This preprint analyzed 230 people with HIV and found that clonal hematopoiesis of indeterminate potential (CHIP) mutations, present in 14% of participants, were associated with increased lymph node metabolic activity rather than direct arterial inflammation or atherosclerosis. The most common mutations occurred in DNMT3A and TET2 genes, with a median variant allele fraction of 2.8%. Surprisingly, CHIP showed no correlation with carotid intima-media thickness or aortic inflammation measured by PET imaging. This challenges the expected direct pathway between CHIP and cardiovascular disease in HIV patients. The lymph node connection suggests CHIP may contribute to HIV-associated atherosclerosis through immune system dysfunction rather than direct vascular inflammation. This finding could reshape understanding of cardiovascular risk mechanisms in HIV, potentially pointing toward immune-targeted interventions rather than traditional anti-inflammatory approaches. However, the study's cross-sectional design limits causal interpretation, and the relatively small CHIP-positive subgroup (32 participants) reduces statistical power. As an unreviewed preprint, these results require peer review confirmation before clinical application, but they offer an intriguing new perspective on the intersection of clonal hematopoiesis, immune function, and cardiovascular disease in HIV.