This low use of lipid-lowering medication is in agreement with th

This low use of lipid-lowering medication is in agreement with the findings of a cross-sectional study of 881 patients, of whom over 80% were on ART [7], and our own previous work evaluating a single site [8]. Although the role of

HAART-related hyperlipidaemia in HIV infection remains to be fully elucidated, the risk of cardiovascular disease is increased in those living with HIV and cholesterol abnormalities are a well-established risk factor [18,19]. Based on our results and other evidence, we VX-770 mouse believe that viral hepatitis status should be included as a variable in studies evaluating cardiovascular disease in HIV infection. Several lines of evidence support the biological plausibility of our observations related to HCV. Hepatitis C virions associate with LDL, very low-density lipoprotein (VLDL) and HDL cholesterol in plasma [18–21]. Specifically, HCV envelope glycoprotein (E2) and HCV core protein interact with VLDL and LDL particles [22–25] and HCV core protein has been identified within cellular lipid storage droplets [26]. It is noteworthy that HCV viral load is diminished in HCV-infected patients following LDL plasmapheresis

[2]. HCV cell binding and entry is mediated, in part, by an LDL receptor-mediated process [26–29] and HDL may facilitate selleck compound HCV entry through the class B type 1 scavenger receptor [28]. Recruitment of apolipoprotein E by nonstructural protein 5A (NS5A) is important for viral assembly and release of old infectious HCV particles

[30,31]. The use of these receptors may not only explain how HCV gains intracellular entry and release but may also provide a mechanism by which HCV perturbs the lipid profile (i.e. by enhanced cellular lipid uptake). HCV proteins may also induce de novo triglyceride synthesis via activation of sterol regulatory element-binding protein 1c (SREBP1c) with concurrent diminished triglyceride secretion, leading to lower serum triglyceride levels and the well-recognized phenomenon of HCV-associated hepatic steatosis [32]. We have described an increase in lipid levels following clearance of chronic HCV infection with antiviral therapy in HIV/HCV coinfection that has been confirmed by others [8,15]. This further supports the validity of the results of the present study. There is little literature describing the influence of HBV on lipid levels. However, at least one group reported lower levels of triglycerides and HDL cholesterol in those chronically infected with HBV without HIV coinfection [33]. It is unclear if and how this observation is related to the observation that the HBV X protein induces lipid accumulation within hepatic cells [34]. Our analysis provides interesting preliminary information on the potential influence of HBV on lipid levels in HIV-infected patients on HAART. However, we acknowledge the limitations of this cohort analysis and the potential influence of confounders.

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