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.