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Immune activation and cardiovascular disease in chronic HIV infection

Chris T Longenecker¹, Claire Sullivan, Jason V Baker

¹aUniversity Hospitals Harrington Heart and Vascular Institute bCase Western Reserve University School of Medicine, Cleveland, Ohio cHennepin County Medical Center dUniversity of Minnesota; Minneapolis, Minnesota, USA.

Current Opinion in HIV and AIDS

|November 25, 2015

Insights

Immune activation contributes to cardiovascular disease (CVD) in people with HIV, even with treatment. Targeting inflammation is crucial for preventing premature CVD in this population.

Area of Science:

Immunology
Cardiovascular Medicine
Infectious Diseases

Background:

Cardiovascular disease (CVD) is a major health concern for individuals with HIV.
Antiretroviral therapy (ART) has improved outcomes, but CVD remains a leading cause of mortality.
Understanding the role of immune activation in HIV-associated CVD is critical.

Purpose of the Study:

To review the contribution of immune activation to the pathogenesis of HIV-associated CVD.
To explore how both adaptive and innate immunity influence CVD risk in people with HIV.
To identify potential targets for CVD prevention strategies in this population.

Main Methods:

Literature review of recent studies on HIV, immune activation, and CVD.
Analysis of T-cell and monocyte/macrophage mechanisms in atherogenesis.
Evaluation of the impact of ART on immune-mediated CVD risk factors.

Main Results:

Persistent T-cell activation and proinflammatory responses contribute to CVD risk.
Copathogens like cytomegalovirus can drive cytotoxic T-cell responses, exacerbating CVD.
Monocyte/macrophage-driven inflammation in atherosclerotic lesions is a key factor.
Innate immune abnormalities may persist despite viral suppression with ART.

Conclusions:

Premature CVD in HIV is partly due to persistent immune activation and inflammation, even with suppressed viral load.
Prevention requires addressing traditional CVD risk factors and exploring immunomodulatory therapies.
Targeting inflammation is essential for comprehensive CVD prevention in people with HIV.

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Abstract

Purpose Of Review:

This article describes the potential contribution of immune activation in the pathogenesis of HIV-associated cardiovascular disease (CVD) - a leading cause of morbidity and mortality among HIV-positive persons with access to antiretroviral therapy (ART).

Recent Findings:

We review recent literature that suggests abnormalities in both adaptive and innate immunity contributes to CVD risk among persons with HIV infection. In particular, potentially atherogenic T-cell mechanisms include persistent high-level T-cell activation (and associated proinflammatory mechanisms), as well as the presence of copathogens (e.g., cytomegalovirus) providing an ongoing stimulus for cytotoxic T-cell responses. More recent data have then emphasized the potential impact of monocyte-/macrophage-mediated inflammation and injury within atherosclerotic lesions. The abnormality driving innate immune activation many not fully reverse with antiretroviral therapy, highlighting the need for interventions that target inflammation as a CVD prevention strategy.

Summary:

Premature CVD among persons with HIV infection is due, in part, to persistent abnormalities in immune activation and systemic inflammation despite viral suppression. Prevention strategies for persons with HIV infection include those that target traditional CVD risk factors, as well as newer candidate treatments with potential immunomodulatory benefits.

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