Even when HIV is effectively suppressed with treatment, small amounts of virus in the blood may more than double the risk of cardiovascular disease. That is the main finding of a new prospective study published in Journal of Infection by researchers from the Netherlands and Belgium, as part of the 2000HIV project.
Thanks to antiretroviral therapy, people living with HIV today can have a nearly normal life expectancy. The treatment prevents the virus from replicating and from being transmitted. However, HIV does not completely disappear from the body. Small amounts of viral material may still be present and could have biological effects.
HIV never fully disappears from the body
Nearly 40 million people worldwide live with HIV, most of whom receive long-term treatment. In Western countries, cardiovascular disease has become one of the leading causes of illness among people with HIV with access to care.
Although standard tests often show no detectable virus, highly sensitive PCR tests can still detect traces of viral RNA. These levels are extremely low and cannot be transmitted to others. This phenomenon is known as residual viremia. Until recently, it was unclear whether these minimal levels had clinical consequences.
In this study, researchers followed 1,895 people with HIV whose virus was considered suppressed. About one-third had residual viremia. After two years, clear differences emerged.
Patients with residual viremia had more than twice the risk of cardiovascular events, including heart attacks, stroke, and peripheral vascular disease. This increased risk remained even after accounting for known risk factors.
Existing cardiovascular risk models also underestimated the number of events in this group by roughly a factor of two. These findings suggest that even very small amounts of virus may contribute directly to cardiovascular risk.
Not explained by inflammation or metabolism
The increased risk of cardiovascular disease in people with HIV has often been linked to chronic inflammation or immune activation. However, this study found no evidence that these factors explain the increased risk in patients with residual viremia.
Researchers performed extensive biological analyses to compare patients with and without residual virus. They found no clear differences in inflammation, lipid metabolism, gut barrier function, or immune activation.
Instead, the results point to a possible direct mechanism. Viral particles or proteins may interact with atherosclerotic plaques, potentially destabilizing them and triggering cardiovascular events. Previous studies have already shown that HIV-related material can be present in vascular plaques, supporting this idea.
A broader link between infections and heart disease
The findings also raise a broader question: can chronic viral infections directly contribute to cardiovascular disease?
Several infections have previously been linked to atherosclerosis, including cytomegalovirus, Chlamydia pneumoniae, herpesviruses, and SARS-CoV-2. However, evidence has often been inconsistent, and the underlying mechanisms remain unclear. HIV may now provide one of the clearest examples of how persistent viral presence can affect cardiovascular health.
The implications of this study go beyond HIV. Infectious diseases and chronic diseases have long been viewed as separate domains. This distinction is now becoming less clear.
Persistent viral presence, even at very low levels, may have long-term effects on the body. This study suggests that a virus that appears clinically controlled can still influence processes such as aging and cardiovascular disease.
These findings highlight the need to better understand how chronic infections contribute to long-term health risks, and how these effects might be prevented in the future.
About the publication
Otten T, Ruijten S, Blaauw M ... Residual HIV viremia strongly increases cardiovascular disease incidence independent of classical risk factors. Journal of Infection, 2026; 92. DOI: 10.1016/j.jinf.2026.106737
