ABSTRACT
BACKGROUND: Angiotensin-converting enzyme 2 (ACE2) is implicated as a host cell receptor that causes infection in the pathogenesis of coronavirus disease 2019 (COVID-19), and its genetic polymorphisms in the ACE2 gene may promote cardiovascular disease and systemic inflammatory injury in COVID-19 patients. Hence, the genetic background may potentially explain the broad interindividual variation in disease susceptibility and/or severity. METHODS: Genetic susceptibility to COVID-19 was analyzed by examining single-nucleotide polymorphisms (SNPs) of ACE2 in 246 patients with COVID-19 and 210 normal controls using the TaqMan genotyping assay. RESULTS: We demonstrated that the ACE2 SNPs rs4646142, rs6632677, and rs2074192 were associated with COVID-19 (for all, p < 0.05), and the differences in the ACE2 SNPs rs4646142 and rs6632677 were correlated with COVID-19-related systemic inflammatory injury and cardiovascular risk. Specifically, rs4646142 was associated with high-sensitivity C-reactive protein (hs-CRP), prealbumin (PAB), apolipoprotein A (APOA), high-density lipoprotein (HDL), and acid glycoprotein (AGP) levels. Rs6632677 was also associated with elevated CRP, acid glycoprotein (AGP), and haptoglobin (HPT). CONCLUSIONS: Our results suggest that the ACE2 SNPs rs4646142 and rs6632677 may be common genetic loci and optimal early identification genetic markers for COVID-19 with cardiovascular risk.
ABSTRACT
BACKGROUND: In December 2019, the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) broke out in Wuhan. Epidemiological and clinical characteristics of patients with COVID-19 have been reported, but the relationships between laboratory features and viral load has not been comprehensively described. METHODS: Adult inpatients (≥18 years old) with COVID-19 who underwent multiple (≥5 times) nucleic acid tests with nasal and pharyngeal swabs were recruited from Renmin Hospital of Wuhan University, including general patients (n = 70), severe patients (n = 195), and critical patients (n = 43). Laboratory data, demographic data, and clinical data were extracted from electronic medical records. The fitted polynomial curve was used to explore the association between serial viral loads and illness severity. RESULTS: Viral load of SARS-CoV-2 peaked within the first few days (2-4 days) after admission, then decreased rapidly along with virus rebound under treatment. Critical patients had the highest viral loads, in contrast to the general patients showing the lowest viral loads. The viral loads were higher in sputum compared with nasal and pharyngeal swab (P = .026). The positive rate of respiratory tract samples was significantly higher than that of gastrointestinal tract samples (P < .001). The SARS-CoV-2 viral load was negatively correlated with portion parameters of blood routine and lymphocyte subsets and was positively associated with laboratory features of cardiovascular system. CONCLUSIONS: The serial viral loads of patients revealed whole viral shedding during hospitalization and the resurgence of virus during the treatment, which could be used for early warning of illness severity, thus improve antiviral interventions.