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The idea of ​​“epidemic constitutions” is attributed to Thomas Sydenham, one of the most eminent physicians of the 17th century. Regardless of the type of disease epidemic (cholera, influenza, smallpox), it aimed to explain what remains unexplained to this day: Why now? And why do some develop serious illness while others do not? In this article, I review some debates that occurred during the cholera epidemics of the 19th century, discuss the idea of ​​telluric “epidemic constitutions”, and propose a reinterpretation, or perhaps just an updated interpretation of Thomas Sydenham's amazing insight into the cause of epidemic constitutions: a confluence between an exciting cause that was in the atmosphere and a predisposing cause that was in the bodies of the sufferers themselves . With what we have learned since then, I explain his insight as representing the process and product of our co-evolution with Influenza A viruses. I explore theoretically how this interpretation would explain differences in rates and distributions of infection, disease and mortality during epidemics, and, propose alternative explanations to the epidemiology of the early emergence of COVID-19 in China and selected countries, based on an epidemiological inquiry on the circulation of influenza viruses during the 2019-2020 influenza season across those countries. The approach brought up new questions that could only emerge from epidemiological (population-based) reasoning (what causes vulnerability?) and epidemiological studies (what was the context of influenza during the emergence of the COVID-19 pandemic?), such as: a) did Influenza B have a role in the production of vulnerability to infection by the SARS-COV2 virus? b) do the SARS-COV2 virus and the H1N1 influenza virus share some immunological attribute conductive to a same type of immune-inflammatory response among non-H1 primed individuals? Or do the sequence B-H1 and B-SARS_COV2 produce similar morbidity? Does a sequence of B – H1 – SARS-COV2 explain the severity of COVID-19 Pandemic in the US? Do the SARS-COV2 viruses and the H1N1 viruses compete in the same ecological spot? What would this mean for future developments of our immune-inflammatory landscape?