Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX, 76107, USA.
Texas Center for Health Disparities, University of North Texas Health Science Center, Fort Worth, TX, 76107, USA.
J Racial Ethn Health Disparities. 2021 Oct;8(5):1153-1160. doi: 10.1007/s40615-020-00871-y. Epub 2020 Sep 23.
Coronavirus disease 2019 (COVID-19) accounts for over 180,000 deaths in the USA. Although COVID-19 affects all racial ethnicities, non-Hispanic Blacks have the highest mortality rates. Evidence continues to emerge, linking the disproportion of contagion and mortality from severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a result of adverse social determinants of health. Yet, genetic predisposition may also play a credible role in disease transmission. SARS-CoV-2 enters cells by interaction between SARS-CoV-2 spike protein and the receptor molecule angiotensin converting enzyme 2 (ACE2) expressed on the surface of the target cells, such that polymorphisms and the expression level of ACE2 influence infectivity and consequent pathogenesis of SARS-CoV-2. Genetic polymorphisms in other multiple genes, such as acetylcholinesterase (AChE) and interleukin-6, are also closely associated with underlying diseases, such as hypertension and type 2 diabetes mellitus, which substantially raise SARS-CoV-2 mortality. However, it is unknown how these genetic polymorphisms contribute to the disparate mortality rates, with or without underlying diseases. Of particular interest is the potential that genetic polymorphisms in these genes may be influencing the disparity of COVID-19 mortality rates in Black communities. Here, we review the evidence that biological predisposition for high-risk comorbid conditions may be relevant to our ability to fully understand and therefore address health disparities of COVID-19 deaths in Blacks.
2019 年冠状病毒病（COVID-19）导致美国超过 180000 人死亡。尽管 COVID-19 影响所有种族和民族，但非西班牙裔黑人的死亡率最高。有证据不断表明，由于健康的不利社会决定因素，严重急性呼吸系统综合征冠状病毒 2（SARS-CoV-2）的传播和死亡率不成比例。然而，遗传易感性也可能在疾病传播中发挥可信的作用。SARS-CoV-2 通过 SARS-CoV-2 刺突蛋白与靶细胞表面表达的受体分子血管紧张素转换酶 2（ACE2）之间的相互作用进入细胞，使得 ACE2 的多态性和表达水平影响 SARS-CoV-2 的感染性和随后的发病机制。其他多个基因，如乙酰胆碱酯酶（AChE）和白细胞介素-6 中的遗传多态性也与高血压和 2 型糖尿病等潜在疾病密切相关，这些疾病大大增加了 SARS-CoV-2 的死亡率。然而，目前尚不清楚这些遗传多态性如何导致死亡率的差异，无论是否存在潜在疾病。特别有趣的是，这些基因中的遗传多态性可能会影响黑人社区 COVID-19 死亡率的差异。在这里，我们回顾了证据，表明高风险合并症的生物学倾向可能与我们充分理解和因此解决黑人 COVID-19 死亡的健康差异有关。
