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Updated: Sep 26, 2025
High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
Published on: March 24, 2015
Interferon-induced transmembrane protein 3 gene polymorphisms are associated with COVID-19 susceptibility and
Yapeng Li1, Lanlan Wei2, Lanye He3
1Rehabilitation Therapy Center, Luoyang Orthopedic Hospital of Henan Province, Orthopedic Hospital of Henan Province, Luoyang, China.
Background:
Recent evidence has linked the interferon-induced transmembrane protein 3 gene (IFITM3) to coronavirus disease 2019 (COVID-19) outcomes, but the results are inconsistent. The purpose of this meta-analysis was to evaluate the association of IFITM3 gene polymorphisms with COVID-19 susceptibility and severity.
Method:
A systematic search was performed with PubMed, Web of Science, Cochrane Library, and Embase from the date of inception to 20 December 2021. The results were analyzed with pooled odds ratios (ORs) and 95% confidence intervals (95% CIs). The robustness was performed using the method of sequential removal for each trial.
Results:
Four studies involving 1989 subjects were included, from which 1114 patients were positive for COVID-19. For IFITM3 rs12252, the pooled OR showed that there was a significant association between the genotype frequencies and infection with COVID-19 in any of the gene models, i.e., the allelic model (OR = 1.91, 95% CI, 1.36-2.68), the dominant model (OR = 1.80, 95% CI, 1.27-2.56), the recessive model (OR = 5.67, 95% CI, 1.01-31.77), the heterozygous model (OR = 1.65, 95% CI, 1.16-2.36) and the homozygous model (OR = 5.88, 95% CI, 1.05-32.98). The results stratified by severity showed that there was a significant correlation only between the allelic (OR = 0.69, 95% CI, 0.49-0.97) and recessive (OR = 0.43, 95% CI, 0.20-0.93) models. Our results did not support the associations between the IFITM3 rs34481144 gene polymorphism and COVID-19 susceptibility or severity in any of the gene models.
Conclusions:
The findings indicated that IFITM3 rs12252 gene polymorphisms were associated with COVID-19 susceptibility and that the rs12252-C variant was particularly critical for severity. Genetic factors should be considered in future vaccine development.
Insights
The interferon-induced transmembrane protein 3 (IFITM3) rs12252 gene variant is linked to increased COVID-19 susceptibility. The rs12252-C variant specifically impacts coronavirus disease 2019 severity, highlighting the role of genetic factors.
Area of Science:
- Genetics
- Immunology
- Infectious Diseases
Background:
- The interferon-induced transmembrane protein 3 (IFITM3) gene's role in coronavirus disease 2019 (COVID-19) outcomes is debated.
- Conflicting evidence necessitates further investigation into IFITM3 gene polymorphisms and their association with COVID-19.
Purpose of the Study:
- To conduct a meta-analysis evaluating the association between IFITM3 gene polymorphisms and COVID-19 susceptibility and severity.
- To clarify the inconsistent findings regarding IFITM3 and COVID-19 outcomes.
Main Methods:
- Systematic literature search of PubMed, Web of Science, Cochrane Library, and Embase up to December 20, 2021.
- Meta-analysis of four studies involving 1989 subjects (1114 COVID-19 positive) using pooled odds ratios (ORs) and 95% confidence intervals (CIs).
- Robustness assessment via sequential removal of trials.
Main Results:
- The IFITM3 rs12252 polymorphism showed a significant association with COVID-19 susceptibility across all genetic models.
- Analysis stratified by severity indicated significant correlations for the allelic (OR=0.69) and recessive (OR=0.43) models.
- No significant association was found for the IFITM3 rs34481144 polymorphism with COVID-19 susceptibility or severity.
Conclusions:
- IFITM3 rs12252 gene polymorphisms are associated with increased COVID-19 susceptibility.
- The rs12252-C variant is a critical factor influencing COVID-19 severity.
- Genetic factors, particularly IFITM3 variants, warrant consideration in future COVID-19 vaccine development.
