The surfactant protein B polymorphisms (rs7316 and rs1130866) and their correlation with disease progression of COVID-19.

COVID-19 SARS-CoV-2 SFTPB gene

Journal

Cytokine
ISSN: 1096-0023
Titre abrégé: Cytokine
Pays: England
ID NLM: 9005353

Informations de publication

Date de publication:
04 Oct 2024
Historique:
received: 11 04 2024
revised: 15 06 2024
accepted: 30 09 2024
medline: 6 10 2024
pubmed: 6 10 2024
entrez: 5 10 2024
Statut: aheadofprint

Résumé

It is critical to examine the pathogenic pathways in coronavirus disease 2019 (COVID-19) that resulted in the development of severe lung injury. Surfactant protein B (SFTPB) is a vital component for sustaining life and serves pivotal functions in the host's defensive mechanisms and alveolar surface tension reduction. Our study aimed to determine the effect of SFTPB rs7316 and rs1130866 variants on the course of disease in COVID-19 patients. The study cohort comprised 3,184 individuals diagnosed with COVID-19. We employed the RFLP approach to determine the variations of the SFTPB genes. SFTPB rs7316 did not exhibit a statistically significant correlation with COVID-19 mortality across different inheritance models. But, after making more changes for SARS-CoV-2 variants, it was found that there was a strong link between the TT and TC genotypes of SFTPB rs7316 and death rates, especially for the Delta variant. Furthermore, our study's findings indicate a significant association between the SFTPB rs1130866 G allele and an elevated risk of mortality in COVID-19 across all variants of SARS-CoV-2. The use of the SFTPB rs1130866 marker has the potential to facilitate the prediction of COVID-19 severity. On the other hand, for SFTPB rs7316, this kind of prediction seems to depend on the particular SARS-CoV-2 variants.

Sections du résumé

BACKGROUND BACKGROUND
It is critical to examine the pathogenic pathways in coronavirus disease 2019 (COVID-19) that resulted in the development of severe lung injury. Surfactant protein B (SFTPB) is a vital component for sustaining life and serves pivotal functions in the host's defensive mechanisms and alveolar surface tension reduction. Our study aimed to determine the effect of SFTPB rs7316 and rs1130866 variants on the course of disease in COVID-19 patients.
METHODS METHODS
The study cohort comprised 3,184 individuals diagnosed with COVID-19. We employed the RFLP approach to determine the variations of the SFTPB genes.
RESULTS RESULTS
SFTPB rs7316 did not exhibit a statistically significant correlation with COVID-19 mortality across different inheritance models. But, after making more changes for SARS-CoV-2 variants, it was found that there was a strong link between the TT and TC genotypes of SFTPB rs7316 and death rates, especially for the Delta variant. Furthermore, our study's findings indicate a significant association between the SFTPB rs1130866 G allele and an elevated risk of mortality in COVID-19 across all variants of SARS-CoV-2.
CONCLUSIONS CONCLUSIONS
The use of the SFTPB rs1130866 marker has the potential to facilitate the prediction of COVID-19 severity. On the other hand, for SFTPB rs7316, this kind of prediction seems to depend on the particular SARS-CoV-2 variants.

Identifiants

pubmed: 39368228
pii: S1043-4666(24)00279-5
doi: 10.1016/j.cyto.2024.156775
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

156775

Informations de copyright

Copyright © 2024 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Amir Behrouzi (A)

Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.

Fatemeh Sakhaee (F)

Department of Mycobacteriology and Pulmonary Research, Pasteur Institute of Iran, Tehran, Iran.

Morteza Ghazanfari Jajin (M)

Department of Mycobacteriology and Pulmonary Research, Pasteur Institute of Iran, Tehran, Iran.

Iraj Ahmadi (I)

Department of Physiology, School of Medicine, Ilam University of Medical Science, Ilam, Iran.

Enayat Anvari (E)

Department of Physiology, School of Medicine, Ilam University of Medical Science, Ilam, Iran.

Fattah Sotoodehnejadnematalahi (F)

Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran. Electronic address: fattah212@gmail.com.

Abolfazl Fateh (A)

Department of Physiology, School of Medicine, Ilam University of Medical Science, Ilam, Iran; Microbiology Research Center (MRC), Pasteur Institute of Iran, Tehran, Iran. Electronic address: afateh2@gmail.com.

Classifications MeSH