HIV/HCV Coinfection and the Risk of Cardiovascular Disease

A Meta-analysis

O. Osibogun; O. Ogunmoroti; E. D. Michos; E. S. Spatz; B. Olubajo; K. Nasir; P. Madhivanan; W. Maziak


J Viral Hepat. 2017;24(11):998-1004. 

In This Article

Abstract and Introduction


The emergence of improved antiretroviral therapy has increased the life expectancy of human immunodeficiency virus (HIV)-infected individuals, although there is an increased susceptibility to developing cardiovascular diseases (CVD). The risk for CVD is purported to be even higher among people with HIV and hepatitis C virus (HCV) coinfection because of the increased inflammatory response, which may synergistically impact CVD risk. However, studies comparing CVD outcomes between HIV alone and HIV/HCV individuals have been discordant. Accordingly, we conducted a meta-analysis to clarify and quantify the association between HIV/HCV coinfection and the risk for CVD. We searched EMBASE, CINAHL, Google Scholar, PubMed, and Web of Science from inception to December 2016 to identify studies that provided information on HIV/HCV coinfection and CVD, defined as coronary artery disease, congestive heart failure and stroke. We used a random-effects model to abstract and pool data on the hazard ratios (HRs) for CVD. HRs were adjusted for traditional CVD risk factors including age, sex, smoking, hypertension, diabetes and LDL cholesterol. Among the 283 articles reviewed, four cohort studies met inclusion criteria with a total of 33 723 participants. The pooled adjusted HRs for the association between HIV/HCV coinfection and CVD were 1.24 (95% CI: 1.07–1.40) compared to HIV monoinfection. The test for heterogeneity was not statistically significant (I 2=0.0%, P=.397). In conclusion, individuals with HIV/HCV coinfection had an increased CVD risk compared to those with HIV monoinfection. More research is needed to further examine the nature of this association, and response to traditional risk-reduction therapies.


According to the World Health Organization, human immunodeficiency virus (HIV) and hepatitis C virus (HCV) infections are major public health issues.[1,2] Worldwide, approximately 36.7 million and 184 million people are living with HIV and HCV, respectively.[3,4] The shared transmission routes of both viruses make coinfection common.[5,6] It is estimated that 15%-30% of HIV-infected individuals are also infected with HCV.[6]

Since the availability of improved antiretroviral therapy (ART), people with HIV are living longer[7] though with an increased risk of chronic diseases such as cardiovascular disease (CVD).[8] The risk of CVD in HIV-infected individuals has been reported to be 61% higher compared to HIV-uninfected individuals.[9] In HCV-infected individuals, the risk of coronary artery disease and stroke has been estimated to be 25% and 27% higher, respectively, compared to HCV-uninfected individuals.[10,11] Moreover, it has been postulated that HIV and HCV have the potential to synergistically increase the risk of CVD in coinfected individuals due to the persistent inflammatory responses of both viruses.[8]

Nevertheless, studies vary in their conclusions about the risk of CVD in HIV/HCV coinfection. Some studies report an increased risk of developing CVD in comparison with individuals with HIV monoinfection because HCV infection is associated with a greater prevalence of some traditional risk factors and biomarkers that cause early atherosclerosis for example type 2 diabetes and endothelial dysfunction,[12,13] while other studies suggest that HCV infection may confer a protective effect on HIV monoinfection because it is associated with lower levels of other CVD risk markers such as total and low-density lipoprotein cholesterol and C-reactive protein.[14–16]

The aim of this meta-analysis is to examine and quantify the risk of developing CVD among individuals with HIV/HCV coinfection in comparison with individuals with HIV monoinfection. We hypothesized that the risk of developing CVD will be higher in those with HIV/HCV coinfection based on the hypothesis that the risk of CVD is synergistically increased by the persistent inflammatory responses of both viruses.