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@#SARS-CoV-2 or 2019-nCov is the Coronavirus first named in 2019 that originated in the city of Wuhan in Hubei province China in December 2019. It causes severe acute respiratory syndrome (SARS). The clinical disease is called COVID-19 by the World Health Organization. SARS-CoV-2 enters the cell via the ACE-2 receptor. COVID-19 rapidly evolved into a pandemic by late February 2020. This review article focuses on the epidemiology, biology, pathogenesis, management and prevention of this virus that has high morbidity and mortality globally. The epicenter of the pandemic rapidly moved from China to Europe, with Italy being the most severely affected; it has since moved to USA, with New York State as the most severely affected. It is transmitted via aerosols and fomites. It causes severe upper and lower respiratory infections. The symptoms include fever, dry cough and malaise. These often rapidly progress to respiratory failure needing aggressive respiratory support. Confirmation of the diagnosis is usually by using Reverse Transcriptase Polymerase Chain Reaction (RTPCR). Some of the WHO recommended preventive measures include, among others, using alcohol based sanitizers, N95 facemask and strict quarantine of patients and contacts.
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ABSTRACT Objective Paraoxonase 1 (PON1) polymorphisms are associated with an increased susceptibility to cardiovascular disease. PON1 Q192R polymorphism (rs662) partially determine PON1 hydrolytic activity and protect against oxidation of LDL and HDL. This study aimed to delineate the association of PON1 status (functional 192 genotype and plasma activity levels) and atherogenicity in urbans residents aged 40 years or more. Materials and methods Anthropometric data, lipid profiles, the atherogenic index of the plasma (AIP) and Framingham score risk were measured. Three kinetic assays were conducted to assay PON1 status using phenylacetate and 4-(chloromethyl)phenyl acetate as substrates. Results Smoking per se did not significantly impact the AIP but the interaction PON1 genotype by smoking significantly increased the AIP. In subjects with the RR genotype smoking increased the AIP index from (estimated mean ± SEM) -0.038 ± 0.039 to 0.224 ± 0.094. The QR genotype increased the Framingham risk index by around 1.3 points. Smoking by RR genotype carriers significantly increased the Framingham risk score (17.23 ± 2.04) as compared to smoking (13.00 ± 1.06) and non-smoking (7.79 ± 0.70) by QQ+QR genotype carriers. The interaction RR genotype by smoking was a more important predictor (odds ratio = 7.90) of an increased Framingham risk score (> 20) than smoking per se (odds ratio = 2.73). The interaction smoking by RR genotype carriers significantly increased triglycerides and lowered HDL cholesterol. Conclusion Smoking per se has no (AIP) or a mild (Framingham risk score) effect on atherogenicity, while the interaction smoking by PON1 RR genotype has a clinically highly significant impact on atherogenicity.