The Immune Response and Immunopathology of COVID-19

Abstract

Coronaviruses were first discovered in the 1960s and are named due to their crownlike shape. Sometimes, but not often, a coronavirus can infect both animals and humans. An acute respiratory disease, caused by a novel coronavirus (severe acute respiratory syndrome coronavirus-2 or SARS-CoV-2 previously known as 2019-nCoV) was identified as the cause of coronavirus disease 2019 (COVID-19) as it spread throughout China and subsequently across the globe. As of 14th July 2020, a total of 13.1 million confirmed cases globally and 572,426 deaths had been reported by the World Health Organization (WHO). SARS-CoV-2 belongs to the β-coronavirus family and shares extensive genomic identity with bat coronavirus suggesting that bats are the natural host. SARS-CoV-2 uses the same receptor, angiotensin-converting enzyme 2 (ACE2), as that for SARS-CoV, the coronavirus associated with the SARS outbreak in 2003. It mainly spreads through the respiratory tract with lymphopenia and cytokine storms occuring in the blood of subjects with severe disease. This suggests the existence of immunological dysregulation as an accompanying event during severe illness caused by this virus. The early recognition of this immunological phenotype could assist prompt recognition of patients who will progress to severe disease. Here we review the data of the immune response during COVID-19 infection. The current review summarizes our understanding of how immune dysregulation and altered cytokine networks contribute to the pathophysiology of COVID-19 patients.

Novel transgenic mice with Cre-dependent co-expression of GFP and human ACE2: a safe tool for study of COVID-19 pathogenesis

“…Clinical observations quickly established that the main cause of the severe course of COVID-19 is not the lung damage itself, but hyperactive immune response leading to cytokine storm, systemic in ammation, and downstream acute respiratory distress syndrome (ARDS) 30 . It was shown that the virus has complex interaction with the innate and adaptive immunity and can directly infect the immune cells.…”

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“…In contrast, Lu et al, (2020) revealed that the viral "S" protein binding of SARS-CoV-2 is comparatively weaker than that of SARS-CoV. Mortaz et al, (2020) demonstrated that after viral adherence to the respiratory tract, ACE2 is released and both of the Inflammatory Nuclear Factor Kappa B (NF-KB) and the Signal Transducer and Activator of Transcription 3 (STAT3) are activated by the SARS-CoV-2 (IL-6 amplifier or IL-6 Amp), resulting in autoimmune and multiple inflammatory diseases. Usually, the Pattern recognition receptors (PRRs) identify the pathogenassociated molecular patterns (PAMPs) such as the viral RNA.…”

“…In addition, the T helper cells play important roles in producing the cytokines. The host immune response is usually suppressed by SARS-CoV-2 through elucidating apoptosis of the T cells, as suggested by Mortaz et al, (2020). According to Huang et al, (2020); Qin et al, (2020); Tan et al, (2020), the number of CD4 + , CD8 + , NK, B cells and the memory helper T cells (CD3 + , CD45, RO + ) were recorded to be significantly decreased in severe COVID-19 patients.…”

“…A recent report of Mortaz et al, (2020) suggested that the mechanism of entry and invasion of the host cells by SARS-CoV-2 is similar to that of SARS-CoV. According to Wan et al, (2020); Lu et al, (2020), human ACE2 acts as a receptor for SARS-CoV-2.…”

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“…The adaptive immune response also comes into play. Helper CD4+, cytotoxic CD8+, and NK cells are activated and play a role in limiting the infection [ 47 ]. Cytotoxic CD8+ cells directly kill virus-infected cells.…”