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Taiwan may have passed COVID-19 peak: Father of coronavirus research

Academician of Academia Sinica Dr. Michael M.C. Lai, the former President of National Cheng Kung University (NCKU), who is currently Chair Professor at China Medical University Institute of Basic Medicine, specialized in coronavirus, the species of virus that causes severe acute respiratory syndrome. His work has led to acknowledgement of Lai as "father of coronavirus research.”
He talked about the global impact of the novel coronavirus (COVID-19) outbreak in a recent interview with reporters in Taiwan. 
The content of the following article is based on Dr. Lai’s comments.
The novel coronavirus (SARS-CoV-2) and SARS virus have similarities between 70-90%, but they have different attribution, the death rate of COVID-19 is 2-3% while SARS is about 10%. However, this death rate tells us little, and several main factors account for much of the difference we’re seeing - down to simply how we screen and counting. Due to higher medical standards now, the death rate is getting lower naturally.
Conversely, the novel coronavirus is extremely infectious, it can spread further, survive longer outside, and may transmit through aerosols. It is infectious during the incubation period before any symptoms appear, even after the symptoms (fever) disappear, asymptomatic carriers will become the source of future infections, hampering screening efforts. These phenomena are giving us a warning that the novel coronavirus will not go away easily and may continue to trouble us.
We do not yet know the reason for such high infectivity of the novel coronavirus, but we can guess that this is related to the adhesion between the virus and cell. When the virus infects a cell, it must first attach to a protein on the cell surface, called a receptor, to enter the cell. The spike protein (S-protein) on the virus surface is used to attach the receptors. Although the spike protein gene sequences of the novel coronavirus and SARS are significantly different, the two viruses use the same receptor, and the novel coronavirus has a few times better binding, making the virus enter cells more easily, therefore higher infectivity. Such evolution is a natural miracle.
It is known that the receptor for SARS-CoV-2 is the angiotensin-converting enzyme 2 (ACE-2), a molecule related to the heart and blood vessels. It is distributed in many organs, including the kidneys, which can explain how patients often have problems with heart vessels and other systems. Note that ACE-2 inhibitors can be used to treat COVID-19, but yet to be approved for clinical use.
If the SARS-CoV-2 spike protein undergoes further mutations, it may make the virus infect other animals, such as pet cats and dogs, and some reports have found this possibility. Why does SARS-CoV-2 have such strong spike protein? It turns out that it is very similar to the pangolin coronavirus. The most likely explanation is that the pangolin coronavirus spike protein gene was transferred to the bat coronavirus and fused into a new RNA via RNA recombination. In addition to mutations, this is another evolution mechanism for the virus.
Generally, viral infections can be classified as acute or persistent. For acute infections such as SARS, pathogens are removed by the body immune system in a short period. Persistent infections are those in which the virus is not cleared from the host following primary infection, but remains associated with some cells, and may reactivate once immune environment changes. Some animals (such as mice) have persistent coronaviruses.
The novel coronavirus may exhibit this characteristic because some recovered COVID-19 patients are testing positive again. Another form is influenza, the virus hides in nature and recurs with the climate season every year, consequently the recurrence of the epidemic. The novel coronavirus may have this ability, so it may not be eliminated.
The best way to effectively control the novel coronavirus is drugs and vaccines. However, the research and development process of drugs is long, from the design and screening of new drugs, animal and clinical trials to the acquisition of drug certificates. It is urgent, but there are some alternative methods: Although viruses are different, their tools for replicating RNA and producing proteins are similar, so drugs used to treat Ebola may also be used for coronaviruses. For example, Remdesivir has been selected. Now it is undergoing clinical trials, and if the clinical trials prove to be effective, this drug can be used in patients immediately without going through another drug review procedure. We will have to wait and see!
Finally, we must remain optimistic and Taiwan may have passed its peak, but the virus remains rampant in Europe and the United States. Underdeveloped and population-dense Asian and African countries are in crisis, coupled with weak medical and public health systems, the epidemic may be imminent. It is not an exaggeration to call it a war.
“If anything kills over 10 million people in the next few decades, it’s most likely to be a highly infectious virus rather than a war - not missiles, but microbes,” warned Bill Gates during a TED Talk back in 2015. I look forward to the public and governments working together to overcome wave after wave of epidemic warfare.
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