A Novel Hypothesis for Original Antigenic Sin in the Severe Disease of SARS-CoV-2 Infection

Monoclon Antib Immunodiagn Immunother. 2020 Aug;39(4):107-111. doi: 10.1089/mab.2020.0029. Epub 2020 Aug 10.

Abstract

In this hypothesis, we address the biological/immunological pathway leading to severe disease or death after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The underlying immune response is described with "original antigenic sin" (OAS) whereby previous infections influence the response to future virus encounters. We cite evidence for OAS-induced immunopathology in HIV-1 disease. We hypothesize that similar immune abnormalities can occur after infection with SARS-CoV-2. This hypothesis is supported by recent analysis of the antibodies in infected patients demonstrating serological and B cell abnormalities. The concept of symmetrical clonal regulation developed earlier for the immune network illustrates the pathway suggested by our hypothesis and may be helpful to develop strategies avoiding severe coronavirus disease 2019.

Keywords: SARS-CoV-2; coronavirus; original antigenic sin.

MeSH terms

  • Antibodies, Monoclonal / immunology
  • Antibodies, Viral / immunology*
  • B-Lymphocytes / immunology*
  • Betacoronavirus / immunology*
  • COVID-19
  • Coronavirus Infections / immunology*
  • Coronavirus Infections / pathology
  • Cross Reactions / immunology
  • Cytokine Release Syndrome / immunology
  • HIV / immunology
  • HIV-1 / immunology
  • Humans
  • Immune Evasion / immunology*
  • Immunoglobulin G / immunology
  • Immunoglobulin M / immunology
  • Immunologic Memory / immunology
  • Pandemics
  • Pneumonia, Viral / immunology*
  • Pneumonia, Viral / pathology
  • SARS-CoV-2

Substances

  • Antibodies, Monoclonal
  • Antibodies, Viral
  • Immunoglobulin G
  • Immunoglobulin M