Abstract
The serological responses to both SARS-CoV-1 and SARS-CoV-2 virus have some unique characteristics that suggest cross-reactive priming by other human coronaviruses (hCoVs). The early kinetics and magnitude of these responses are, in some cases, associated with worse clinical outcomes in SARS and COVID-19. Cross-reactive hCoV antibody responses have been detected in both SARS and COVID-19 patients. There is also evidence that pre-existing T cell immunity to common cold coronaviruses can prime the response to SARS-CoV-2. Studies in non-human primates show that SARS-CoV-1 S-protein vaccine-induced antibodies are associated with acute lung injury in macaques challenged with SARS-CoV-1. Here we discuss the potential of cross-reactive immunity to drive the immunopathogenesis of COVID-19 and its implications for current efforts to develop immune-based therapies and vaccines.
Highlights
The new SARS-CoV-2 pandemic has overwhelmed the world with its high contagiousness and range of severity, presenting from asymptomatic infection or mild symptoms to severe acute respiratory syndrome with severe morbidity and mortality
There is evidence that pre-existing T cell immunity to common cold coronaviruses can prime the response to SARSCoV-2
Based on the available data on COVID-19 patients and data from the previous SARS-CoV-1 and MERS outbreaks, there is substantial evidence that cross-reactive B and T cell responses may establish an unfavorable environment for the primary immune response to SARS-CoV-2 virus
Summary
The new SARS-CoV-2 pandemic has overwhelmed the world with its high contagiousness and range of severity, presenting from asymptomatic infection or mild symptoms to severe acute respiratory syndrome with severe morbidity and mortality. The authors suggested two possible effects of this mutation on the viral phenotype: (a) a reduction of S1–S2 subunit interaction, resulting in increased shedding of S1 from viral-membranebound S2 and (b) a potential induction of ADE: the D614G mutation is located deep within an immunodominant linear epitope of the SARS-CoV-1 Spike (S597–603) This peptide has been recognized as a major immunodominant epitope of SARSCoV-1 by analyzing sera from convalescent patients infected during the 2001 outbreak. Control of virus replication may be less efficient in SARS patients since the peak in viral load coincides with the first appearance of the antibody response, approximately 10 days after the onset of symptoms [16] Consistent with these conclusions, previous administration of anti-S-IgG in Chinese macaques leads to acute lung injury due to a massive accumulation of monocytes/ macrophages in the lungs [6]
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