Abstract
The burden of tuberculosis and cardiovascular disease (CVD) is enormous worldwide. CVD rates are rapidly increasing in low- and middle-income countries. Public health programs have been challenged with the overlapping tuberculosis and CVD epidemics. Monocyte/macrophages, lymphocytes and cytokines involved in cellular mediated immune responses against Mycobacterium tuberculosis are also main drivers of atherogenesis, suggesting a potential pathogenic role of tuberculosis in CVD via mechanisms that have been described for other pathogens that establish chronic infection and latency. Studies have shown a pro-atherogenic effect of antibody-mediated responses against mycobacterial heat shock protein-65 through cross reaction with self-antigens in human vessels. Furthermore, subsets of mycobacteria actively replicate during latent tuberculosis infection (LTBI), and recent studies suggest that LTBI is associated with persistent chronic inflammation that may lead to CVD. Recent epidemiologic work has shown that the risk of CVD in persons who develop tuberculosis is higher than in persons without a history of tuberculosis, even several years after recovery from tuberculosis. Together, these data suggest that tuberculosis may play a role in the pathogenesis of CVD. Further research to investigate a potential link between tuberculosis and CVD is warranted.
Highlights
Non-communicable diseases caused 38 of the 56 million deaths reported globally in 2012
A study of the mechanism of Epstein Barr virus (EBV) in cardiovascular disease (CVD) showed that the presence of neutralizing antibodies to an early EBV protein was associated with higher levels of IL-6 and Intracellular adhesion molecule-1 (ICAM-1) in patients with acute myocardial infarction (AMI) compared to patients with stable angina [25]
A significant correlation between anti-HSP65 antibodies and carotid atherosclerosis has been reported [48, 49]. These data suggest that tuberculosis could have a pathogenic role in CVD through molecular mimicry and auto-immunity mediated by anti-HSP65 antibodies
Summary
Non-communicable diseases caused 38 of the 56 million deaths reported globally in 2012. Recent studies suggest that latent tuberculosis infection (LTBI) is associated with chronic inflammation a connection between LTBI and CVD seems plausible [30, 31]. For an infectious disease to cause CVD via an increase in inflammation it stands to reason that the infection must trigger host immunologic responses similar to those implicated in atherogenesis.
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