The immune response to SARS-CoV-2 and COVID-19 immunopathology – Current perspectives

Abstract

SARS-CoV-2 is a new beta coronavirus, similar to SARS-CoV-1, that emerged at the end of 2019 in the Hubei province of China. It is responsible for coronavirus disease 2019 (COVID-19), which was declared a pandemic by the World Health Organization on March 11, 2020. The ability to gain quick control of the pandemic has been hampered by a lack of detailed knowledge about SARS-CoV-2-host interactions, mainly in relation to viral biology and host immune response. The rapid clinical course seen in COVID-19 indicates that infection control in asymptomatic patients or patients with mild disease is probably due to the innate immune response, as, considering that SARS-CoV-2 is new to humans, an effective adaptive response would not be expected to occur until approximately 2–3 weeks after contact with the virus. Antiviral innate immunity has humoral components (complement and coagulation-fibrinolysis systems, soluble proteins that recognize glycans on cell surface, interferons, chemokines, and naturally occurring antibodies) and cellular components (natural killer cells and other innate lymphocytes). Failure of this system would pave the way for uncontrolled viral replication in the airways and the mounting of an adaptive immune response, potentially amplified by an inflammatory cascade. Severe COVID-19 appears to be due not only to viral infection but also to a dysregulated immune and inflammatory response. In this paper, the authors review the most recent publications on the immunobiology of SARS-CoV-2, virus interactions with target cells, and host immune responses, and highlight possible associations between deficient innate and acquired immune responses and disease progression and mortality. Immunotherapeutic strategies targeting both the virus and dysfunctional immune responses are also addressed.

Age-Adjusted Associations Between Comorbidity and Outcomes of COVID-19: A Review of the Evidence From the Early Stages of the Pandemic

“…Whilst the mechanisms remain poorly understood, there are numerous biologically plausible explanations. The pathogenesis of severe COVID-19 is thought to involve dysregulated proinflammatory immune response and subsequent multi-system damage (39)(40)(41). Many underlying conditions may leave affected individuals more vulnerable to the effects of this.…”

A modular molecular framework for quickly estimating the binding affinity of the spike protein of SARS-CoV-2 variants for ACE2, in presence of mutations at the spike receptor binding domain

“…Furthermore, THOP1 appears to play a crucial role in the regulation of MHC I cell-surface expression [72][73][74]. Due to the shown high expression of THOP1 in several brain compartments and in the effector CD8 T-cells of COVID-19 patients [71], it raises the question about a possible relationship between different SARS-CoV-2 immune responses [75,76], neurological disorders observed in long covid patients, and THOP1 involvement in MHC-class I regulation in COVID-19 patients [77][78][79].…”

Changes in Dietary Patterns and Clinical Health Outcomes in Different Countries during the SARS-CoV-2 Pandemic

“…Antiviral innate immunity consists of coagulant factor, and components of the complement and fibrinolytic systems, soluble proteins that recognize glycans on cell surfaces, interferons, chemokines, and naturally occurring antibodies (mainly IgM but also IgA and IgG). The cellular components are natural killer cells and other innate lymphoid cells but also gamma delta T cells, which generally limit the spread of viral infection [ 64 ]. The viral spike protein preferentially binds to the angiotensin converting enzyme 2 receptor (ACE-2), prevalent in cells in the mammalian respiratory tract.…”