Abstract
ObjectivesInfection with co-pathogens is one of the postulated factors contributing to persistent inflammation and non-AIDS events in virologically-suppressed HIV-infected patients. We aimed to investigate the relationship of human herpesvirus-8 (HHV-8), a vasculotropic virus implicated in the pathogenesis of Kaposi's sarcoma, with inflammation and subclinical atherosclerosis in HIV-infected patients.MethodsProspective study including virologically suppressed HIV-infected patients. Several blood biomarkers (highly-sensitive C-reactive protein [hsCRP], tumour necrosis factor-α, interleukin-6, monocyte chemoattractant protein-1, vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, malondialdehyde, plasminogen activator inhibitor [PAI-1], D-dimer, sCD14, sCD163, CD4/CD38/HLA-DR, and CD8/CD38/HLA-DR), serological tests for HHV-8 and the majority of herpesviruses, carotid intima-media thickness, and endothelial function through flow-mediated dilatation of the brachial artery were measured.ResultsA total of 136 patients were included, 34.6% of them infected with HHV-8. HHV-8-infected patients were more frequently co-infected with herpes simplex virus type 2 (HSV-2) (P<0.001), and less frequently with hepatitis C virus (HCV) (P = 0.045), and tended to be older (P = 0.086). HHV-8-infected patients had higher levels of hsCRP (median [interquartile range], 3.63 [1.32–7.54] vs 2.08 [0.89–4.11] mg/L, P = 0.009), CD4/CD38/HLA-DR (7.67% [4.10–11.86]% vs 3.86% [2.51–7.42]%, P = 0.035) and CD8/CD38/HLA-DR (8.02% [4.98–14.09]% vs 5.02% [3.66–6.96]%, P = 0.018). After adjustment for the traditional cardiovascular risk factors, HCV and HSV-2 infection, the associations remained significant: adjusted difference between HHV-8 positive and negative patients (95% confidence interval) for hsCRP, 74.19% (16.65–160.13)%; for CD4/CD38/HLA-DR, 89.65% (14.34–214.87)%; and for CD8/CD38/HLA-DR, 58.41% (12.30–123.22)%. Flow-mediated dilatation and total carotid intima-media thickness were not different according to HHV-8 serostatus.ConclusionIn virologically suppressed HIV-infected patients, coinfection with HHV-8 is associated with increased inflammation and immune activation. This might contribute to increase the risk of non-AIDS events, including accelerated atherosclerotic disease.
Highlights
The spectrum of diseases causing morbidity and mortality in HIV-infected persons has shifted from AIDS-defining to nonAIDS related events, similar to those occurring in the general population [1,2,3]
Excess morbidity and mortality do occur in HIV-infected compared to uninfected persons, and deaths from cardiovascular and liver diseases, non-AIDS defining cancer and suicide have been reported to be more frequent among patients with highly access to antiretroviral therapy (ART) [4]
We evaluated the relationship of human herpesvirus-8 (HHV-8) with carotid intima-media thickness (c-IMT), and endothelial function through flow-mediated dilatation measurement
Summary
The spectrum of diseases causing morbidity and mortality in HIV-infected persons has shifted from AIDS-defining to nonAIDS related events, similar to those occurring in the general population [1,2,3]. This was related to the advent of combination antiretroviral therapy (ART), and its effects on immune dysfunction, lymphocyte activation and inflammation. Several studies support increased immune activation and inflammation among virologically-suppressed HIV patients, and even in elite controllers, compared to the general population [7,8,9,10].
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