#كوفيد19_يتقهقر_ويضعف_مع_مرور_الوقت
#أخبار_سارة
#عبدالجبار_الظفري
🔹#الخبر_قبل_يومان،
أثبتت دراسات بحثية أن فيروس كورونا مع مرور الزمن والوقت يضعف وذلك بتحولات جينية جعلته أضعف من بدايته بكثير..
فقد فقد الفيروس 60٪ من شراسته السابقة
و هو متجه في الأسابيع القادمة إلى تحولات جينية أخرى بحيث يصبح غير ممرض للبشر وأضعف بكثر من بدايته، (بإذن الله تعالى) و هو حاله حال جميع الفيروسات السابقة مثل فيروس الحمى الألمانية والإنفلونزا الأسبانية وعائلة كوفيد٢...الخ ، اللهم الوباء و البلاء وسائر الأمراض والأسقام يا رب العالمين.
🔴 المصدر :الدراسة الألمانية ؛ و BBC
#COVID_19
#كوفيد_19
#انشروا_الأمل🌹
المصادر والفيديو أسفل المقال👇
Although the exact mechanisms remain unknown, evidence suggests that after the virus attaches itself, the host cell snips the spike protein at one of its dedicated ‘cleavage sites’, exposing fusion peptides — small chains of amino acids that help to pry open the host cell’s membrane so that the virus’s membrane can merge with it. Once the invader’s genetic material gets inside the cell, the virus commandeers the host’s molecular machinery to produce new viral particles. Then, those progeny exit the cell to go and infect others.
Power spikes
SARS-CoV-2 is uniquely equipped for forcing entry into cells. Both SARS-CoV and SARS-CoV-2 bind with ACE2, but the receptor-binding domain of SARS-CoV-2 is a particularly snug fit. It is 10–20 times more likely to bind ACE2 than is SARS-CoV9. Wendtner says that SARS-CoV-2 is so good at infecting the upper respiratory tract that there might even be a second receptor that the virus could use to launch its attack.
Even more troubling is the fact that SARS-COV-2 seems to make use of the enzyme furin from the host to cleave the viral spike protein. This is worrying, researchers say, because furin is abundant in the respiratory tract and found throughout the body. It is used by other formidable viruses, including HIV, influenza, dengue and Ebola to enter cells. By contrast, the cleavage molecules used by SARS-CoV are much less common and not as effective.
The simulations driving the world’s response to COVID-19
Scientists think that the involvement of furin could explain why SARS-CoV-2 is so good at jumping from cell to cell, person to person and possibly animal to human. Robert Garry, a virologist at Tulane University in New Orleans, Louisiana, estimates that it gives SARS-CoV-2 a 100–1,000 times greater chance than SARS-CoV of getting deep into the lungs. “When I saw SARS-CoV-2 had that cleavage site, I did not sleep very well that night,” he says.
The mystery is where the genetic instructions for this particular cleavage site came from. Although the virus probably gained them through recombination, this particular set-up has never been found in any other coronavirus in any species. Pinning down its origin might be the last piece in the puzzle that will determine which animal was the stepping stone that allowed the virus to reach humans.
End game
Some researchers hope that the virus will weaken over time through a series of mutations that adapt it to persist in humans. By this logic, it would become less deadly and have more chances to spread. But researchers have not yet found any sign of such weakening, probably because of the virus’s efficient genetic repair mechanism. “The genome of COVID-19 virus is very stable, and I don’t see any change of pathogenicity that is caused by virus mutation,” says Guo Deyin, who researches coronaviruses at Sun Yat-sen University in Guangzhou.
Rambaut, too, doubts that the virus will become milder over time and spare its host. “It doesn’t work that way,” he says. As long as it can successfully infect new cells, reproduce and transmit to new ones, it doesn’t matter whether it harms the host, he says.
But others think there is a chance for a better outcome. It might give people antibodies that will offer at least partial protection, says Klaus Stöhr, who headed the World Health Organization’s SARS research and epidemiology division. Stöhr says that immunity will not be perfect — people who are reinfected will still develop minor symptoms, the way they do now from the common cold, and there will be rare examples of severe disease. But the virus’s proofreading mechanism means it will not mutate quickly, and people who were infected will retain robust protection, he says.
“By far the most likely scenario is that the virus will continue to spread and infect most of the world population in a relatively short period of time,” says Stöhr, meaning one to two years. “Afterwards, the virus will continue to spread in the human population, likely forever.” Like the four generally mild human coronaviruses, SARS-CoV-2 would then circulate constantly and cause mainly mild upper respiratory tract infections, says Stöhr. For that reason, he adds, vaccines won’t be necessary.
Some previous studies support this argument. One10 showed that when people were inoculated with the common-cold coronavirus 229E, their antibody levels peaked two weeks later and were only slightly raised after a year. That did not prevent infections a year later, but subsequent infections led to few, if any, symptoms and a shorter period of viral shedding.
الورقه البحثية الخاصة بالموضوع👇
https://media.nature.com/original/magazine-assets/d41586-020-01315-7/d41586-020-01315-7.pdf
لمزيد من المعلومات والبحوث حول الموضوع👇
https://www.nature.com/articles/d41586-020-01315-7
بخصوص الموضوع وفيديو بالعربي👇
https://m.akhbarelyom.com/news/newdetails/3036044/1/فيديو--علماء--كورونا-يضعف-مع-مرور-الوقت