Advanced search
Start date
Betweenand
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Heat shock proteins HSPB8 and DNAJC5B have HCV antiviral activity

Full text
Author(s):
Silva Braga, Ana Claudia [1] ; Carneiro, Bruno Moreira [1, 2] ; Batista, Mariana Nogueira [1] ; Akinaga, Monica Mayumi [1] ; Bittar, Cintia [1] ; Rahal, Paula [1]
Total Authors: 6
Affiliation:
[1] UNESP IBILCE, Lab Estudos Genom, Sao Jose Do Rio Preto, SP - Brazil
[2] UFMT CUR, Inst Ciencias Exatas & Nat, Rondonopolis, Mato Grosso - Brazil
Total Affiliations: 2
Document type: Journal article
Source: PLoS One; v. 12, n. 11 NOV 28 2017.
Web of Science Citations: 1
Abstract

Hepatitis C is a disease caused by the hepatitis C virus (HCV), and an estimated 3% of the world population is infected with the virus. During replication, HCV interacts with several cellular proteins. Studies have shown that several heat shock proteins (HSPs) have an altered expression profile in the presence of the virus, and some HSPs interact directly with HCV proteins. In the present study, we evaluated the expression levels of heat shock proteins in vitro in the presence and absence of HCV. The differential expression of 84 HSPs and chaperones was observed using a qPCR array, comparing HCV uninfected and infected Huh7.5 cells. To validate qPCR array, the differentially expressed genes were tested by real-time PCR in three different HCV models: subgenomic HCV replicon cells (SGR-JFH-1), JFH-1 infected cells (both genotype 2a) and subgenomic S52 cells (genotype 3). The HSPB8 gene showed increased expression in all three viral models. We silenced HSPB8 expression and observed an increase in viral replication. In contrast, when we increased the expression of HSPB8, a decrease in the HCV replication rate was observed. The same procedure was adopted for DNAJC5B, and HCV showed a similar replication pattern as that observed for HSPB8. These results suggest that HSPB8 may act as an intracellular factor against hepatitis C virus replication and that DNAJC5B has the same function, with more relevant results for genotype 3. We also evaluated the direct interactions between HCV and HSP proteins, and the IP experiments showed that the HCV NS4B protein interacts with HSPB8. These results contribute to a better understanding of the mechanisms involved in HCV replication. (AU)

FAPESP's process: 13/17253-9 - Regulating the Expression of Heat Shock Proteins by Hepatitis C Virus
Grantee:Ana Cláudia Silva Braga
Support type: Scholarships in Brazil - Doctorate