Marc Souris, Léon Tshilolo, Destin Mbongi, Baltazar Phoba, Marie-Anasthasie Tshilolo, René Mbungu, Daniel Parzy, Line Lobaloba Ingoba, Francine Ntoumi, Rachel Kamgaing, Martin Samuel Sosso, Nadine Fainguem, Tandakha Ndiaye Dieye, Moussa Ndour, Massamba Sylla, Pierre Morand and Jean-Paul Gonzalez
More than a year after the emergence of COVID-19, significant regional differences in terms of morbidity persist, showing in particular lower incidence rates in some regions of Africa or Asia. The work reported here aims to test for a pre-pandemic natural immunity among populations in central and western Africa and a suspected SARS-CoV-2 original antigenic sin. To identify such pre-existing immunity, sera samples collected before the emergence of COVID-19 were tested to detect the presence of IgG antibodies reacting against SARS-CoV-2 proteins of major significance. Sera samples from blood donors of France also collected before the pandemic were used as control. The results showed a statistically highly significant difference for antibodies prevalence between the samples collected in Africa and the control samples. Our results suggest that in the tested African sub-regions the populations have been potentially pre-exposed before the COVID-19 pandemic to the antigens of a SARS-CoV-2-like virus.
COVID-19 and flu are both transmissible respiratory illnesses, but they are caused by much type of viruses. COVID-19 is instigated by infection with a coronavirus first recognized in 2019, and flu is instigated by infection with influenza viruses. The viruses that cause COVID-19 and the flu spread in parallel ways. They can both spread between people who are in close contact (within 6 feet, or 2 meters). The viruses feast through respiratory droplets or aerosols unconfined through sneezing, talking, or coughing. These droplets can land in the mouth or nose of someone close. These viruses can also spread if a person traces a surface with one of the viruses on it and then traces his or her mouth, eyes or nose.
Drug repurposing is a fast way to rapidly discover a drug for clinical use. In such circumstances of the spreading of the highly contagious COVID-19, searching for already known drugs is a worldwide demand. In this study, many drugs were evaluated by molecular docking. Among the test compounds, aliskiren (the best), dipyridamole, mopidamol and rosuvastatin showed higher energies of binding than that of the co-crystallized ligand N3 with COVID-19 main protease Mpro. Rolitetracycline showed the best binding with the catalytic center of the protease enzyme through binding with CYS 145 and HIS 41. Metamizole showed about 86% of the binding energy of the ligand N3 while the protease inhibitor darunavir showed little bit lower binding energy than N3. These results are promising for using these drugs in the treatment and management of the spreading of COVID-19 virus. Also, it could stimulate clinical trials for the use of these drugs by systemic or inhalation route.
Yves Muscat Baron* and Liberato Camilleri
Background: The atmospheric pollutant PM2.5 has been implicated in the pathogenesis of COVID-19. Some of the variants of SARS-CoV-2 possess the attributes of increased transmissibility and immune escape and appear to have been naturally selected to promulgate the pandemic. Variants of SARS-CoV-2 resulted due to a number of persistent SARS-CoV-2 mutations found in widely disparate and distant regions. This paper examines a possible association between airborne pollutant PM2.5 and the emergence of ten SARS-CoV-2 variants.
Methods: The daily mean levels of PM2.5 of a number of cities, where SARS-CoV-2 variants were detected, were obtained from the World Air Quality Index (WAQI). The mean daily PM2.5 levels were evaluated just before the occurrence of the first cluster of PM2.5 peaks’ atmospheric concentration, till after the emergence of the SARS- CoV-2 variants. Where available the daily number of new cases of COVID-19 diagnosed was matched to the PM2.5 levels.
Results: There appears to be a common pattern of PM2.5 in most of the regions prior to the emergence of the SARS-CoV-2 variants. An initial cluster of PM2.5 peaks was noted on average 50 days prior to the emergence of the variants and another group of smaller peaks in PM2.5 were noted just before or contemporaneous with the emergence of the SARS-CoV-2 variants. In the regions where the quantity of daily new cases was available, a number of significant correlations were obtained between PM2.5 levels and the number of new cases of SARS-CoV-2 variants.
Conclusion: In most regions two clusters of PM2.5 peaks were noted prior to the emergence of SARS-CoV-2 variants. The first cluster of PM2.5 peaks may suggest that anthropogenic activity was increased possibly reflecting augmented human to human contact. Due to elevated levels of PM2.5, a consequent propagation of the respiratory ACE-2 receptor (port of viral entry into the cell) ensued. Coronavirus- laden PM2.5 may have induced intra-host mutagenesis in the SARS-CoV-2 genome, contemporaneously diminishing pulmonary immunity. With the second cluster of PM2.5 peaks, this airborne pollutant may have also acted as a viral vector. The above findings suggest that antecedent peaks in PM2.5 prior to SARS-CoV-2 variants’ emergence not only contributed to transmission, but also impacted the immediate viral environs which may have led to SARS-CoV-2’s natural selection.
Yves Muscat Baron* and Liberato Camilleri
Background: Tobacco smoking has been shown to increase the severity of COVID-19 infection and the risk for intra-tracheal ventilation in smokers. Tobacco smoking exposes the user and nearby individuals to very high concentrations of particulate matter in a short period of time. Genes coding for SARS-CoV-2 have been found adherent to particulate matter which has been linked to COVID-19 related mortality PM2.5. The aim of the study was to observe the incidence of SARS-CoV-2 infection rates in the USA, comparing States differentiated by the degree of smoking bans, exploring a possible link between tobacco smoke-related particulate matter and SARS-CoV-2 transmission.
Methodology: Two groups of USA States, differentiated by the degree of smoking legislative restrictions, had a number of variables compared. Variables related to COVID-19 were obtained from the John Hopkins Coronavirus Resource Centre between the 20th and the 26th September 2020. The degree of smoking bans and the percentage of the smoking population in the USA States were obtained from the websites of the Nonsmokers Rights Foundation and the Centres of Disease Control database respectively. Population characteristics were obtained from databases concerning USA demographics.
Results: The incidence of COVID-19 infection in the States with limited bans on tobacco smoking was 2046/100,000 (sd+/-827) while the infection incidence in States with more restrictive rulings on tobacco smoking was 1660/100,000 (sd+/-686) (p<0.038). The population percentage of smokers in States with minor limitations to smoking was 18.3% (sd+/-3.28), while States with greater smoking restrictions had a smoking population percentage of 15.2% (sd+/-2.68) (p<0.0006). Significant correlations were noted between the percentage of the states’ population which was below the poverty line and access to Healthcare. Population density correlated significantly with the case-fatality ratio (R=0.66 p<0.0001).
Conclusion: States in the USA with high levels of tobacco smoking and limited regulation had significantly higher rates of COVID-19 infection incidences than States with greater smoking restrictions. The State population percentage living in poverty, and access to healthcare were significantly different between both groups of States. Densely populated USA States with partial bans on tobacco smoking, with elevated percentages of the population living in poverty and with limited access to healthcare had high incidences of COVID-19 rates during the time period assessed.
Virology: Current Research received 187 citations as per Google Scholar report