Lack of Effects of the Genetic Polymorphisms of Interleukin-10 in Clinical Outcomes of COVID-19

Avendaño-Félix, Mariana; Ochoa‐Ramírez, Luis Antonio; Ramos‐Payán, Rosalío; Aguilar‐Medina, Maribel; Ayala-Ham, Alfredo; Rendón-Aguilar, Horacio; Lizárraga-Verdugo, Erik; Peraza-Garay, Felipe de Jesús; Ríos‐Tostado, Juan José; Velarde‐Félix, Jesús Salvador

doi:10.1089/vim.2021.0022

Cited by 17 publications

(11 citation statements)

References 31 publications

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“…In case of IL-10 ( rs1800872) gene polymorphism, a significant protective role of CC genotype was observed in preventing COVID-19 severity among infected patients ( p = 0.010). A study on Mexican population reported a similar finding where frequency of CC genotype was higher in mild (52.1%) as compared to severe COVID-19 patients (50.7%) but their results were not found to be significant [ 22 ]. The frequency of AA genotype was found to be 9.4% and 13.3% in our mild and severe cases respectively which is a bit higher when compared to Mexican COVID-19 patients (5.3% and 10.7%, respectively).…”

Section: Discussionmentioning

confidence: 82%

Implication of single nucleotide polymorphisms in Interleukin-10 gene (rs1800896 and rs1800872) with severity of COVID-19

Rizvi

Raza

Abbas³

et al. 2022

Egypt J Med Hum Genet

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Background Coronavirus disease 2019 (COVID-19) is an ongoing pandemic which has emerged as a new challenge for the medical sciences. Severity of COVID-19 is mostly determined with overexpressed proinflammatory cytokines eventually leading to endothelial dysfunction causing vital organ injury, especially in the lungs. It has been postulated that various genetic mutations might be associated with an increased risk of disease severity in COVID-19. This study was thus carried out to determine the association of rs1800896 and rs1800872 genetic polymorphism in IL-10 gene in determining COVID-19 severity. Methods The study included 160 RT-PCR confirmed COVID-19 patients with mild (n = 85) and severe (n = 75) conditions. All subjects were genotyped for Interleukin-10 (rs1800896 and rs1800872) gene polymorphisms using PCR–RFLP technique followed by statistical analysis. Results This study found a significant gender and age-based discrepancy in COVID-19 severity with 1.85-and 3.81-fold increased risk of COVID-19 in males of mild and severe groups as compared to females (p = 0.046 and p < 0.001) and 4.35-fold high risk in subjects ≥ 50 (p < 0.001). Genotyping analysis showed that IL-10 (rs1800872) gene polymorphism was strongly associated with COVID-19 severity (p = 0.01) whereas, IL-10 rs1800896 polymorphism was not found to confer the risk of COVID-19 severity in our population. Conclusion In this regard, the present study provided an evidence that IL-10 (rs1800872) gene polymorphism is strongly associated with COVID-19 severity and CC genotype confer a protective role in preventing severe disease progression. More detailed studies with a larger sample size on the genetic variations are required to establish the role of studied IL-10 gene polymorphisms with COVID-19 severity.

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Section: Discussionmentioning

confidence: 82%

Implication of single nucleotide polymorphisms in Interleukin-10 gene (rs1800896 and rs1800872) with severity of COVID-19

Rizvi

Raza

Abbas³

et al. 2022

Egypt J Med Hum Genet

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“…In addition, HLA‐A*11:01, B*51:01, and C*14:02 alleles constitute the most significant risk alleles predisposing for severity 101 . Other immune molecules, like cytokines and chemokines, were also significantly associated with the majority of the studies 102–105 …”

Section: Resultsmentioning

confidence: 98%

“…101 Other immune molecules, like cytokines and chemokines, were also significantly associated with the majority of the studies. [102][103][104][105] The most significant association signals of another GWAS in UK patients were reported to be harbored in the gene cluster of OAS1, OAS2, and OAS3 (rs10735079), in DPP9 (rs2109069), in IFNAR2 (rs2236757) near the gene TYK2 (rs74956615). 106 DNAH7, CLUAP1, DES, SPEG, STXBP5, TOMM7, and WSB1 have been also associated with COVID-19 mortality in another GWAS.…”

Section: Findings From Genetic Association and Cohort Studies Of Covi...mentioning

confidence: 99%

Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review

Tziastoudi

Cholevas

Stefanidis

et al. 2022

Ann Clin Transl Neurol

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COVID‐19 and ME/CFS present with some similar symptoms, especially physical and mental fatigue. In order to understand the basis of these similarities and the possibility of underlying common genetic components, we performed a systematic review of all published genetic association and cohort studies regarding COVID‐19 and ME/CFS and extracted the genes along with the genetic variants investigated. We then performed gene ontology and pathway analysis of those genes that gave significant results in the individual studies to yield functional annotations of the studied genes using protein analysis through evolutionary relationships (PANTHER) VERSION 17.0 software. Finally, we identified the common genetic components of these two conditions. Seventy‐one studies for COVID‐19 and 26 studies for ME/CFS were included in the systematic review in which the expression of 97 genes for COVID‐19 and 429 genes for ME/CFS were significantly affected. We found that ACE, HLA‐A, HLA‐C, HLA‐DQA1, HLA‐DRB1, and TYK2 are the common genes that gave significant results. The findings of the pathway analysis highlight the contribution of inflammation mediated by chemokine and cytokine signaling pathways, and the T cell activation and Toll receptor signaling pathways. Protein class analysis revealed the contribution of defense/immunity proteins, as well as protein‐modifying enzymes. Our results suggest that the pathogenesis of both syndromes could involve some immune dysfunction.

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“…In addition, the significant association of IL‐17A AG (rs2275913), IL17F TT (rs763780), and IL10 AG (rs1800896) SNPs with international severity and death outcome due to the COVID‐19 has been deciphered 73 . Noticeably, IL10 rs1800871 and rs1800872 genotypes among 193 COVID‐19 patients, were not significantly associated with the disease severity 76 (Table 1). IL17 gene polymorphisms have been associated with ARDS, SARS COV, MERS, and SARS‐COV‐2 in which the decrease in the IL17 levels was protective, but increased levels were related to the disease severity.…”

Section: Interleukins Polymorphismsmentioning

confidence: 98%

Individual genetic variability mainly of Proinflammatory cytokines, cytokine receptors, and toll‐like receptors dictates pathophysiology of COVID‐19 disease

Vakil

Mansoori

Al-Awsi

et al. 2022

Journal of Medical Virology

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Innate and acquired immunity responses are crucial for viral infection elimination. However, genetic variations in coding genes may exacerbate the inflammation or initiate devastating cytokine storms which poses severe respiratory conditions in coronavirus disease-19 (COVID-19). Host genetic variations in particular those related to the immune responses determine the patients' susceptibility and COVID-19 severity and pathophysiology. Gene polymorphisms such as single nucleotide polymorphisms (SNPs) of interferons, TNF, IL1, IL4, IL6, IL7, IL10, and IL17 predispose patients to the severe form of COVID-19 or severe acute respiratory syndrome coronavirus-2 (SARS-COV-2). These variations mainly alter the gene expression and cause a severe response by B cells, T cells, monocytes, neutrophils, and natural killer cells participating in a cytokine storm. Moreover, cytokines and chemokines SNPs are associated with the severity of COVID-19 and clinical outcomes depending on the corresponding effect. Additionally, genetic variations in genes encoding toll-like receptors (TLRs) mainly TLR3, TLR7, and TLR9 have been related to the COVID-19 severe respiratory symptoms. The specific relation of these mutations with the novel variants of concern (VOCs) infection remains to be elucidated. Genetic variations mainly within genes encoding proinflammatory cytokines, cytokine receptors, and TLRs predispose patients to COVID-19 disease severity. Understanding host immune gene variations associated with the SARS-COV-2 infection opens insights to control the pathophysiology of emerging viral infections.

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Lack of Effects of the Genetic Polymorphisms of Interleukin-10 in Clinical Outcomes of COVID-19

Cited by 17 publications

References 31 publications

Implication of single nucleotide polymorphisms in Interleukin-10 gene (rs1800896 and rs1800872) with severity of COVID-19

Implication of single nucleotide polymorphisms in Interleukin-10 gene (rs1800896 and rs1800872) with severity of COVID-19

Genetics of COVID‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review

Individual genetic variability mainly of Proinflammatory cytokines, cytokine receptors, and toll‐like receptors dictates pathophysiology of COVID‐19 disease

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