Morbidity and mortality profile of human immunodeficiency virus-infected patients with and without hepatitis C co-infection

Retrovirus Research Center, and Department of Microbiology, Universidad Central del Caribe, School of Medicine, Bayamón, Puerto Rico.
The American journal of tropical medicine and hygiene (Impact Factor: 2.7). 03/2006; 74(2):239-45.
Source: PubMed


Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) co-infection is an important and frequent scenario, predominantly in injecting drug users (IDUs). The present study evaluated morbidity and mortality variation in HIV-infected patients with and without HCV co-infection. Co-infection prevalence was determined in 356 HIV-infected persons. Their clinical manifestations, laboratory findings, risk factors, HIV therapies, and mortality rates were evaluated. The prevalence of HCV was 54% in the overall group and 81% in IDUs, with a predominance of HCV genotype 1. Mortality rates were similar in patients with and without co-infection; however, co-infected patients had significantly higher liver damage as a cause of mortality when compared with those who were not co-infected. The high prevalence of HCV and an emerging mortality from liver diseases showed the significance of this co-infection in the HIV epidemic. Primary and secondary prevention are necessary to reduce the expanding impact of HCV infection in HIV patients.

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    • "These HIV/HCV co-infected persons account for approximately 25% of all HIV-infected persons all over the world [1]. Injection drug users (IDUs) are shown to be the highest risk factor of HIV/HCV co-infection [2-5]. According to a study investigation performed in 2008, approximately 63.2% of HIV-infected patients were co-infected with HCV in different areas of China [6], and the prevalence was 96.6% in IDUs and 92.9% in former paid blood donors (FBD) [7]. "
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    ABSTRACT: Co-infection with hepatitis C (HCV) is very common in human immunodeficiency virus 1 (HIV-1) infected patients. Although HIV co-infection clearly accelerates progression of HCV-related fibrosis and liver disease, controversy remains as to the impact of HCV on HIV disease progression in co-infected patients. HIV can cause immune dysfunction, in which the regulatory function of T helper (Th) cells is very essential. Moreover, cytokines derived from Th cells play a prominent role in viral infection. Investigating the functional changes of Th1 and Th2 cells in cytokine level can improve the understanding of the effect of co-infected HCV on HIV infection. In this study, we measured the baseline Th1/Th2 cytokine concentration in sera by using flow cytometry in HIV/HCV co-infection, HIV mono-infection, HCV mono-infection, and healthy control group, as well as the dynamic changes of these cytokine levels after receiving highly active antiretroviral therapy (HAART). The ratio of Th1 and Th2 cytokine concentration in HIV/HCV co-infection was higher than HCV mono-infection and healthy control group, while lower than HIV mono-infection group. After HAART was initiated, the Th1/Th2 ratio of HIV/HCV co-infection group decreased to the same level of healthy control, while HIV mono-infection group was still higher than the control group. There was no significant evidence showing co-infected with HCV had negative effect on HIV related diseases. However, co-infected with HCV can decrease Th1/Th2 ratio by affecting Th1 cytokine level, especially the secretion of IFN-γ. With the initiation of HAART, Th1 and Th2 cytokine levels were progressively reduced. HIV was the main stimulating factor of T cells in HIV/HCV co-infection group.
    BMC Infectious Diseases 04/2012; 12(1):102. DOI:10.1186/1471-2334-12-102 · 2.61 Impact Factor
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    ABSTRACT: HCV-infected "speedball" users (n = 30) were selected from an original cohort of 400 intravenous drug users for cytokine analysis. Cytokine concentrations (TNF-alpha, IL-1beta, IL-6, IFN-gamma, IL-2, IL-4, IL-10 and IL-12) were determined in plasma and peripheral blood mononuclear cells (PBMC) cultures derived ex vivo from these patients. In addition, lymphocyte proliferation was measured in 49 HCV-positive "speedball" users. TNF-alpha, IL-6, IFN-gamma, IL-2, IL-4, IL-10, IL-12 cytokines and not IL-1beta were significantly increased in plasma from HCV-positive "speedball" users compared with healthy controls. Except for IL-10, all other cytokines measured were augmented in phytohemagglutinin-stimulated PBMC cultures from HCV-positive "speedball" users. Likewise, overproduction of cytokines TNF-alpha, IL-1beta, IL-6 and IFN-gamma, was consistently detected when PBMC cultures from HCV-positive "speedball" users were stimulated with a biological response modifier. However, HCV-infected "speedball" users showed significant reduction in lymphoproliferative activity. Compared with healthy subjects, there was a consistent overproduction of both TH1 and TH2 type cytokines in the plasma and PBMC's of HCV-infected "speedball" users. Furthermore, there was a persistent reduction of lymphoproliferative activity in this group. These immunologic abnormalities, coupled with the range of response between the two TH-types in HCV-infected "speedball" users, suggest impairment in the regulatory mechanism of the TH1-TH2 system.
    Drug and Alcohol Dependence 01/2007; 85(3):236-43. DOI:10.1016/j.drugalcdep.2006.05.013 · 3.42 Impact Factor
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    ABSTRACT: Many human immunodeficiency virus (HIV) infected persons are coinfected with hepatitis C virus (HCV) and with the use of highly active antiretroviral therapy, liver disease from HCV has become an important cause of morbidity and mortality. The current guidelines recommend that human immunodeficiency virus and HCV coinfected patients be evaluated and treated for HCV if there are no major contraindications to treatment. Coinfected patients treated with pegylated interferon-a and ribavirin have sustained virologic responses (SVRs) of 27% to 40% which for a variety of reasons are lower than those reported in HCV mono-infected patients. Understanding that most patients will not achieve SVRs, strategies to evaluate for the role of maintenance interferon in delaying complications of liver disease are being evaluated. In patients who have failed prior treatment, cannot tolerate treatment, or who have contraindications to HCV treatment, the use of highly active antiretroviral therapy with careful monitoring for hepatotoxicity and aggressive counseling on alcohol and substance abuse may slow down fibrosis progression. As the data on liver transplantation in coinfected patients accumulate, patients with end stage liver disease should be referred early for evaluation in a transplant center. As new drugs for HCV are being developed, it will be of utmost importance to include coinfected patients earlier in the process on new drug trials and therapeutic strategies.
    Journal of Clinical Gastroenterology 02/2007; 41(1):75-87. DOI:10.1097/01.mcg.0000225592.16448.f3 · 3.50 Impact Factor
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