PMID- 38271561 OWN - NLM STAT- MEDLINE DCOM- 20240229 LR - 20240229 IS - 1557-8976 (Electronic) IS - 0882-8245 (Linking) VI - 37 IP - 1 DP - 2024 Jan-Feb TI - Interaction Between Genetic Susceptibility and COVID-19 Pathogenesis in Pediatric Multisystem Inflammatory Disorders: The Role of Immune Responses. PG - 1-11 LID - 10.1089/vim.2023.0074 [doi] AB - Numerous studies have highlighted the emergence of coronavirus disease (COVID-19) symptoms reminiscent of Kawasaki disease in children, including fever, heightened multisystem inflammation, and multiorgan involvement, posing a life-threatening complication. Consequently, extensive research endeavors in pediatric have aimed to elucidate the intricate relationship between COVID-19 infection and the immune system. COVID-19 profoundly impacts immune cells, culminating in a cytokine storm that particularly inflicts damage on the pulmonary system. The gravity and vulnerability to COVID-19 are closely intertwined with the vigor of the immune response. In this context, the human leukocyte antigen (HLA) molecule assumes pivotal significance in shaping immune responses. Genetic scrutiny of HLA has unveiled the presence of at least one deleterious allele in children afflicted with multisystem inflammatory syndrome in children (MIS-C). Furthermore, research has demonstrated that COVID-19 exploits the angiotensin-converting enzyme 2 (ACE-2) receptor, transmembrane serine protease type 2, and various other genes to gain entry into host cells, with individuals harboring ACE-2 polymorphisms being at higher risk. Pediatric studies have employed diverse genetic methodologies, such as genome-wide association studies (GWAS) and whole exome sequencing, to scrutinize target genes. These investigations have pinpointed two specific genomic loci linked to the severity and susceptibility of COVID-19, with the HLA locus emerging as a notable risk factor. In this comprehensive review article, we endeavor to assess the available evidence and consolidate data, offering insights into current clinical practices and delineating avenues for future research. Our objective is to advance early diagnosis, stabilization, and appropriate management strategies to mitigate genetic susceptibility's impact on the incidence of COVID-19 in pediatric patients with multisystem inflammation. FAU - Chen, Li-Na AU - Chen LN AD - Department of Pediatric, Affiliated Hospital of Shaoxing University, Shaoxing, China. FAU - Shou, Zhang-Xuan AU - Shou ZX AD - Department of Pharmacy, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China. FAU - Jin, Xue AU - Jin X AUID- ORCID: 0000-0002-9388-0558 AD - Department of Pharmacy, Center for Clinical Pharmacy, Cancer Center, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, China. LA - eng PT - Journal Article PT - Review DEP - 20240125 PL - United States TA - Viral Immunol JT - Viral immunology JID - 8801552 RN - 0 (HLA Antigens) RN - pediatric multisystem inflammatory disease, COVID-19 related SB - IM MH - Humans MH - Child MH - *COVID-19/genetics/epidemiology/*complications MH - SARS-CoV-2 MH - Genome-Wide Association Study MH - Inflammation MH - HLA Antigens/genetics MH - Immunity MH - Genetic Predisposition to Disease MH - *Systemic Inflammatory Response Syndrome OTO - NOTNLM OT - COVID-19 OT - genetic susceptibility OT - immune responses OT - multisystem inflammatory disorders OT - pediatric EDAT- 2024/01/25 18:42 MHDA- 2024/02/29 06:43 CRDT- 2024/01/25 14:23 PHST- 2024/02/29 06:43 [medline] PHST- 2024/01/25 18:42 [pubmed] PHST- 2024/01/25 14:23 [entrez] AID - 10.1089/vim.2023.0074 [doi] PST - ppublish SO - Viral Immunol. 2024 Jan-Feb;37(1):1-11. doi: 10.1089/vim.2023.0074. Epub 2024 Jan 25.