Xuefei Huang
The more we find out about COVID-19, the more we need to scrutinize our suspicions about it. Right off the bat in the COVID-19 pandemic, our data about the illness originated from clinical case reports of COVID-19 and what we thought about flu pandemics and the serious intense respiratory condition (SARS) coming about because of SARS-CoV.
SARS-CoV is a coronavirus that imparts 82% of its genome to SARS-CoV-2. In 2003, it caused a global SARS pandemic.
It immediately turned out to be evident that COVID-19 was altogether different than occasional flu, with higher mortality and infectivity, yet it took more time to understand that there were significant contrasts and similitudes with SARS.
For example, COVID-19 is irresistible in any event, during the presymptomatic stage. Likewise, physiological cycles that are destructive in one period of the malady may get supportive later. For instance, the angiotensin changing over protein 2 (ACE2) receptor, which permits the infection to enter the body, may likewise be vital to the security of the lungs in the later periods of the sickness.
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