Innate immunity and hepatitis C virus: eluding the host cell defense

10.2741/3579 ◽  
2009 ◽  
Vol 14 (1) ◽  
pp. 4950 ◽  
Author(s):  
Deborah, R. Taylor
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Host Cell ◽  
Cell Defense

The hepatitis C virus non-structural 3/4A protease activates Akt-dependent host cell signaling which is required for sufficient viral replication

2009 ◽  
Vol 47 (01) ◽  
Author(s):  
ED Brenndörfer ◽  
J Karthe ◽  
P Cebula ◽  
A Erhardt ◽  
L Frelin ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Viral Replication ◽  
Cell Signaling ◽  
Host Cell ◽  
Host Cell Signaling

scholarly journals Innate immunity and hepatitis C virus infection: a microarray's view

2012 ◽  
Vol 7 (1) ◽  
Author(s):  
Luigi Buonaguro ◽  
Annacarmen Petrizzo ◽  
Maria Lina Tornesello ◽  
Franco M Buonaguro
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Hepatitis C Virus Infection

Hepatitis C virus NS2 protease inhibits host cell antiviral response by inhibiting IKKε and TBK1 functions

2012 ◽  
Vol 85 (1) ◽  
pp. 71-82 ◽  
Author(s):  
Pasi Kaukinen ◽  
Maarit Sillanpää ◽  
Laura Nousiainen ◽  
Krister Melén ◽  
Ilkka Julkunen
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Host Cell ◽  
Antiviral Response

scholarly journals Insights into antiviral innate immunity revealed by studying hepatitis C virus

Cytokine ◽  
2015 ◽  
Vol 74 (2) ◽  
pp. 190-197 ◽  
Author(s):  
Stacy M. Horner
Keyword(s):  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Antiviral Innate Immunity

scholarly journals Hepatitis C Virus E2—Host Cell Receptor, HSPA5, Binding Site Prediction

2020 ◽  
Author(s):  
Alaa Elgohary ◽  
Abdo Elfiky
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Host Cell ◽  
Cyclic Peptide ◽  
Causative Factor ◽  
Cell Receptor ◽  
Binding Mode ◽  
Structural Protein ◽  
The Unfolded Protein Response

Hepatitis C Virus (HCV) is the main causative factor for liver cirrhosis and the development of liver cancer, with a confirmed ~ 180 million infections worldwide. E2 is an HCV structural protein responsible for virus entry to the host cell. Heat Shock Protein A5 (HSPA5), also termed BiP and GRP78, is the master regulator of the unfolded protein response mechanism, where it mainly localizes in the lumen of the Endoplasmic Reticulum (ER) in normal conditions. Under the stress of HCV infection or carcinogenesis, HSPA5 is upregulated. Consequently, HSPA5 escapes the ER retention localization and translocates to the cytoplasm and plasma membrane. Pep42, a cyclic peptide that was reported to target explicitly cell-surface HSPA5 in vivo. Owing to the high sequence and structural conservation between the C554-C566 region of HCV E2 and the Pep42, then we propose that the HCV E2 C554-C566 region could be the recognition site. The motivation of this work is to predict the possible binding mode between HCV E2 and HSPA5 by implementing molecular docking to test such proposed binding. Docking results reveal the high potent binding of the HCV E2 C554-C566 region to HSPA5 substrate-binding domain β (SBDβ). Moreover, the full-length HCV E2 also exhibits high binding potency to HSPA5 SBDβ. Defining the binding mode between HCV E2 and HSPA5 is of significance, so one can interfere with such binding and reducing the viral infection.

scholarly journals Dissecting the Interferon-Induced Inhibition of Hepatitis C Virus Replication by Using a Novel Host Cell Line

2005 ◽  
Vol 79 (21) ◽  
pp. 13778-13793 ◽  
Author(s):  
Marc P. Windisch ◽  
Michael Frese ◽  
Artur Kaul ◽  
Martin Trippler ◽  
Volker Lohmann ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Host Cell ◽  
Cell Line ◽  
Nuclear Translocation ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Adaptive Mutations ◽  
Antiviral Compounds ◽  
Ifn Γ

ABSTRACT The Hepatitis C virus (HCV), a member of the family Flaviviridae, is a major cause of chronic liver disease. Patients are currently treated with alpha interferon (IFN-α) that is given alone or in combination with ribavirin. Unfortunately, this treatment is ineffective in eliminating the virus in a large proportion of individuals. IFN-induced antiviral activities have been intensively studied in the HCV replicon system. It was found that both IFN-α and IFN-γ inhibit HCV replicons, but the underlying mechanisms have not yet been identified. Of note is that nearly all of these studies were performed with the human hepatoma cell line Huh-7. Here, we report that genotypes 1b and 2a replicons also replicate in the human hepatoblastoma cell line HuH6. Similar to what has been described for Huh-7 cells, we observed that efficient HCV replication in HuH6 cells depends on the presence of cell culture-adaptive mutations and the permissiveness of the host cell. However, three major differences exist: in HuH6 cells, viral replication is (i) independent from ongoing cell proliferation, (ii) less sensitive to certain antiviral compounds, and (iii) highly resistant to IFN-γ. The latter is not due to a general defect in IFN signaling, as IFN-γ induces the nuclear translocation of signal transducer and activator of transcription 1 (STAT1), the enhanced transcription of several IFN-regulated genes, and the inhibition of unrelated viruses such as influenza A virus and Semliki Forest virus. Taken together, the results establish HuH6 replicon cells as a valuable tool for IFN studies and for the evaluation of antiviral compounds.

scholarly journals Innate Immune Response against Hepatitis C Virus: Targets for Vaccine Adjuvants

Vaccines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 313
Author(s):  
Daniel Sepulveda-Crespo ◽  
Salvador Resino ◽  
Isidoro Martinez
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Innate Immune Response ◽  
Vaccine Development ◽  
Innate Immune ◽  
World Health ◽  
Cell Immune Response ◽  
Vaccine Adjuvants

Despite successful treatments, hepatitis C virus (HCV) infections continue to be a significant world health problem. High treatment costs, the high number of undiagnosed individuals, and the difficulty to access to treatment, particularly in marginalized susceptible populations, make it improbable to achieve the global control of the virus in the absence of an effective preventive vaccine. Current vaccine development is mostly focused on weakly immunogenic subunits, such as surface glycoproteins or non-structural proteins, in the case of HCV. Adjuvants are critical components of vaccine formulations that increase immunogenic performance. As we learn more information about how adjuvants work, it is becoming clear that proper stimulation of innate immunity is crucial to achieving a successful immunization. Several hepatic cell types participate in the early innate immune response and the subsequent inflammation and activation of the adaptive response, principally hepatocytes, and antigen-presenting cells (Kupffer cells, and dendritic cells). Innate pattern recognition receptors on these cells, mainly toll-like receptors, are targets for new promising adjuvants. Moreover, complex adjuvants that stimulate different components of the innate immunity are showing encouraging results and are being incorporated in current vaccines. Recent studies on HCV-vaccine adjuvants have shown that the induction of a strong T- and B-cell immune response might be enhanced by choosing the right adjuvant.

scholarly journals Hepatitis C virus NS3 protein modulates the biological behaviors of malignant hepatocytes by altering the expression of host cell microRNA

2015 ◽  
Vol 12 (4) ◽  
pp. 5109-5115 ◽  
Author(s):  
JUN ZHANG ◽  
YASUHITO ISHIGAKI ◽  
TSUTOMU TAKEGAMI
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Host Cell ◽  
Ns3 Protein
Sign in / Sign up

Export Citation Format

Share Document