Racial Disparities in Mortality During the 1918 Influenza Pandemic in United States Cities.

Against a backdrop of extreme racial health inequality, the 1918 influenza pandemic resulted in a striking reduction of non-White to White influenza and pneumonia mortality disparities in United States cities. We provide the most complete account to date of these reduced racial disparities, showing that they were unexpectedly uniform across cities. Linking data from multiple sources, we then examine potential explanations for this finding, including city-level sociodemographic factors such as segregation, implementation of nonpharmaceutical interventions, racial differences in exposure to the milder spring 1918 "herald wave," and racial differences in early-life influenza exposures, resulting in differential immunological vulnerability to the 1918 flu. While we find little evidence for the first three explanations, we offer suggestive evidence that racial variation in childhood exposure to the 1889-1892 influenza pandemic may have shrunk racial disparities in 1918. We also highlight the possibility that differential behavioral responses to the herald wave may have protected non-White urban populations. By providing a comprehensive description and examination of racial inequality in mortality during the 1918 pandemic, we offer a framework for understanding disparities in infectious disease mortality that considers interactions between the natural histories of particular microbial agents and the social histories of those they infect.

Thromboses and Hemostasis Disorders Associated with COVID-19: The Possible Causal Role of Cross-Reactivity and Immunological Imprinting.

By examining the issue of the thromboses and hemostasis disorders associated with severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) through the lens of cross-reactivity, it was found that 60 pentapeptides are shared by SARS-CoV-2 spike glycoprotein (gp) and human proteins that- when altered, mutated, deficient or, however, improperly functioning- cause vascular diseases, thromboembolic complications, venous thrombosis, thrombocytopenia, coagulopathies, and bleeding, inter alia. The peptide commonality has a relevant immunological potential as almost all of the shared sequences are present in experimentally validated SARS-CoV-2 spike gp-derived epitopes, thus supporting the possibility of cross-reactions between the viral gp and the thromboses-related human proteins. Moreover, many of the shared peptide sequences are also present in pathogens to which individuals have previously been exposed following natural infection or vaccinal routes, and of which the immune system has stored imprint. Such an immunological memory might rapidly trigger anamnestic secondary cross-reactive responses of extreme affinity and avidity, in this way explaining the thromboembolic adverse events that can associate with SARS-CoV-2 infection or active immunization.