2026/06/01 by Daniel Petkov, Summer Siddiqui, David X Liu +5 · 1 voice
Medicine · Immunology and Microbiology · #HIV-related health complications and treatments #HIV Research and Treatment #Immune cells in cancer
paper · doi:10.1093/jleuko/qiag069
openalex publication_date 2026/06/01 · openalex created_date 2026/06/06 · openalex updated_date 2026/07/27
People living with HIV experience an earlier risk for onset of aging-related chronic inflammatory comorbidities, including cardiovascular disease. We previously showed that the proportion of macrophages was higher in the heart of older rhesus macaques (Macaca mulatta) with normal histopathology as well as in all age groups of macaques with cardiac pathology. In the present study, we investigated the effects of simian immunodeficiency virus (SIV) infection on cell density and macrophages in heart tissues of adult rhesus macaques. Heart tissues were evaluated by hematoxylin and eosin staining and immunofluorescence staining to assess the number and phenotype of heart macrophages that could change with SIV infection. Cardiac cellularity was lower in hearts of SIV-infected young and adult macaques, as well as in uninfected aged macaques, compared with uninfected adult rhesus macaques. This lower cellularity was associated with higher percentages of CD163+ macrophages in hearts of SIV-infected young adult macaques, similar to that of uninfected aged macaques. Higher percentages of CD163+ macrophages were also observed in diseased hearts of both SIV-infected and uninfected adult animals that appeared to be short-lived macrophages, based on 5-bromo-2'-deoxyuridine labeling. In contrast, macrophages retaining in vivo-administered dextran, indicative of long-lived macrophages, predominated among cardiac macrophages in both SIV-infected and uninfected animals of all ages. Together, these results suggest SIV infection induces changes in cardiac cellularity and macrophage composition that resemble those observed during aging. This rhesus macaque model supports continued studies to further dissect the shifting dynamics of macrophage subsets and their role in heart adaptations in response to HIV infection and aging.