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Regulation of Inflammatory and Immune Responses in Flaviviridae Family: Emphasis on HCV, DENV, and ZIKV

Call for Papers

Hepacivirus and Flavivirus are two of the four genera belonging to Flaviviridae family. Among Hepacivirus and Flavivirus, the hepatitis C virus (HCV), dengue virus (DENV), and zika virus (ZIKV) represent significant public health concerns for humans. DENV and ZIKV are arboviruses and important causes of acute febrile disease in tropical areas, while HCV is a hepatotropic RNA virus and is the leading cause of virus-induced liver diseases. Dengue fever is an acute febrile disease caused by any of the four serotypes DENV-1, DENV-2, DENV-3, and DENV-4, ranging from a nonspecific febrile illness to a more severe disease characterized by bleeding and plasma leakage. Although the symptoms associated with Zika virus infection are generally mild, severe neurological complications have been reported including Guillain-Barré syndrome (GBS), microcephaly, and other neurological fetal complications mainly in regions with DENV circulation. The critical point of DENV pathophysiology is plasma leakage mediated by inflammatory mediators such as cytokines and chemokines. Importantly, activated inflammatory cells in the liver are associated with liver fibrosis and damage during chronic HCV infection. The pathogenesis of ZIKV infection still remains poorly understood.

We invite authors to submit original research and review articles exploring aspects of innate and adaptive antiviral immunity in humans and also in animal models. We are interested in articles describing the role of inflammatory mediators in the pathogenesis of DENV, ZIKV, or HCV virus infections as well as new insights into pathophysiological mechanisms using animal models.

Potential topics include but are not limited to the following:

  • Investigating innate and adaptive responses
  • The influence on the antiviral and inflammatory responses of the DENV, ZIKV, or HCV in mono- and coinfected patients
  • The influence of HIV coinfection on DENV, ZIKV, or HCV antiviral and inflammatory responses
  • New cellular and animal models to evaluate immunity to virus infection
  • Identifying inflammatory biomarkers/correlates of protective immunity
  • Identifying immunogenic epitopes recognized by human infected individuals

Authors can submit their manuscripts through the Manuscript Tracking System at https://mts.hindawi.com/submit/journals/mi/ricm/.

Submission DeadlineFriday, 24 November 2017
Publication DateApril 2018

Papers are published upon acceptance, regardless of the Special Issue publication date.

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