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Cellular and Humoral Immune Responses in Covid-19 and Immunotherapeutic Approaches
Amal Hasan1, Ebaa Al-Ozairi2,3, Zahraa Al-Baqsumi1
1Department of Immunology and Microbiology, Research Division, Dasman Diabetes Institute, Dasman, Kuwait City, Kuwait.
Abstract:
Coronavirus disease 2019 (Covid-19), caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can range in severity from asymptomatic to severe/critical disease. SARS-CoV-2 uses angiotensin-converting enzyme 2 to infect cells leading to a strong inflammatory response, which is most profound in patients who progress to severe Covid-19. Recent studies have begun to unravel some of the differences in the innate and adaptive immune response to SARS-CoV-2 in patients with different degrees of disease severity. These studies have attributed the severe form of Covid-19 to a dysfunctional innate immune response, such as a delayed and/or deficient type I interferon response, coupled with an exaggerated and/or a dysfunctional adaptive immunity. Differences in T-cell (including CD4+ T-cells, CD8+ T-cells, T follicular helper cells, γδ-T-cells, and regulatory T-cells) and B-cell (transitional cells, double-negative 2 cells, antibody-secreting cells) responses have been identified in patients with severe disease compared to mild cases. Moreover, differences in the kinetic/titer of neutralizing antibody responses have been described in severe disease, which may be confounded by antibody-dependent enhancement. Importantly, the presence of preexisting autoantibodies against type I interferon has been described as a major cause of severe/critical disease. Additionally, priorVaccine and multiple vaccine exposure, trained innate immunity, cross-reactive immunity, and serological immune imprinting may all contribute towards disease severity and outcome. Several therapeutic and preventative approaches have been under intense investigations; these include vaccines (three of which have passed Phase 3 clinical trials), therapeutic antibodies, and immunosuppressants.
Insights
Severe COVID-19 is linked to immune system dysfunction, including impaired interferon responses and altered T-cell and B-cell activity. Pre-existing autoantibodies against interferon are a significant factor in severe disease progression.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, presents a spectrum of illness from asymptomatic to critical.
- SARS-CoV-2 infection triggers an inflammatory response, particularly pronounced in severe cases, involving the angiotensin-converting enzyme 2 receptor.
- Understanding immune response variations is crucial for predicting and managing COVID-19 severity.
Purpose of the Study:
- To elucidate the differences in innate and adaptive immune responses between mild and severe COVID-19 cases.
- To identify key immune cell populations and antibody dynamics associated with disease severity.
- To explore the role of pre-existing immunity and autoantibodies in COVID-19 outcomes.
Main Methods:
- Comparative analysis of immune cell profiles (T-cells, B-cells) in patients with varying COVID-19 severity.
- Assessment of neutralizing antibody kinetics and potential antibody-dependent enhancement.
- Investigation of autoantibodies against type I interferon as a potential cause of severe disease.
Main Results:
- Severe COVID-19 is associated with a delayed/deficient type I interferon response and exaggerated/dysfunctional adaptive immunity.
- Distinct alterations in T-cell subsets (CD4+, CD8+, Tfh, γδT, Treg) and B-cell populations are observed in severe cases.
- Pre-existing autoantibodies against type I interferon are identified as a major contributor to severe/critical COVID-19.
- Factors like prior vaccination, trained immunity, and immune imprinting may influence disease severity.
Conclusions:
- Immune dysregulation, characterized by impaired interferon signaling and aberrant adaptive immunity, underlies severe COVID-19.
- Autoantibodies against type I interferon represent a critical risk factor for severe disease.
- Further research into immune responses and pre-existing immunity is vital for developing effective COVID-19 therapeutics and vaccines.
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