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Asymptomatic COVID-19: disease tolerance with efficient anti-viral immunity against SARS-CoV-2

ABSTRACT: The immune responses and mechanisms limiting symptom progression in asymptomatic cases of SARS-CoV-2 infection remain unclear. We comprehensively characterized transcriptomic profiles, cytokine responses, neutralization capacity of antibodies and cellular immune phenotypes of asymptomatic patients with acute SARS-CoV-2 infection to identify potential protective mechanisms. Compared to symptomatic patients, asymptomatic patients had higher counts of mature neutrophils and lower proportion of CD169+ expressing monocytes in the peripheral blood. Systemic levels of pro-inflammatory cytokines were also lower in asymptomatic patients, accompanied by milder pro-inflammatory gene signatures. Mechanistically, a more robust systemic Th2 cell signature with a higher level of virus-specific Th17 cells and a weaker yet sufficient neutralizing antibody profile against SARS-CoV-2 was observed in asymptomatic patients. In addition, asymptomatic COVID-19 patients had higher systemic levels of growth factors that are associated with cellular repair. Together, asymptomatic patients mount less pro-inflammatory and more protective immune responses against SARS-CoV-2 indicative of disease tolerance. Insights from this study highlight key immune pathways that could serve as therapeutic targets to prevent disease progression in COVID-19.

ORGANISM(S): Homo sapiens

PROVIDER: GSE166424 | GEO | 2021/04/24

REPOSITORIES: GEO

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Project description:Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has provoked, up to date, more than 5 million deaths worldwide. While asymptomatic individuals are responsible of many potential transmissions, the difficulty to identify and isolate them at the high peak of infection constitutes still a real challenge in the actual pandemic. Moreover, apart from the effect over the respiratory system, SARS-CoV-2 provokes severe vascular damage and thromboembolic events in critical COVID-19 patients, deriving in many related deaths and long-hauler symptoms. Understanding how these processes are triggered in response to the virus as well as the potential sequelae at the long term, even in asymptomatic donors, becomes essential. Methods: We have evaluated, by application of a proteomics-based quantitative approach, the effect of serum of COVID-19 asymptomatic individuals over circulating angiogenic cells (CACs). Thus, healthy CACs were incubated ex-vivo with the serum of either COVID-19 negative (PCR-/IgG-, n:8) or COVID-19 positive asymptomatic donors, at different infective stages: PCR+/ IgG- (n:8) and PCR-/IgG+ (n:8). Also, a label free quantitative approach was applied to identify and quantify protein differences between these serums. Results: Our results confirmed that SARS-CoV-2 promotes changes at the protein level in the serum of infected asymptomatic individuals, mainly correlated with altered coagulation and inflammatory processes (Fibrinogen, Von Willebrand Factor, Thrombospondin-1). At the cellular level, proteins like ICAM-1, TLR2 or Ezrin/Radixin were only up-regulated in CACs treated with the serum of asymptomatic patients at the highest peak of infection (PCR+/IgG-), but not with the serum of PCR-/IgG+ individuals. Many of these proteins correlate with the initial response of the endothelium against the virus. Conclusions: The incubation ex vivo of CACs with the serum of asymptomatic COVID-19 donors at different stages of infection promoted protein changes representative of the endothelial dysfunction and inflammatory response that occur after viral infection, together with activation of the coagulation process. The current approach constitutes an optimal model to study the response of vascular cells to SARS-CoV-2 infection, as well as an alternative to test potential inhibitors targeting either the virus entry pathway or molecules involved in the immune responses following SARS-CoV-2 infection.

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Asymptomatic COVID-19: disease tolerance with efficient anti-viral immunity against SARS-CoV-2

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