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HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection
Hepatitis B virus/hepatitis C virus (HBV/HCV) dual infection is common among high-risk individuals. To characterize the virological and immunological features of patients with HBV/HCV dual infection, we enrolled 1,049 individuals who have been identified as injection drug users. Patients were divide...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5180099/ https://www.ncbi.nlm.nih.gov/pubmed/28009018 http://dx.doi.org/10.1038/srep39409 |
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author | Chen, Fei Zhang, Jian Wen, Bo Luo, Shan Lin, Yingbiao Ou, Wensheng Guo, Fengfan Tang, Ping Liu, Wenpei Qu, Xiaowang |
author_facet | Chen, Fei Zhang, Jian Wen, Bo Luo, Shan Lin, Yingbiao Ou, Wensheng Guo, Fengfan Tang, Ping Liu, Wenpei Qu, Xiaowang |
author_sort | Chen, Fei |
collection | PubMed |
description | Hepatitis B virus/hepatitis C virus (HBV/HCV) dual infection is common among high-risk individuals. To characterize the virological and immunological features of patients with HBV/HCV dual infection, we enrolled 1,049 individuals who have been identified as injection drug users. Patients were divided into single and dual infection groups according to the serological markers. We found the average HCV RNA level was significantly lower; however, HBV viral load was significantly higher in HBV/HCV dual-infected patients (n = 42) comparing HCV single infection (n = 340) or HBV single infection (n = 136). The level of anti-HBs in patients who experienced spontaneous HBV clearance was higher than that in HCV single-infected patients with HBV spontaneous clearance. The level of anti-HCV E2 in HBV/HCV dual infection was lower than that detected in HCV single infection. Serum levels of IL-6, IL-8, and TNF-α were significantly lower in HBV/HCV dual-infected patients than in patients infected with HBV or HCV alone. Taken together, two viral replications are imbalanced in dual infected patients. The anti-HBs and anti-HCV E2 antibody production were impaired and proinflammatory IL-6, IL-8, and TNF-α also downregulated due to dual infection. These findings will help further understanding the pathogenesis of HBV/HCV dual infection. |
format | Online Article Text |
id | pubmed-5180099 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-51800992016-12-29 HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection Chen, Fei Zhang, Jian Wen, Bo Luo, Shan Lin, Yingbiao Ou, Wensheng Guo, Fengfan Tang, Ping Liu, Wenpei Qu, Xiaowang Sci Rep Article Hepatitis B virus/hepatitis C virus (HBV/HCV) dual infection is common among high-risk individuals. To characterize the virological and immunological features of patients with HBV/HCV dual infection, we enrolled 1,049 individuals who have been identified as injection drug users. Patients were divided into single and dual infection groups according to the serological markers. We found the average HCV RNA level was significantly lower; however, HBV viral load was significantly higher in HBV/HCV dual-infected patients (n = 42) comparing HCV single infection (n = 340) or HBV single infection (n = 136). The level of anti-HBs in patients who experienced spontaneous HBV clearance was higher than that in HCV single-infected patients with HBV spontaneous clearance. The level of anti-HCV E2 in HBV/HCV dual infection was lower than that detected in HCV single infection. Serum levels of IL-6, IL-8, and TNF-α were significantly lower in HBV/HCV dual-infected patients than in patients infected with HBV or HCV alone. Taken together, two viral replications are imbalanced in dual infected patients. The anti-HBs and anti-HCV E2 antibody production were impaired and proinflammatory IL-6, IL-8, and TNF-α also downregulated due to dual infection. These findings will help further understanding the pathogenesis of HBV/HCV dual infection. Nature Publishing Group 2016-12-23 /pmc/articles/PMC5180099/ /pubmed/28009018 http://dx.doi.org/10.1038/srep39409 Text en Copyright © 2016, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Chen, Fei Zhang, Jian Wen, Bo Luo, Shan Lin, Yingbiao Ou, Wensheng Guo, Fengfan Tang, Ping Liu, Wenpei Qu, Xiaowang HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection |
title | HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection |
title_full | HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection |
title_fullStr | HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection |
title_full_unstemmed | HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection |
title_short | HBV/HCV dual infection impacts viral load, antibody response, and cytokine expression differently from HBV or HCV single infection |
title_sort | hbv/hcv dual infection impacts viral load, antibody response, and cytokine expression differently from hbv or hcv single infection |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5180099/ https://www.ncbi.nlm.nih.gov/pubmed/28009018 http://dx.doi.org/10.1038/srep39409 |
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