الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged a new disease named coronavirus disease 2019 (COVID-19) and developed an epidemic resulting in about 6 million deaths around the world till December 2022 according to the reports of the World Health Organization (WHO).
The COVID-19 infection varied greatly in severity among those who were infected. Understanding why serious diseases develop in some persons is critically important. It has long been established that heritable variables affect an individual’s susceptibility to and severity of infectious disease.
Numerous investigations have been conducted on the cellular proteins and innate defense mechanisms involved in immunity to pathogen infection. Interferon-stimulating genes (ISGs) are expressed as a result of the induction of type I and type III interferons (IFNs) as part of the innate immune responses. It has been determined that interferon-induced transmembrane proteins (IFITMs) are important ISGs that obstruct viral endosomal membrane fusion and nascent virions’ ability to spread. Even in the absence of IFN induction, the IFITM-3 protein is widely expressed in human tissues; yet, all three forms of IFNs have the strong ability to upregulate it.
The single nucleotide polymorphism (SNP) rs12252, which is found in the first exon of the IFITM3 gene, has been linked to a higher severity of influenza infection and a more rapid development of acquired immunodeficiency syndrome (AIDS) after infection with human immunodeficiency virus (HIV-1). It was first proposed that this SNP could result in an alternate splicing site created by the G allele, leading to a protein with an N-terminal deletion of 21 amino acids. The shortened form of the protein was primarily translocated to the plasma membrane, as demonstrated by model tests employing ∆21-IFITM3, and as a result, it did not prevent HIV-1 or influenza viruses from infecting cells.
In this study, we aimed to investigate the association between interferon-induced transmembrane protein 3 gene (IFITM3) rs12252 polymorphism with disease severity in coronavirus disease.
The study was conducted on 87 laboratory-confirmed COVID-19 patients from Alexandria University Hospitals, (23 patients with mild disease course, 36 patients with moderate disease course, and 28 patients with severe disease course) and 75 age and sex-matched apparently healthy controls. Laboratory confirmation was defined as a positive result at real-time reverse-transcription polymerase chain reaction (RT-PCR) assay of nasopharyngeal swab specimens.
All subjects in this study