Science: Heavy! Why is the new coronavirus highly contagious? Scientists have found their "weaknesses."

Since Qingdao cold chain food packaging isolated to the new crown live virus, China's new crown epidemic prevention and control focus has shifted from "anti-human" to "people and prevention."
to find the "weakness" of sars-CoV-2 virus as soon as possible, and the development of vaccines and drugs is the only solution.
Unlike other coronavirus, which causes symptoms of the common cold and mild respiratory tract, SARS-CoV-2 is highly contagious, but so far the main question remains unanswered as to why SARS-CoV-2 is susceptible to infection with organs outside the respiratory system, such as the brain and heart.
A major study published in the journal Science on October 20th, an international team of researchers led by the University of Technology in Munich, Germany, and the University of Helsinki in Finland, identified the cause of SARS-CoV-2's highly contagious and rapid spread in human cells - neuroclear protein 1 (NRP-1).
experiments using laboratory-cultured cells with artificial and naturally occurring viruses that mimic SARS-CoV-2 have shown that NRP-1 can promote infection in the presence of ACE2, and that infection can be suppressed by blocking NRP-1 with antibody specificity.
NRP1 promotes the entry of cells of SARS-CoV-2 prosthetic particles into cells that have been identified as coronavirus SARS-CoV-2 infected through the subject ACE2.
if ACE2 is considered a "door" to the cell, NRP-1 may be the factor that directs the virus to the door.
ACE2 is very low in most cells, so it's not easy for the virus to find the entry gate, so other factors, such as NRP-1, may be necessary to help the virus find the gate.
mice showed that NRP-1 was able to transport tiny virus-sized particles from the nasal mucous membranes to the central nervous system.
nanoparticles are chemically engineered to bind to NRP-1.
when nanoparticles are used on an animal's nose, they reach neurons and capillaries in the brain within hours, while control particles that have no affinity for NRP-1 do not.
NRP mediated nanoparticles into cultured cells, olfactory superstructures, and the central nervous system in mice because loss of smell is one of the symptoms of COVID-19, and NRP-1 is mainly present in the cell layer of the nasal cavity, so the researchers examined tissue samples from 6 COVID-19 patients and 8 uninfected control patients to see if cells equipped with NRP-1 were actually infected by SARS-CoV-2.
the results showed that this was true: five out of six COVID-19 patients detected an olfactory endoskin infection, and infected olfactory endoskin cells showed high expression of NRP1.
SSAR-CoV-2 is infected with olfactory onskin, said Mikael Simons, a professor of molecular neurobiology at the University of Technology in Munich.
, however, we can't draw conclusions about whether SARS-CoV-2 is the same, because in most patients this pathway is likely to be suppressed by the immune system.
currently only speculate on the molecular processes involved, and further research is needed to shed light on the problem.
, however, once the prickly protein is determined to bind to NRP-1, this interaction can be shown to help enhance SARS-CoV-2's invasion of human cells.
More importantly, the potential therapeutic value of this discovery in the fight against COVID-19 is highlighted by reducing SARS-CoV-2's ability to infect human cells by using monoclonal antibodies, laboratory-created proteins similar to natural antibodies, or selective drugs that block interactions.
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