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      Genotypic distribution and hepatic fibrosis among HIV/HCV co-infected individuals in Southern China: a retrospective cross-sectional study

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          Abstract

          Background

          End-stage liver disease and hepatocellular carcinoma due to hepatitis C virus (HCV) co-infection are increasingly common causes of death among HIV-infected individuals. However, there are few clinical investigations of HIV/HCV co-infected individuals from low and middle-income nations. Here, we compare the epidemiology of HCV-infected and HIV/HCV co-infected individuals in Southern China and examine hepatic fibrosis scores in co-infected individuals.

          Methods

          We conducted a retrospective cross-sectional study of treatment-naïve HIV/HCV co-infected and HCV mono-infected subjects. Bivariate and multivariate models were used to examine the association between demographics and HCV genotype. Among co-infected individuals, we also studied the relationship between fibrosis scores derived from non-invasive studies and HCV genotype.

          Results

          Data were collected from 175 HCV-infected individuals, including 89 (51 %) HIV/HCV co-infected individuals. HIV/HCV co-infection was correlated with intravenous drug use (AOR 46.25, p < 0.001) and not completing high school (AOR 17.39, p < 0.001) in a multivariate model. HIV/HCV co-infected individuals were more likely to be infected with HCV genotype 6a ( p < 0.0001) or 3a ( p < 0.023), whereas increased fibrosis (FIB-4 score) was associated with HCV genotype 3a infection (β 2.18, p < 0.001).

          Discussion

          Our results suggest that intravenous drug use is driving HIV/HCV co-infection in Southern China. While additional studies are needed, HCV genotype 6a is more common and genotype 3a appears to be associated with more severe hepatic fibrosis in co-infected individuals.

          Conclusions

          Future HIV/HCV co-infection research in China should focus on at risk populations, HCV testing uptake, and genotype-specific treatment.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s12879-015-1135-1) contains supplementary material, which is available to authorized users.

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          Most cited references42

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          The global burden of hepatitis C.

          Hepatitis C is of concern both to industrialized and developing countries. Preliminary unpublished estimates of the global burden of disease (GBD) attributable to HCV-related chronic liver disease seem to be substantial. Therefore, the reduction of global mortality and morbidity related to chronic hepatitis C should be a concern to public health authorities, and primary, secondary and tertiary prevention activities should be implemented and monitored in each country, with precise targets set to be reached. In order to decide on national health policies, there is a need to estimate the burden of disease, globally, regionally and nationally. To evaluate the GBD, three components have to be assessed: 1) The global, regional and national burden of morbidity and mortality associated with HCV infection, based on prevalence, incidence, transmission and economics; 2) The natural history of HCV infection, including 'healthy individuals'; and 3) The areas for which more research is needed. A working group was created to assist the World Health organization (WHO) in estimating the GBD associated with HCV infection.
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            Sofosbuvir for hepatitis C genotype 2 or 3 in patients without treatment options.

            Patients chronically infected with hepatitis C virus (HCV) genotype 2 or 3 for whom treatment with peginterferon is not an option, or who have not had a response to prior interferon treatment, currently have no approved treatment options. In phase 2 trials, regimens including the oral nucleotide polymerase inhibitor sofosbuvir have shown efficacy in patients with HCV genotype 2 or 3 infection. We conducted two randomized, phase 3 studies involving patients with chronic HCV genotype 2 or 3 infection. In one trial, patients for whom treatment with peginterferon was not an option received oral sofosbuvir and ribavirin (207 patients) or matching placebo (71) for 12 weeks. In a second trial, patients who had not had a response to prior interferon therapy received sofosbuvir and ribavirin for 12 weeks (103 patients) or 16 weeks (98). The primary end point was a sustained virologic response at 12 weeks after therapy. Among patients for whom treatment with peginterferon was not an option, the rate of a sustained virologic response was 78% (95% confidence interval [CI], 72 to 83) with sofosbuvir and ribavirin, as compared with 0% with placebo (P<0.001). Among previously treated patients, the rate of response was 50% with 12 weeks of treatment, as compared with 73% with 16 weeks of treatment (difference, -23 percentage points; 95% CI, -35 to -11; P<0.001). In both studies, response rates were lower among patients with genotype 3 infection than among those with genotype 2 infection and, among patients with genotype 3 infection, lower among those with cirrhosis than among those without cirrhosis. The most common adverse events were headache, fatigue, nausea, and insomnia; the overall rate of discontinuation of sofosbuvir was low (1 to 2%). In patients with HCV genotype 2 or 3 infection for whom treatment with peginterferon and ribavirin was not an option, 12 or 16 weeks of treatment with sofosbuvir and ribavirin was effective. Efficacy was increased among patients with HCV genotype 2 infection and those without cirrhosis. In previously treated patients with genotype 3 infection, 16 weeks of therapy was significantly more effective than 12 weeks. (Funded by Gilead Sciences; POSITRON and FUSION ClinicalTrials.gov numbers, NCT01542788 and NCT01604850, respectively.).
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              The increasing burden of mortality from viral hepatitis in the United States between 1999 and 2007.

              The increasing health burden and mortality from hepatitis B virus (HBV) and hepatitis C virus (HCV) in the United States are underappreciated. To examine mortality from HBV; HCV; and, for comparison, HIV. Analysis of U.S. multiple-cause mortality data from 1999 to 2007 from the National Center for Health Statistics. All U.S. states and the District of Columbia. Approximately 22 million decedents. Age-adjusted mortality rates from HBV, HCV, and HIV. Logistic regression analyses of 2007 data generated 4 independent models per outcome (HCV- or HBV-related deaths) that each included 1 of 4 comorbid conditions and all sociodemographic characteristics. Between 1999 and 2007, recorded deaths from HCV [corrected] increased significantly to 15,106, whereas deaths from HIV declined to 12,734 by 2007. Factors associated with HCV-related deaths included chronic liver disease, HBV co-infection, alcohol-related conditions, minority status, and HIV co-infection. Factors that increased odds of HBV-related death included chronic liver disease, HCV co-infection, Asian or Pacific Islander descent, HIV co-infection, and alcohol-related conditions. Most deaths from HBV and HCV occurred in middle-aged persons. A person other than the primary physician of the decedent frequently completed the death certificate, and HCV and HBV often were not detected and thus not reported as causes of death. By 2007, HCV had superseded HIV as a cause of death in the United States, and deaths from HCV and HBV disproportionately occurred in middle-aged persons. To achieve decreases in mortality similar to those seen with HIV requires new policy initiatives to detect patients with chronic hepatitis and link them to care and treatment. Centers for Disease Control and Prevention.
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                Author and article information

                Contributors
                kalizhou26@gmail.com
                gz8hhfy@126.com
                charles_wang@brown.edu
                gz8hxm@126.com
                lanyun.vip@126.com
                jmorano@health.usf.edu
                smlemon@med.unc.edu
                jdtucker@med.unc.edu
                gz8hcwp@126.com
                Journal
                BMC Infect Dis
                BMC Infect. Dis
                BMC Infectious Diseases
                BioMed Central (London )
                1471-2334
                30 September 2015
                30 September 2015
                2015
                : 15
                : 401
                Affiliations
                [ ]Guangzhou Eighth People’s Hospital, Guangzhou, China
                [ ]UNC-Project – China, Division of Infectious Diseases, Department of Medicine, UNC Chapel Hill School of Medicine, Chapel Hill, NC USA
                [ ]Department of Medicine, Division of Gastroenterology Providence, Brown University School of Medicine, Rhode Island, USA
                [ ]University of South Florida, Morsani College of Medicine, USF International, Tampa, FL USA
                [ ]Division of Infectious Diseases, Department of Medicine, UNC Chapel Hill School of Medicine, Chapel Hill, NC USA
                Article
                1135
                10.1186/s12879-015-1135-1
                4589973
                26424404
                7b874dae-6d9f-4d0a-bf76-cb2327ed07d7
                © Zhou et al. 2015

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 9 January 2015
                : 21 September 2015
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2015

                Infectious disease & Microbiology
                hepatitis c,human immunodeficiency virus,hiv/hcv co-infection,epidemiology,hcv genotype,hepatic fibrosis

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