重症新型冠状病毒肺炎患者遗传易感性研究进展

doi:10.16288/j.yczz.22-058

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Hereditas(Beijing) ›› 2022, Vol. 44 ›› Issue (8): 672-681.doi: 10.16288/j.yczz.22-058

• Review • Previous Articles Next Articles

Genetic predisposition in patients with severe COVID-19

Wenbing Liu^1,²(), Dan Liu¹, Jin Yan¹, Xin Liu^1,², Qianfei Wang^1,²()

1. CAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics (China National Center for Bioinformation), Chinese Academy of Sciences, Beijing 100101, China
2. University of Chinese Academy of Sciences, Beijing 100049, China

Received:2022-03-06 Revised:2022-05-25 Online:2022-08-20 Published:2022-06-10
Contact: Wang Qianfei E-mail:liuwenbing@big.ac.cn;wangqf@big.ac.cn
Supported by:
Beijing Natural Science Foundation(M21022)

Abstract

Abstract:

The coronavirus disease 2019 (COVID-19) is a global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. COVID-19 has a variety of clinical manifestations, ranging from asymptomatic infection or mild symptoms to severe symptoms. Severe COVID-19 patients experience cytokine storm, resulting in multi-organ failure and even death. Male gender, old age, and pre-existing comorbidities (such as hypertension and diabetes ) are risk factors for COVID-19 severity. Recently, a series of studies suggested that genetic defects might also be related to disease severity and the cytokine storm occurence. Genetic variants in key viral immune genes, such as TLR7 and UNC13D, have been identified in severe COVID-19 patients from previous reports. In this review, we summarize the mechanisms underlying immune responses against SARS-CoV-2 and genetic variants that associated with the severity of COVID-19. The study of genetic basis of COVID-19 will be of great benefit for early disease detection and intervention.

Key words: severe COVID-19 patients, germline variants, immunodeficiency

Wenbing Liu, Dan Liu, Jin Yan, Xin Liu, Qianfei Wang. Genetic predisposition in patients with severe COVID-19[J]. Hereditas(Beijing), 2022, 44(8): 672-681.

Figures/Tables 2

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分类	基因	突变/多态性	突变表型	参考文献
病毒入侵	ACE2	rs190509934	降低表达	[18]
病毒入侵	ACE2	rs41303171	预测影响蛋白结构	[19]
病毒入侵	TMPRSS2	rs12329760	预测影响蛋白结构	[20~22]
血型系统	ABO	rs657152	无相关报道	[27]
HLA	HLA-A	HLA-A*11:01	无相关报道	[21]
HLA	HLA-B	HLA-B*51:01	无相关报道	[21]
HLA	HLA-C	HLA-C*14:02	无相关报道	[21]
HLA	HLA-DRB1	HLA-DRB1*14:04	无相关报道	[21]
HLA	HLA-DQA1	HLA-DQA1*01:01	无相关报道	[21]
HLA	HLA-C	HLA-C*04:01	无相关报道	[31]
HLA	HLA-DRB1	HLA-DRB1*15:01	无相关报道	[32]
HLA	HLA-DQB1	HLA-DQB1*06:02	无相关报道	[32]
HLA	HLA-B	HLA-B*27:07	无相关报道	[32]
干扰素通路	TLR7	c.2129_2132del;p.(Gln710Argfs*18)	降低表达	[34]
干扰素通路	TLR7	c.2383G>T;p.(Val795Phe)	降低表达	[34]
炎症因子风暴	UNC13D	c.2588G?>?A:p.(Gly863Asp)	预测影响蛋白结构	[41]
炎症因子风暴	AP3B1	c.2779G?>?A:p.(Gly927Ser)	预测影响蛋白结构	[41]
炎症因子风暴	AP3B1	c.911?C?>?T:p.(Thr304Ile)	预测影响蛋白结构	[41]

Genetic predisposition in patients with severe COVID-19

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[1]	Yinglun Han, Qingwei Li. Application progress of CRISPR/Cas9 genome editing technology in the treatment of HIV-1 infection [J]. HEREDITAS(Beijing), 2016, 38(1): 9-16.
[2]	Jianyuan Zhao, Jiwei Ding, Zeyun Mi, Tao Wei, Shan Cen. Identification and characterization of HIV-1 transmitted /founder viruses [J]. HEREDITAS(Beijing), 2015, 37(5): 419-425.