A ideia de “constituições epidêmicas” é atribuída a Thomas Sydenham, um dos médicos mais eminentes do século XVII. Independentemente do tipo de epidemia de doença (cólera, gripe, varíola), ela visava explicar o que permanece inexplicável até hoje: Por que agora? E por que alguns desenvolvem doenças graves enquanto outros não? Neste artigo, reviso alguns debates que ocorreram durante as epidemias de cólera do século XIX, discuto a ideia de “constituições epidêmicas” telúricas e proponho uma reinterpretação, ou talvez apenas uma interpretação atualizada da incrível percepção de Thomas Sydenham sobre a causa das constituições epidêmicas: uma confluência entre uma causa excitante que estava na atmosfera e uma causa predisponente que estava nos corpos dos próprios sofredores. Com o que aprendemos desde então, explico sua percepção como representando o processo e o produto de nossa co-evolução com os vírus da Influenza A. Eu exploro teoricamente como essa interpretação explicaria diferenças em taxas e distribuições de infecção, doença e mortalidade durante epidemias e proponho explicações alternativas para a epidemiologia do surto inicial de COVID-19 na China e em países selecionados, com base em uma investigação epidemiológica sobre a circulação de vírus influenza durante a temporada de influenza de 2019-2020 nesses países. A abordagem levantou novas questões que só poderiam emergir do raciocínio epidemiológico (baseado na população) (o que causa vulnerabilidade?) e estudos epidemiológicos (qual era o contexto da influenza durante o surgimento da pandemia de COVID-19?), como: a) a Influenza B teve um papel na produção de vulnerabilidade à infecção pelo vírus SARS-COV2? b) o vírus SARS-COV2 e o vírus influenza H1N1 compartilham algum atributo imunológico condutivo a um mesmo tipo de resposta imunoinflamatória entre indivíduos não preparados para H1? Ou a sequência B-H1 e B-SARS_COV2 produzem morbidade semelhante? Uma sequência de B – H1 – SARS-COV2 explicaria a gravidade da Pandemia de COVID-19 nos EUA? Os vírus SARS-COV2 e os vírus H1N1 disputam o mesmo lugar ecológico? O que isso significaria para os desenvolvimentos futuros de nossa constituição imunoinflamatória?
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