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Clonal hematopoiesis of indeterminate potential in persons with HIV
Andreas D Knudsen1,2, Christian Winther Eskelund3, Thomas Benfield4
1Department of Infectious Diseases 8632.
Insights
In older individuals with HIV, over a quarter had clonal hematopoiesis (CHIP). CHIP was not linked to inflammation or coronary artery disease (CAD) in this population.
Area of Science:
- Hematology
- Immunology
- Cardiology
Background:
- Clonal hematopoiesis of indeterminate potential (CHIP) is linked to aging, inflammation, and coronary artery disease (CAD) risk.
- Older persons with HIV (PWH) often have increased inflammation and CAD risk.
- The relationship between CHIP, inflammation, and CAD in PWH remains unclear.
Purpose of the Study:
- To determine the prevalence of CHIP in older PWH.
- To investigate the association between CHIP and inflammatory markers.
- To explore the association between CHIP and CAD in older PWH.
Main Methods:
- Analysis of data from the Copenhagen Comorbidity in HIV Infection (COCOMO) study, including 190 PWH aged over 55.
- CHIP defined as variant allele fraction ≥2%.
- CAD assessed via CT angiography, categorizing severity from no atherosclerosis to obstructive CAD (≥50% stenosis).
Main Results:
- CHIP mutations were found in 26% of participants, with DNMT3A, TET2, and ASXL1 being the most common.
- CHIP prevalence was associated with age and sex, but not with inflammatory markers (IL-1β, IL-6, TNF-α, etc.).
- No significant association was found between CHIP and any atherosclerosis or obstructive CAD after adjustments.
Conclusions:
- Over one in four older, well-treated PWH in Scandinavia exhibit CHIP.
- This study found no evidence linking CHIP to inflammatory markers or CAD in this cohort.
- CHIP is unlikely to be the mechanism explaining the inflammation-CAD association in treated HIV infection.
Background:
Clonal hematopoiesis of indeterminate potential (CHIP) has been associated with older age, inflammation and with risk of coronary artery disease (CAD). We aimed to characterize the burden of CHIP, and to explore the association between CHIP, inflammatory markers, and CAD in older persons with HIV (PWH).
Methods:
From the Copenhagen Comorbidity in HIV Infection (COCOMO) study, we included 190 individuals older than 55 years of age. We defined CHIP as variant allele fraction at least 2%. CAD was categorized according to the most severe coronary artery lesion on coronary computed tomography (CT) angiography as no coronary atherosclerosis; any atherosclerosis defined as at least 1% stenosis and obstructive CAD defined as at least 50% stenosis.
Results:
In the entire population (median age 66 years, 87% men), we identified a total of 62 mutations distributed among 49 (26%) participants. The three most mutated genes were DNMT3A , TET2 , and ASXL1 , accounting for 49, 25, and 16% of mutations, respectively. Age and sex were the only variables associated with CHIP. IL-1β, IL-1Ra, IL-2, IL-6, IL-10, soluble CD14, soluble CD163 and TNF-α were not associated with CHIP, and CHIP was not associated with any atherosclerosis or with obstructive CAD in adjusted analyses.
Conclusion:
In older, well treated, Scandinavian PWH, more than one in four had at least one CHIP mutation. We did not find evidence of an association between CHIP and inflammatory markers or between CHIP and CAD. CHIP is an unlikely underlying mechanism to explain the association between inflammation and CAD in treated HIV disease.
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