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Polymorphisms in the ACE I/D (rs4646994) and ACE2 G8790A (rs2285666) in Young Children Living in the Amazon Region
Yan Cardoso Pimenta1,2,3, Flávia Freitas de Oliveira Bonfim1, Carlos Eduardo da Silva Figueiredo1,3,4
1Laboratory of Comparative and Environmental Virology, Oswald °Cruz Institute, Oswald °Cruz Foundation, Fiocruz, Avenida Brasil, 4365, Manguinhos, Rio de Janeiro 21040-360, RJ, Brazil.
Abstract:
COVID-19 infection caused by SARS-CoV-2 continues to cause significant mortality and morbidity. ACE2 is a key regulator of the renin-angiotensin-aldosterone system (RAAS). Differences in COVID-19 severity are thought to be due to the imbalance of RAAS/ACE mutations. This retrospective study evaluated the detection and genetic susceptibility to SARS-CoV-2 infection in 202 children ≤3 years of age living in the Amazon region in 2021. The angiotensin-converting enzyme ACE I/D (rs4646994) and ACE2 G8790A (rs2285666) polymorphisms were detected by SYBR GREEN real-time PCR and PCR-RFLP/Alul digestion, respectively. SARS-CoV-2 detection was performed by RT-qPCR in feces and saliva samples collected simultaneously from the same children presenting acute gastroenteritis (AGE) or acute respiratory infection (ARI). The frequency of SARS-CoV-2 detected by qRT-PCR in children was low (5.9%, 12/202), although higher in the group of children with AGE (8.9%, 9/101) than with ARI (2.9%, 3/101). Susceptibility to SARS-CoV-2 infection was not verified due to the low frequency. Homozygous II (rs4646994) children were the majority (87.1%, 176/202). Boys with genotype A (rs2285666) were more susceptible to ARI and pneumonia symptoms than AGE (OR = 3.8, 95% CI 1.4-10.3, p 0.007). Boys with genotype G (rs4646994) or the combination II + G were more susceptible to acquiring AGE. Surveillance, along with understanding their causes, is crucial to controlling ARI and COVID-19 in children living in low-income countries.
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