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. 2020 Jul 3:11:1662.
doi: 10.3389/fimmu.2020.01662. eCollection 2020.

Cell-Mediated Immune Responses to COVID-19 Infection

Amélie Guihot  1   2 , Elena Litvinova  2 , Brigitte Autran  1 , Patrice Debré  1   2 , Vincent Vieillard  1
Affiliations

Cell-Mediated Immune Responses to COVID-19 Infection

Amélie Guihot et al. Front Immunol. .

Abstract

An unprecedented outbreak of pneumonia caused by a novel coronavirus (CoV), subsequently termed COVID-19 by the World Health Organization, emerged in Wuhan City (China) in December 2019. Despite rigorous containment and quarantine efforts, the incidence of COVID-19 continues to expand, causing explosive outbreaks in more than 160 countries with waves of morbidity and fatality, leading to significant public health problems. In the past 20 years, two additional epidemics caused by CoVs have occurred: severe acute respiratory syndrome-CoV, which has caused a large-scale epidemic in China and 24 other countries; and respiratory syndrome-CoV of the Middle East in Saudi Arabia, which continues to cause sporadic cases. All of these viruses affect the lower respiratory tract and manifest as pneumonia in humans, but the novel SARS-Cov-2 appears to be more contagious and has spread more rapidly worldwide. This mini-review focuses on the cellular immune response to COVID-19 in human subjects, compared to other clinically relevant coronaviruses to evaluate its role in the control of infection and pathogenesis and accelerate the development of a preventive vaccine or immune therapies.

Keywords: COVID-19; SARS - CoV-2; adaptive immunity; coronavirus; innate immunity.

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Figures

Figure 1
Figure 1
Proposed host immune responses during SARS-CoV-2 infection. Aerosolized uptake of SARS CoV-2 leads to infection of ACE2-expressing target cells, such as alveolar type 2 pneumocytes or other unknown target cells. The virus may dampen antiviral IFN-α/β responses resulting in uncontrolled viral replication. The influx of neutrophils and monocytes/macrophages results in hyperproduction of pro-inflammatory cytokines. The immunopathology of lung may be the result of the “cytokine storm.” NK cells and specific T cells may be activated and contribute to exacerbating inflammatory responses, and then to an acute respiratory distress syndrome (ARDS). SARS-CoV-2 specific Abs may help neutralize viruses, participate to antibody-dependent cell-mediated cytotoxicity (ADCC) or on the contrary to induce antibody-dependent enhancement (ADE). To date, most events remain speculative or unknown.
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