African Americans (AAs) are disproportionately affected by COVID‐19, likely due to interacting biological, environmental, and social factors.[ 41 ] Immunogenetic differences also exist among populations, affecting the immune cell repertoire and resulting in racial differences in immune profiles. For instance, variations in serum cytokine levels between AAs and European Americans (EAs) have been observed. AAs are significantly more likely to carry genetic variants of proinflammatory cytokines.[ 42 43 ] Furthermore, aggravatingly, they often bear genotypes (including variants of IL‐1, IL‐6, IL‐10, and TNF‐α) known to tamp down the anti‐inflammatory responses.[ 42 ] Consistently, various inflammatory diseases are more common among AAs.[ 44 ] These immunogenetic differences may also explain why AAs have a higher risk of developing lung cancer than EAs.[ 45 ]

AAs have been subject to marginalization and discrimination, resulting in socio‐economic and health disparities. The engendered stress causes the release of inflammatory mediators (e.g., CRP, IL‐6, NF‐κB, TNF‐α) via the activation of the sympathetic nervous system and the hypothalamic‐pituitary‐adrenal axis.[ 46 ] Continuous social and environmental stresses induce chronic inflammation that is at the root of most disease etiologies. Importantly, a higher prevalence of low‐grade inflammation has been shown in young AAs subjected to racial discrimination compared to those who identified positively with their racial identities.[ 47 ] Environmental and social factors may also modulate epigenetic modifications (DNA methylation, histone modifications, and alterations in the expression of non‐coding RNAs), thereby affecting disease susceptibility.[ 46 ] Considering the higher levels of proinflammatory cytokines in AAs, a pronounced impact of COVID‐19 is comprehensible. It remains unclear, however, whether AAs are more susceptible to COVID‐19 sequelae, including cancer.

Cancer as a prospective sequela of long COVID‐19 – PMC (