Host Immune Response to Dengue Virus Infection: Friend or Foe?
DENV belongs to the Flaviviridae family and possesses a single-stranded RNA genome of positive polarity. DENV infection manifests in mild subclinical forms or severe forms that may be dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS). Despite a lot of effort worldwide, the exact mechanis...
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MDPI AG
2024-11-01
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| author | Priya Dhole Amir Zaidi Hardik K. Nariya Shruti Sinha Sandhya Jinesh Shivani Srivastava |
| author_facet | Priya Dhole Amir Zaidi Hardik K. Nariya Shruti Sinha Sandhya Jinesh Shivani Srivastava |
| author_sort | Priya Dhole |
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| description | DENV belongs to the Flaviviridae family and possesses a single-stranded RNA genome of positive polarity. DENV infection manifests in mild subclinical forms or severe forms that may be dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS). Despite a lot of effort worldwide, the exact mechanism underlying the pathogenesis of severe DENV infection remains elusive. It is believed that both host and viral factors contribute to the outcome of dengue disease. The host factors are age at the time of infection, sex, nutrition, and immune status, including the presence of pre-existing antibodies or reactive T cells. Viral factors include the serotype, genotype, and mutation(s) due to error-prone RNA-dependent polymerase leading to the development of quasispecies. Accumulating bodies of literature have depicted that DENV has many ways to invade and escape the immune system of the host. These invading strategies are directed to overcome innate and adaptive immune responses. Like other viruses, once the infection is established, the host also mounts a series of antiviral responses to combat and eliminate the virus replication. Nevertheless, DENV has evolved a variety of mechanisms to evade the immune system. In this review, we have emphasized the strategies that DENV employs to hijack the host innate (interferon, IFN; toll-like receptors, TLR; major histocompatibility complex, MHC; autophagy; complement; apoptosis; RNAi) and adaptive (antibody-dependent enhancement, ADE; T cell immunity) immune responses, which contribute to the severity of DENV disease. |
| format | Article |
| id | doaj-art-317b14d180c34e57bf0072d2ecaf60da |
| institution | Kabale University |
| issn | 2673-5601 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | MDPI AG |
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| series | Immuno |
| spelling | doaj-art-317b14d180c34e57bf0072d2ecaf60da2024-12-27T14:30:34ZengMDPI AGImmuno2673-56012024-11-014454957710.3390/immuno4040033Host Immune Response to Dengue Virus Infection: Friend or Foe?Priya Dhole0Amir Zaidi1Hardik K. Nariya2Shruti Sinha3Sandhya Jinesh4Shivani Srivastava5Division of Microbiology and Immunology, Emory National Primate Research Center, Emory University, Atlanta, GA 30322, USADepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USADivision of Microbiology and Immunology, Emory National Primate Research Center, Emory University, Atlanta, GA 30322, USAMicrobiology Department, School of Allied Sciences, Dev Bhoomi Uttarakhand University, Dehradun 248007, UA, IndiaCVS Health, 5065 Main Street, Trumbull, CT 06611, USADepartment of Pathology, School of Medicine, Yale University, New Haven, CT 06510, USADENV belongs to the Flaviviridae family and possesses a single-stranded RNA genome of positive polarity. DENV infection manifests in mild subclinical forms or severe forms that may be dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS). Despite a lot of effort worldwide, the exact mechanism underlying the pathogenesis of severe DENV infection remains elusive. It is believed that both host and viral factors contribute to the outcome of dengue disease. The host factors are age at the time of infection, sex, nutrition, and immune status, including the presence of pre-existing antibodies or reactive T cells. Viral factors include the serotype, genotype, and mutation(s) due to error-prone RNA-dependent polymerase leading to the development of quasispecies. Accumulating bodies of literature have depicted that DENV has many ways to invade and escape the immune system of the host. These invading strategies are directed to overcome innate and adaptive immune responses. Like other viruses, once the infection is established, the host also mounts a series of antiviral responses to combat and eliminate the virus replication. Nevertheless, DENV has evolved a variety of mechanisms to evade the immune system. In this review, we have emphasized the strategies that DENV employs to hijack the host innate (interferon, IFN; toll-like receptors, TLR; major histocompatibility complex, MHC; autophagy; complement; apoptosis; RNAi) and adaptive (antibody-dependent enhancement, ADE; T cell immunity) immune responses, which contribute to the severity of DENV disease.https://www.mdpi.com/2673-5601/4/4/33dengue virusantibody-dependent enhancement |
| spellingShingle | Priya Dhole Amir Zaidi Hardik K. Nariya Shruti Sinha Sandhya Jinesh Shivani Srivastava Host Immune Response to Dengue Virus Infection: Friend or Foe? Immuno dengue virus antibody-dependent enhancement |
| title | Host Immune Response to Dengue Virus Infection: Friend or Foe? |
| title_full | Host Immune Response to Dengue Virus Infection: Friend or Foe? |
| title_fullStr | Host Immune Response to Dengue Virus Infection: Friend or Foe? |
| title_full_unstemmed | Host Immune Response to Dengue Virus Infection: Friend or Foe? |
| title_short | Host Immune Response to Dengue Virus Infection: Friend or Foe? |
| title_sort | host immune response to dengue virus infection friend or foe |
| topic | dengue virus antibody-dependent enhancement |
| url | https://www.mdpi.com/2673-5601/4/4/33 |
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