Paper Information

Journal:   HEPATITIS MONTHLY   JUNE 2014 , Volume 14 , Number 6; Page(s) 0 To 0.
 
Paper: 

HCV NS3 BLOCKING EFFECT ON IFN INDUCED ISGS LIKE VIPERIN AND IL28 WITH AND WITHOUT NS4A

 
 
Author(s):  KHANLARI ZAHRA, SABAHI FARZANEH*, HOSSEINI SEYED YOUNES, GHADERI MOSTAFA
 
* DEPARTMENT OF MEDICAL VIROLOGY, FACULTY OF MEDICAL SCIENCES, TARBIAT MODARES UNIVERSITY, TEHRAN, IR IRAN
 
Abstract: 

Background: Hepatitis C virus (HCV) is able to down-regulate innate immune response. It is important to know the immune pathways that this virus interacts with. HCV non-structural protein 3 (NS3) plays an important role in this viral feature. HCV NS3 protein could affect the expression of antiviral protein such as viperin, and interleukin 28whichare important proteins in antiviral response.
Objectives: HCV has developed different mechanisms to maintain a persistent infection, especially by disrupting type I interferon response and subsequent suppression of expression of Interferon stimulatory genes (ISGs). Viperin, a member of ISGs, is considered as a host antiviral protein, which interferes with viral replication. Since it is a good target for some viruses to evade host responses, it is interesting to study if HCV has evolved a mechanism to interfere with this member of ISGs.
Materials and Methods: We evaluated the impact of NS3, NS3/4A and a mutated nonfunctional NS3 on ISGs expression such as viperin and IL-28 after the induction of IFN signaling Jak-STAT pathway using IFN-.
Results: NS3 protein disrupted the expressions of viperin gene and IL-28, an inducer for the expression of ISGs and viperin itself. By comparing the roles of NS3 and NS3/4A protease activities in suppressing the innate immune responses, we also showed that NS3 (without NS4A) has the ability to down-regulate ISGs expression, similar to that of NS3/4A.
Conclusions: ISGs expression is impeded by NS3 protease activity and its interaction with Jak-STAT pathway proteins. In addition, the NS3/4A substrates spectrum seems to be similar to those of NS3.

 
Keyword(s): HEPATITIS C, NS3, INTERFERON-LAMBDA PROTEIN
 
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