4.8 Article

BCG vaccination provides protection against IAV but not SARS-CoV-2

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CELL REPORTS
卷 38, 期 10, 页码 -

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CELL PRESS
DOI: 10.1016/j.celrep.2022.110502

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资金

  1. Histopathology Platforms at RI-MUHC
  2. UHN Toronto
  3. IUCPQ Quebec City
  4. Animal Research Division at RI-MUHC
  5. Canadian Institutes of Health Research (CIHR) [MM1-174910]
  6. McGill Interdisciplinary Initiative in Infection and Immunity (MI4) Emergency COVID-19 Research Funding awards
  7. Fonds de Recherche du Quebec -Sante (FRQS) Award
  8. Strauss Chair in Respiratory Diseases
  9. Canada Research Chair in Barrier Immunity
  10. Peter Munk Chair in Aortic Disease Research
  11. FRQS Award
  12. FRQS
  13. CIHR
  14. University of Toronto's Medicine by Design initiative

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A study found that while BCG vaccine can provide protection against influenza virus, it is ineffective against SARS-CoV-2. This may be due to the unique pulmonary vasculature damage caused by SARS-CoV-2, which facilitates the virus to spread to other organs, including the central site for BCG-induced trained immunity. In addition, individuals vaccinated with BCG show a strong immune response to influenza virus but minimal response to SARS-CoV-2.
Since the vast majority of species solely rely on innate immunity for host defense, it stands to reason that a critical evolutionary trait like immunological memory evolved in this primitive branch of our immune system. There is ample evidence that vaccines such as bacillus Calmette-Guerin (BCG) induce protective innate immune memory responses (trained immunity) against heterologous pathogens. Here we show that while BCG vaccination significantly reduces morbidity and mortality against influenza A virus (IAV), it fails to provide protection against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). In contrast to IAV, SARS-CoV-2 infection leads to unique pulmonary vasculature damage facilitating viral dissemination to other organs, including the bone marrow (BM), a central site for BCG-mediated trained immunity. Finally, monocytes from BCG-vaccinated individuals mount an efficient cytokine response to IAV infection, while this response is minimal following SARS-CoV-2. Collectively, our data suggest that the protective capacity of BCG vaccination is contingent on viral pathogenesis and tissue tropism.

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