In order to understand the treatment, we need to clarify "ACE2" first. Many previous studies have shown that ACE2 plays an important and complicated role in the diseases caused by COVID-19. On the one hand, ACE2 is the receptor that COVID-19 recognized when he entered the cell. In the mouse model, the higher the expression level of ACE2, the more serious the disease is. On the other hand, ACE2 has a certain protective effect. If the expression level of ACE2 is low, the lung injury of mice will be more serious.
Simply put, if there is too much ACE2 in the human body, the higher the risk and severity of COVID-19's disease. But we can't eliminate all ACE2, because if there is too little ACE2 in the human body, the lungs will be damaged.
Suck the virus away! The infectivity has dropped by 5000 times, so the researchers put forward a new idea, that is, can "recombinant human ACE2 protein" purified in vitro prevent COVID-19 infection?
The logic behind this is simple: COVID-19 will recognize and bind human ACE2 protein. Then, the researchers added "recombinant human ACE2 protein" from the outside, and these proteins added from the outside would "suck away" COVID-19 like a magnet, making it impossible to invade cells. In this way, the infectivity of the virus to human body can be eliminated.
To test this idea, researchers first isolated COVID-19 and then infected cultured cells with them. Interestingly, if the viruses contact with recombinant human ACE2 protein for 30 minutes before infecting cells, the infectivity of these viruses will be obviously weakened. The researchers estimate that the weakening range is about 1000-5000 times.
In organ experiments, it can also inhibit infection. After the positive results of cell experiments, the researchers conducted follow-up research in the "organ-like" model. Compared with the cell model, the quasi-organ can better reflect some key features of the organ, so it has better representative significance.
The researchers used human capillaries and kidney-like organs, and the results of previous cell experiments were similar: adding recombinant human ACE2 protein can significantly reduce the infection in COVID-19. In the kidney model, this inhibitory ability also showed dose-dependence, that is, the higher the concentration of ACE2 protein added, the better the inhibitory ability. The preliminary data of safety also showed that ACE2 protein added in vitro was not toxic in capillary model and kidney model.
Scientists need to further test the efficacy in the lungs. However, this treatment idea is not perfect. The researchers pointed out that it also has several obvious limitations.
First of all, this study is aimed at the early infection stage of the virus, with the goal of preventing COVID-19 from invading the host cells at an early stage. Whether human recombinant ACE2 protein still has inhibitory effect in the later stage of the disease is unknown.
Secondly, although capillaries and kidney-like organs have certain scientific basis in pathology, researchers have not detected lung-like organs, which are the hardest hit areas of COVID-19 infection; Finally, in the actual physiological environment, the signal pathway and regulation mode related to ACE2 are more complicated. We need to do more research to understand the possible role of additional human recombinant ACE2 protein.
Before summarizing vaccine, antidote, protein therapy or other treatment ideas, the author pointed out in the paper that these results indicate that soluble ACE2 is expected to inhibit COVID-19 and prevent them from entering cells. At a time when various drugs have not been clinically verified for a long time, and vaccines need 12- 18 months to be born, this research undoubtedly brings new ideas to prevent virus infection.
Of course, the results of these cell experiments and organ-like experiments alone are far from enough. In order to verify its preventive potential, we need to do more exploration. Interestingly, for some other purposes, the purified human recombinant ACE2 protein has completed 1 and phase 2 clinical trials in the past. This is a good start, and we hope that scientists will not spend too long following up.