Gene polymorphism</subject><subject>Genetic factors</subject><subject>Genomics</subject><subject>Humans</subject><subject>Immune 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attributed to complex interplay between virus, host genes and host immune response. Host factors such as antibody-dependent enhancement (ADE), memory cross-reactive T cells, anti-DENV NS1 antibodies, autoimmunity as well as genetic factors are major determinants of disease susceptibility. NS1 protein and anti-DENV NS1 antibodies were believed to be responsible for pathogenesis of severe dengue. The cytokine response of cross-reactive CD4+ T cells might be altered by the sequential infection with different DENV serotypes, leading to further elevation of pro-inflammatory cytokines contributing a detrimental immune response. Fcγ receptor-mediated antibody-dependent enhancement (ADE) results in release of cytokines from immune cells leading to vascular endothelial cell dysfunction and increased vascular permeability. Genomic variation of dengue virus and subgenomic flavivirus RNA (sfRNA) suppressing host immune response are viral determinants of disease severity. Dengue infection can lead to the generation of autoantibodies against DENV NS1antigen, DENV prM, and E proteins, which can cross-react with several self-antigens such as plasminogen, integrin, and platelet cells. Apart from viral factors, several host genetic factors and gene polymorphisms also have a role to play in pathogenesis of DENV infection. This review article highlights the various factors responsible for the pathogenesis of dengue and also highlights the recent advances in the field related to biomarkers which can be used in future for predicting severe disease outcome.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33231723</pmid><doi>10.1007/s00284-020-02284-w</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-0740-1443</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antibodies Antibodies, Viral Antibody-Dependent Enhancement Antigens Autoantibodies Autoantigens Autoimmune diseases Autoimmunity Biomarkers Biomedical and Life Sciences Biotechnology CD4 antigen Cytokines Dengue Dengue fever Dengue hemorrhagic fever Dengue Virus Endothelial cells Gene polymorphism Genetic factors Genomics Humans Immune response Immune system Immunological memory Infections Inflammation Life Sciences Lymphocytes Lymphocytes T Memory cells Microbiology NS1 protein Pathogenesis Permeability Proteins Review Review Article Ribonucleic acid RNA RNA viruses Serotypes Vector-borne diseases Virus Diseases Viruses |
title | Current Understanding of the Pathogenesis of Dengue Virus Infection |
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