Association of HIV infection and HIV/HCV coinfection with C-reactive protein levels: The fat redistribution and metabolic change in HIV infection (FRAM) study

University of California, San Francisco, San Francisco, CA, USA.
JAIDS Journal of Acquired Immune Deficiency Syndromes (Impact Factor: 4.56). 07/2008; 48(2):142-8. DOI: 10.1097/QAI.0b013e3181685727
Source: PubMed


Inflammation is a potential mechanism to explain the accelerated atherosclerosis observed in HIV- and hepatitis C virus (HCV)-infected persons. We evaluated C-reactive protein (CRP) in HIV-infected and HIV/HCV-coinfected individuals in the era of effective antiretroviral (ARV) therapy.
Cross-sectional study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM) cohort and controls from the Coronary Artery Risk Development in Young Adults (CARDIA) study.
CRP levels were measured in 1135 HIV-infected participants from the FRAM cohort and 281 controls from the CARDIA study. The associations of HIV and HIV/HCV infection with CRP levels were estimated by multivariable linear regression.
Compared with controls, HIV monoinfection was associated with an 88% higher CRP level in men (P < 0.0001) but with no difference in women (5%; P = 0.80) in multivariate analysis. CRP levels were not associated with ARV therapy, HIV RNA level, or CD4 cell count. Compared with controls, HIV/HCV coinfection was associated with a 41% lower CRP level in women (P = 0.012) but with no difference in men (+4%; P = 0.90). Among HIV-infected participants, HCV coinfection was associated with 50% lower CRP levels after multivariable analysis (P < 0.0001) in men and women. Greater visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were strongly associated with CRP levels. Among HIV-infected participants, CRP levels were 17% (P < 0.001) and 21% (P = 0.002) higher per doubling of VAT and SAT; among controls, CRP levels were 34% (P < 0.001) and 61% (P = 0.009) higher, respectively.
In the absence of HCV coinfection, HIV infection is associated with higher CRP levels in men. HCV coinfection is associated with lower CRP levels in men and women.

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Available from: Steven B Heymsfield, Dec 15, 2014
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    • "Findings from our study are consistent with those from prior studies investigating the association between HIV/HCV status and TNF-α [27-30], CRP [31,32], IL-10 [30,33], IFN-γ [30,34,36], IL-6 [28] and cystatin C [35]. However, some differences between our work and these prior studies may reflect different biomarker outcome categorization (quartiles versus detection, secretion, or means), HIV/HCV categorization (viremia versus antibody detection, in vitro stimulation with viral proteins) sources of biomarkers (serum versus intrahepatic), referent groups (participants with undetectable HIV and HCV viremia versus HIV or HCV mono-infected participants) and adjustment covariates. "
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    ABSTRACT: Assessing whether hepatitis C (HCV) co-infection with human immunodeficiency virus (HIV) is associated with increased inflammation is complex. The liver, integral to inflammatory biomarker synthesis, is compromised by HCV and alcohol abuse. Using single liver-synthesized biomarkers (e.g. C-reactive protein) to represent inflammation may not be appropriate in HIV/HCV co-infection. We hypothesized that 1) detectable HIV/HCV RNA was independently associated with increased inflammation; 2) a composite inflammation measure describes inflammation differently from single inflammatory biomarkers. We compared inflammation by HIV/HCV group in a cohort of 361 HIV infected participants from the HIV-Longitudinal Interrelationships of Viruses and Ethanol study. Inflammatory biomarkers >75th percentile were considered elevated. Associations between HIV/HCV group and elevated biomarkers were analyzed as a composite measure (inflammatory burden) or individually. We defined inflammatory burden as number of concurrently elevated biomarkers. Biomarkers included interleukin-6 (IL-6), C-reactive protein (CRP), cystatin C, serum amyloid-A (SAA), tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10). Covariates: alcohol, liver fibrosis, comorbidities, CD4 count, antiretroviral therapy, substance use. Detectable HIV and HCV RNA (OR = 2.49; 95%CI = 1.05--5.89) and detectable HCV RNA alone (2.95; 1.08--8.01) were independently associated with increased odds of having a greater inflammatory burden compared to undetectable viremia. Elevated IL-10 (7.79; 1.90--31.97) and TNF-alpha (7.70; 1.42--41.83) were independently associated with detectable HIV and HCV RNA. Elevated IL-10 was also associated with detectable HCV RNA alone (5.51; 1.17, 25.84). Detectable HIV and HCV replication versus undetectable replication was associated with inflammatory burden and certain inflammatory biomarkers independently of alcohol consumption, liver fibrosis and other comorbidities.
    BMC Infectious Diseases 08/2013; 13(1):399. DOI:10.1186/1471-2334-13-399 · 2.61 Impact Factor
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    • "The treatment failure might be affected by the high proportion of IDU and, consequently, the high proportion of HIV/HCV coinfection, which strongly affects patient adherence to HAART treatment. In spite of the fact that the mechanisms through which HCV infection worsens the condition of HIV patients and increases its complications and AIDS-related deaths are not clear, it likely activates immune cells with the CD4 apoptosis marker and causes a severe defect in the immune system [42], decreasing the power of recovery in CD4 T cells after HAART treatment [43]; increasing the production of cryoglobulin by activation of B cells [44], decreasing the production of CRP [45]; and activating the replication of HCV in lymphoid [46] and lymphoblastic [47] tissues as well as in environmental CD4 T cells in HIV patients [48]. The present study revealed that HAART treatment is highly effective in HIV patients in Iran. "
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    ABSTRACT: HIV and HCV infections are basic issues of many health systems. Since HIV and HCV are transmitted similarly, it is common to become infected by them simultaneously. No consensus exists on the effect of HCV infection on the survival of HIV-infected patients. This study aimed to investigate the issue in a relatively large cohort of patients who had a high prevalence of this coinfection in Shiraz (South of Iran). In this historical cohort study, we evaluated the survival time of 1338 HIV-infected individuals who had been referred to a behavioral consultation center in Shiraz over 10 years (from April 2001 to July 2011). Kaplan-Meier method and log-rank test were used to investigate patient survival and compare their survival curves, respectively. Moreover, Cox proportional hazards model was used to examine the effect of HCV infection on patient survival after control for age, sex, having the injection drug use (IDU) risk factor, CD4 count at baseline, more than a 30% decline in CD4 cell count, and highly active antiretroviral therapy (HAART). In our cohort, 1044 patients (78.03%) were infected by HCV. The median follow-up was 43.48 months (95% CI = 61.18-26.63). The median survival time in HCV-infected and uninfected patients was 163.8 and 194.8 months, respectively (P = 0.039). After controlling for other covariates, HCV infection increased the mortality rate 2.13 times more in HCV-infected patients than HCV -uninfected patients (CI: 95%; 1.1-4.52). HCV infection increases AIDS-related deaths. To control HCV infection and transmission and eliminate HCV, timely diagnosis and treatment and serious harm reduction programs must be implemented.
    Hepatitis Monthly 02/2012; 12(2):106-11. DOI:10.5812/hepatmon.839 · 1.93 Impact Factor
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    • "Also, the presence of HIV has a negative impact on the natural history of HCV since the progression to cirrhosis is higher in coinfected [54, 55]. HCV/HIV coinfection is associated to develop other complications, such as hematologic disorders [56, 57], kidney disease [58, 59], cardiovascular disease [60, 61], and neurologic status [62–65]. "
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    ABSTRACT: NATURAL HISTORY OF HCV RELATED CHRONIC HEPATITIS IS INFLUENCED AND MODIFIED BY MANY FACTORS: virus features, coinfections and host characteristics. In particular, a peculiar genetic background of the host by conditioning the occurrence of intracellular metabolic derangements (i.e., insulin resistance) might contribute to accelerate the rate of progression to cirrhosis and eventually the occurrence of hepatocellular carcinoma (HCC) and death. Likely, direct interplays between virus genotype and host genetic background might be hypothesized at this level. Morbidity and mortality in cirrhosis is primarily associated with complications of liver cirrhosis (ascites, hepatic encephalopathy, jaundice, and gastroesophageal bleeding) and HCC occurrence. Therefore the main goal of therapy is to clear viral infection and decrease liver necro-inflammation that directly relates to development of cirrhosis and HCC. Among patients treated with Interferon-based therapy, those with sustained viral response showed a significant reduction of progression to cirrhosis and development of HCC. However, a residual risk of hepatocellular carcinoma still remains indicating the need for careful follow-up using ultrasonography every six months in cirrhotic patients, even in those showing persistently normal ALT and undetectable HCV RNA levels after antiviral therapy.
    11/2011; 2011:314301. DOI:10.4061/2011/314301
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