Letter Topical Sections

Antibodies and infected monocytes and macrophages in COVID-19 patients

  • Received: 28 May 2022 Accepted: 31 May 2022 Published: 08 June 2022
  • The SARS-CoV-2 virus causes the COVID-19 disease associated with over 6.2 million deaths globally. Multiple early indicators raised the potential risk of the SARS-CoV-2 virus infecting monocytes and macrophages via Fc-receptor antibody binding based on closely related beta coronaviruses. Antibody Fc-receptor infection of phagocytic monocytes and macrophages is one type of antibody dependent enhancement of disease. Increased COVID-19 severity correlated with early high antibody responses on initial infection for unvaccinated adults. Clinical evidence suggests that for moderate antibody titer levels, antibodies binding to SARS-CoV-2 may contribute to viral spread, cytokine dysregulation, and enhanced COVID-19 disease severity. Primary immune responses appear to have too low of antibody titer to significantly contribute to Fc-receptor uptake by monocytes and macrophages for COVID-19 patients. Very high antibody titers created by SARS-CoV-2 vaccines also appear to inhibit Fc-receptor uptake and infection of monocytes and macrophages; this inhibition appears to decrease as antibody titer levels decrease. Cross reactive antibodies to other coronaviruses or moderate levels of SARS-CoV-2 antibodies may be contributing to antibody dependent enhancement of disease in critical COVID-19 patients.

    Citation: Darrell O. Ricke. Antibodies and infected monocytes and macrophages in COVID-19 patients[J]. AIMS Allergy and Immunology, 2022, 6(2): 64-70. doi: 10.3934/Allergy.2022007

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  • The SARS-CoV-2 virus causes the COVID-19 disease associated with over 6.2 million deaths globally. Multiple early indicators raised the potential risk of the SARS-CoV-2 virus infecting monocytes and macrophages via Fc-receptor antibody binding based on closely related beta coronaviruses. Antibody Fc-receptor infection of phagocytic monocytes and macrophages is one type of antibody dependent enhancement of disease. Increased COVID-19 severity correlated with early high antibody responses on initial infection for unvaccinated adults. Clinical evidence suggests that for moderate antibody titer levels, antibodies binding to SARS-CoV-2 may contribute to viral spread, cytokine dysregulation, and enhanced COVID-19 disease severity. Primary immune responses appear to have too low of antibody titer to significantly contribute to Fc-receptor uptake by monocytes and macrophages for COVID-19 patients. Very high antibody titers created by SARS-CoV-2 vaccines also appear to inhibit Fc-receptor uptake and infection of monocytes and macrophages; this inhibition appears to decrease as antibody titer levels decrease. Cross reactive antibodies to other coronaviruses or moderate levels of SARS-CoV-2 antibodies may be contributing to antibody dependent enhancement of disease in critical COVID-19 patients.



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