Surviving the Rookie Virus, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2): The Immunopathology of a SARS-CoV2 Infection
Author(s) -
Sheng Feng Tsai,
Kang-Yun Lu,
Hong-Meng Chuang,
Ching-Ann Liu
Publication year - 2021
Publication title -
cell transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.043
H-Index - 100
eISSN - 1555-3892
pISSN - 0963-6897
DOI - 10.1177/0963689721993769
Subject(s) - virology , covid-19 , immunopathology , coronavirus , medicine , severe acute respiratory syndrome coronavirus , respiratory system , severe acute respiratory syndrome , betacoronavirus , virus , immunology , pathology , infectious disease (medical specialty) , disease , outbreak
Until July 29th, the number of confirmed coronavirus (COVID-19) cases worldwide has risen to over 16 million, within which 655 k deaths. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) emerges as the 11th global pandemic disease, showing the highest infectivity and lowest infection fatality rate. In this review, we compare the immunopathology among SARS-CoV, Middle East respiratory syndrome coronavirus, and SARS-CoV2. SARS-CoV2 is similar to SARS-CoV; it can cause lymphocytopenia and a rising granulocyte count. Here we point out the human body and concentrated society make for an excellent incubator for virus evolution. Most research energies put into developing the SARS-CoV2 vaccine are trying to block virus infection. Sixty-five percent of severe patients die with multiple organ failure, inflammation, and cytokine storm, which indicates that the patient’s immune system maintains functionality. Finding a way to trigger the specific T cell subset and plasmablast in our body is the best shot to get away with SARS-CoV2.
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