Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) results in a variety of clinical symptoms ranging from no or mild to severe disease. Currently, there are multiple postulated mechanisms that may push a moderate to severe disease into a critical state. Human serum contains abundant evidence of the immune status following infection. Cytokines, chemokines, and antibodies can be assayed to determine the extent to which a patient responded to a pathogen. We examined serum and plasma from a cohort of patients infected with SARS-CoV-2 early in the pandemic and compared them to negative-control sera. Cytokine and chemokine concentrations varied depending on the severity of infection, and antibody responses were significantly increased in severe cases compared to mild to moderate infections. Neutralization data revealed that patients with high titers against an early 2020 SARS-CoV-2 isolate had detectable but limited neutralizing antibodies against the emerging SARS-CoV-2 Alpha, Beta and Delta variants. This study highlights the potential of re-infection for recovered COVID-19 patients.

Highlights

  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) results in a variety of clinical symptoms ranging from no or mild to severe disease

  • We found that infection with SARS-CoV-2 resulted in significant changes in multiple cytokines and chemokines compared to negative control serum and plasma (Fig. 1)

  • Since the beginning of the COVID-19 pandemic, clinicians and scientists have sought to investigate the components of patient serum for evidence of either sufficient or aberrant immune responses

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Summary

Introduction

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) results in a variety of clinical symptoms ranging from no or mild to severe disease. Cytokine and chemokine concentrations varied depending on the severity of infection, and antibody responses were significantly increased in severe cases compared to mild to moderate infections. In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in the city of Wuhan, Hubei province, China, causing variably severe respiratory tract pathology termed coronavirus disease 2019 (COVID-19). Critical cases of COVID-19 do occur, and are characterized by severe pneumonia and acute respiratory distress ­syndrome[1] leading to organ failure and d­ eath[2]. In many severely affected patients, SARS-CoV-2 infection triggers an overactive immune response known as a “cytokine storm.”. Besides cytokine and chemokine production following infection, antibodies generated by COVID-19 patients have been studied and reported in detail. The beta and delta variants both have displayed decreased sensitivity to pre-existing neutralizing a­ ntibodies[15,19–21]

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