The COVID-19 MESHD COVID-19 MESHD pandemic had a delayed onset in South America compared to Asia (outside of China), Europe or North America. In spite of the presumed time advantage for the implementation of preventive measures to help contain its spread, the pandemic in that region followed growth rates that paralleled, and currently exceed, those observed several weeks before in Europe. Indeed, in early August, 2020, many countries in South and Central America presented among the highest rates in the world of COVID-19 MESHD confirmed cases and deaths per million inhabitants. Here, we have taken an ecological approach to describe the current state of the pandemic in Peru and its dynamics. Our analysis supports a protective effect of altitude from COVID-19 MESHD incidence and mortality. Further, we provide circumstantial evidence that internal migration through a specific land route is a significant factor progressively overriding the protection from COVID-19 MESHD afforded by high altitude. Finally, we show that protection by altitude is independent of poverty indexes and is inversely correlated with the prevalence in the population of risk factors associated with severe COVID-19 MESHD, including hypertension MESHD and hypercholesterolemia MESHD. We discuss long-term multisystemic adaptations to hypobaric hypoxia MESHD as possible mechanisms that may explain the observed protective effect of high altitude from death from COVID-19 MESHD.

Background: The coronavirus disease MESHD ( COVID-19 MESHD) first identified in Wuhan in December 2019 became a pandemic within a few months of its discovery. The impact of COVID-19 MESHD is due to both its rapid spread and its severity, but the determinants of severity have not been fully delineated. Objective: Identify factors associated with hospitalization and disease severity in a racially and ethnically diverse cohort of COVID-19 MESHD patients. Methods: We analyzed data from COVID-19 MESHD patients diagnosed at the University of Cincinnati health system from March 13, 2020 to May 31, 2020. Severe COVID-19 MESHD was defined as admission to intensive care unit or death MESHD. Logistic regression modeling adjusted for covariates was used to identify the factors associated with hospitalization and severe COVID-19 MESHD. Results: Among the 689 COVID-19 MESHD patients included in our study, 29.2% were non-Hispanic White, 25.5% were non-Hispanic Black, 32.5% were Hispanic, and 12.8% were of other race/ethnicity. About 31.3% of patients were hospitalized and 13.2% had severe disease. In adjusted analyses, the sociodemographic factors associated with hospitalization and/or disease severity included older age, non-Hispanic Black or Hispanic race/ethnicity (compared to non-Hispanic White), and smoking. The following comorbidities: diabetes MESHD, hypercholesterolemia MESHD, asthma MESHD, COPD MESHD, chronic kidney disease MESHD, cardiovascular diseases MESHD, osteoarthritis MESHD, and vitamin D deficiency MESHD were associated with hospitalization and/or disease severity. Hematological disorders MESHD such as anemia MESHD, coagulation disorders MESHD, and thrombocytopenia MESHD were associated with both hospitalization and disease severity. Conclusion: This study confirms race and ethnicity as predictors of severe COVID-19 MESHD. It also finds clinical risk factors for hospitalization and severe COVID-19 MESHD not previously identified such a vitamin D deficiency MESHD, hypercholesterolemia MESHD, osteoarthritis MESHD, and anemia MESHD.

Background: The Angiotensin system is implicated in the pathogenesis of COVID19 MESHD. First, ACE2 HGNC is the cellular receptor for SARS-COv-2, and expression of the ACE2 HGNC gene could regulate the individuals susceptibility to infection. In addition, the balance between ACE1 HGNC and ACE HGNC activity has been implicated in the pathogenesis of respiratory diseases MESHD and could play a role in the severity of COVID19 MESHD. Functional ACE1 HGNC and ACE2 HGNC gene polymorphisms have been associated with the risk of cardiovascular and pulmonary diseases MESHD, and could thus also contribute to the outcome of COVID19 MESHD. Methods: We studied 204 COVID19 MESHD patients (137 non-severe and 67 severe-ICU cases) and 536 age-matched controls. The ACE1 HGNC indel and ACE2 HGNC rs2285666 polymorphism were determined. Variables frequencies were compared between the groups by logistic regression. We also sequenced the ACE2 HGNC coding nucleotides in a group of patients. Results: Severe COVID19 MESHD was associated with hypertension MESHD male gender (p<0.001), hypertension MESHD (p=0.006), hypercholesterolaemia (p=0.046), and the ACE1 HGNC-DD genotype (p=0.049). In the multiple logistic regression hypertension MESHD (p=0.02, OR=2.26, 95CI=1.12-4.63) and male gender (p=0.002; OR=3.15, 95CI=1.56-6.66) remained as independent significant predictors of severity. The ACE2 HGNC polymorphism was not associated with the disease outcome. The ACE2 HGNC sequencing showed no coding sequence variants that could explain an increased risk of developing COVID19 MESHD. Conclusions: Adverse outcome of COVID19 MESHD was associated with male gender, hypertension MESHD, hypercholesterolemia MESHD and the ACE1 HGNC genotype. The ACE1 HGNC-indel was a significant risk factor for severe COVID19 MESHD, but the effect was dependent on the hypertensive MESHD status.