Innate Immune Evasion Mediated by Flaviviridae Non-Structural Proteins.

Shun Chen, Zhen Wu, Mingshu Wang, Anchun Cheng
Author Information
  1. Shun Chen: Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China. shunchen@sicau.edu.cn.
  2. Zhen Wu: Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China. zhenwu@stu.sicau.edu.cn.
  3. Mingshu Wang: Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China. mshwang@163.com.
  4. Anchun Cheng: Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China. chenganchun@vip.163.com. ORCID

Abstract

Flaviviridae-caused diseases are a critical, emerging public health problem worldwide. Flaviviridae infections usually cause severe, acute or chronic diseases, such as liver damage and liver cancer resulting from a hepatitis C virus (HCV) infection and high fever and shock caused by yellow fever. Many researchers worldwide are investigating the mechanisms by which Flaviviridae cause severe diseases. Flaviviridae can interfere with the host's innate immunity to achieve their purpose of proliferation. For instance, dengue virus (DENV) NS2A, NS2B3, NS4A, NS4B and NS5; HCV NS2, NS3, NS3/4A, NS4B and NS5A; and West Nile virus (WNV) NS1 and NS4B proteins are involved in immune evasion. This review discusses the interplay between viral non-structural Flaviviridae proteins and relevant host proteins, which leads to the suppression of the host's innate antiviral immunity.

Keywords

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MeSH Term

Animals
Antiviral Agents
Flaviviridae
Flaviviridae Infections
Humans
Immune Evasion
Immunity, Innate
Mice
Viral Nonstructural Proteins

Chemicals

Antiviral Agents
Viral Nonstructural Proteins

Word Cloud

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