SARS‐CoV‐2‐mediated immune system activation and potential application in immunotherapy

Abstract

Although novel severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2)‐mediated pulmonary inflammation has recently attracted great attention, its pathology and pathogenesis are not clear. Notably, due to both its high infective and pathogenicity, SARS‐CoV‐2 infection may cause a severe sometimes fatal respiratory disease. A specific vaccine, which relies on the analysis of SARS‐CoV‐2 structural protein‐derived antigenic peptides, is indispensable for restraining the spread and reducing the mortality of SARS‐CoV‐2. SARS‐CoV‐2 infections activate cytototxic, myeloid‐derived suppressor cells, dendritic cells, macrophages, as well as natural killer, B, helper T, and regulatory T cells, thus further stimulating innate and antigen‐specific immune responses. Nevertheless, many immune effector cells cause hyperinflammation and pulmonary immunopathology by releasing proinflammatory cytokines and chemokines, including interferon (IFN)‐α, IFN‐β, IFN‐γ, monocyte chemoattractant protein‐1, macrophage inflammatory protein (MIP)‐1A, MIP1B, interleukin (IL)‐1, IL‐2, IL‐4, IL‐6, IL‐7, IL‐8, IL‐9, IL‐12, IL‐17, and IL‐18, platelet‐derived growth factor, fibroblast growth factor, tumor necrosis factor‐α, and induced protein 10. Interestingly, related products derived from SARS‐CoV‐2 are likely to trigger immune evasion. Therefore, investigating SARS‐CoV‐2‐specific vaccines, blocking immunopathology, and prohibiting immune evasion are urgently required for treating SARS‐CoV‐2 infection. In this review, we emphatically illuminated the development of a SARS‐CoV‐2‐specific vaccine based on the analysis of epitopes, also expounding the molecular mechanisms of SARS‐CoV‐2‐mediated cytokine release syndrome. Furthermore, we comprehensively discussed SARS‐CoV‐2‐associated immune evasion and lung immunopathology. Lastly, potential therapeutic strategies against SARS‐CoV‐2 were explored.

Recurrence of alopecia areata after covid‐19 vaccination: A report of three cases in Italy

“…This cascade promotes NK cell activation and the escalation of the cytokine storm. 12 Similarly, COVID-19 vaccines may play a role in the activation of immunological events leading to an aberrant autoimmune Thus, in patients with pre-existing inflammatory dysregulated pathways, the interaction between the immune system and vaccines may enhance other autoimmune mechanisms.…”

The human pandemic coronaviruses on the show: The spike glycoprotein as the main actor in the coronaviruses play

“…Comparing both viruses, the infection caused by SARS-CoV-2 is recognized by a broader clinical spectrum that comes from asymptomatic infection to severe viral pneumonia with respiratory failure and death [ 8 , 12 , 13 ]. In contrast to SARS-CoV and MERS-CoV, many SARS-CoV-2-infected patients developed low-titer of neutralizing antibody, leading them to suffer with prolonged severe symptoms and illness, suggesting a more effective SARS-CoV-2 immune surveillance evasion than SARS-CoV and MERS-CoV [ [14] , [15] , [16] , [17] , [18] ].…”

Identifying The “Core” Transcriptome of SARS-CoV-2 Infected Cells

“…Reports have shown that the virus is capable of not only affecting lung function, showing similar results as pneumonia, but also influences the function of various organs throughout the body, such as the heart, kidney, testis, liver, lymphocytes and nervous system [26], leading to a plethora of other symptoms of variable nature and severity in patients. Previous research has also shown that infection with SARS-CoV-2 leads to activation and upregulation of various aspects of the immune system, including recruiting cytokines and chemokines, as well as cell migration and degranulation [27]. Other studies have established the downregulation of several genes upon viral infection, such as angiopoietin-1, a powerful protector of the vascular system [28] and retinoic acid-induced protein 2, a gene responsible for cellular development and growth [24].…”