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<p>Dengue virus (DENV), an arboviral pathogen, causes important morbidity and mortality around the globe. DENV non-structural protein 1 (NS1) plays an important role in the entire life cycle of the virus and directly influences both replication of viruses and immune responses in host cells. Studies recently uncovered that DENV NS1 interacts with the host’s complement system, a fundamental component of innate immunity. The complement system is composed of several proteins that function in a cascade to enhance inflammation and facilitate the removal of pathogens. However, NS1 interferes with complement activation; it does this either by directly interacting with complement proteins or through modulation of the complement cascade, leading to immune evasion. These interactions may lead to a dysregulated immune response, contributing to the pathogenesis of dengue fever and its more severe forms, such as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). This study discusses the molecular mechanisms behind the interactions between DENV NS1 and complement pathway proteins, shedding light on the implications for viral persistence, immune evasion, and disease progression. These interactions may thus hold the key to unveiling novel therapeutic targets for developing complement-based interventions to treat dengue infections.</p>

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Interaction of Dengue virus NS1 with complement pathway proteins: an in silico study

  • 期刊论文

  • 发表日期：

    2025年7月21日

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  • Dwaipayan Chaudhuri,
  • Kalyan Giri

摘要

Dengue virus (DENV), an arboviral pathogen, causes important morbidity and mortality around the globe. DENV non-structural protein 1 (NS1) plays an important role in the entire life cycle of the virus and directly influences both replication of viruses and immune responses in host cells. Studies recently uncovered that DENV NS1 interacts with the host’s complement system, a fundamental component of innate immunity. The complement system is composed of several proteins that function in a cascade to enhance inflammation and facilitate the removal of pathogens. However, NS1 interferes with complement activation; it does this either by directly interacting with complement proteins or through modulation of the complement cascade, leading to immune evasion. These interactions may lead to a dysregulated immune response, contributing to the pathogenesis of dengue fever and its more severe forms, such as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). This study discusses the molecular mechanisms behind the interactions between DENV NS1 and complement pathway proteins, shedding light on the implications for viral persistence, immune evasion, and disease progression. These interactions may thus hold the key to unveiling novel therapeutic targets for developing complement-based interventions to treat dengue infections.