The African-American population with a low allele frequency of SNP rs1990760 (T allele) in IFIH1 predicts less IFN-beta
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The African-American population with a low allele frequency of SNP rs1990760 (T allele) in IFIH1 predicts less IFN-beta expression and potential vulnerability to COVID-19 infection Amit K. Maiti 1 Received: 14 May 2020 / Accepted: 23 July 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Covid-19 has caused worldwide devastation. IFIH1 is a pattern recognition receptor that senses coronavirus RNA and triggers interferon production as a first line of viral immune defense. The role of IFIH1 polymorphism, rs1990760 (C>T; aaA946T) in the epidemiology of viral infection is well studied, and the minor allele T resists viral infection. Knock-in mice with mutated IFIH1 protein (946T) for this allele have enhanced interferon production and protection from lethal viral infection. The minor allele frequency (Tmaf) varies widely from Africans (0.06 to 0.35) to Chinese (0.19 to 0.23) to Caucasians (0.56 to 0.69). During the initial days of infection when the social restrictions were not imposed, I show that the infection rate in Italy was lower as expected from its higher Tmaf (0.56) than that in China (Tmaf for southern China, 0.23). The infection rate in the USA and Spain was intermediate between those two countries despite higher Caucasian overall Tmaf (0.69), perhaps due to a more admixed African population in these countries. These analyses suggest that African-Americans and Chinese with low Tmaf of rs1990760 are more vulnerable to SARS-COV2 infection, apart from other genetic factors or socioeconomic conditions in these population. Taken together, an IFN-beta supplement might aid in preventing COVID-19 infection and help in development of herd immunity. Keywords SARS-COV2 . COVID-19 . IFIH1 . Polymorphism . Interferon-beta
Recently, novel coronavirus (virus, SARS-COV2; disease, COVID-19) infection and its related mortality are so severe internationally that the WHO declared it as a pandemic. Although mortality rates differ in various countries, such as in Wuhan (little more than 3%) but in Italy, it was so far more than 5% of infected people. The principle mode of transmission of SARS-COV2 is air-droplet-borne, and eventually, the virus enters lung alveolar cells through the upper respiratory tract to multiply and cause disease. SARS-COV2 has a protein coat with spikes and a positive ~ 30-kb (29,903 base) RNA strand (Ren et al. 2020). After attaching to the host cells with its spikes, it uses the ACE2 receptor as well as the TMPRSS2 enzyme to enter into host cells and uses its host machinery to replicate its RNA genome to make thousands of RNA molecules (Hoffmann et al. 2020). It also uses host protein synthesis system to synthesize its coat proteins to pack its RNA * Amit K. Maiti [email protected]; [email protected] 1
Department of Genetics and Genomics, Mydnavar, 2645 Somerset Boulevard, Troy, MI 48084, USA
genetic material to become a new full-fledged virus and bursts the host cells to come out to infect other cells. Lung cells damaged or destroyed by infection
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