Research team at Nankai University finds the new virus SARS-CoV-2 has mutated gene similar to those found in HIV and Ebola which makes it is far more likely to bond to human cells than Sars.
The mutation could not be found in Sars, Mers or Bat-CoVRaTG13, the bat coronavirus that was considered to be the original source of the new coronavirus SARS-CoV-2 containing 96% genes similarity. Confirmed by another research team led by Professor Li Hua from Huazhong University of Science and Technology.
Professor Ruan Jishou team at Nankai University in Tianjin found a section of mutated genes that did not exist in Sars, but were similar to those found in HIV and Ebola.
Claims the published paper in Chinaxiv.org, a platform used by the Chinese Academy of Sciences where scientific research papers are first released.
The study proposes that the virus uses the outreaching spike protein to hook on to the host cell, the mutation can generate a structure known as a cleavage site in the new coronavirus’ spike protein. Normally this protein is inactive. The cleavage site structure aims to trick the human furin protein, to cut and activate the spike protein and cause a “direct fusion” of the viral and cellular membranes. This entry mechanism is “100 to 1,000 times” more efficient then SARS according to the study.
To wrap my mind around those concepts, I watched the amazing quick and easy to understand video below by Armando Hasudungan.
Why older people are more likely to be affected by this virus
Another study by Etienne Decroly a french scientist from Aix-Marseille University, published in the scientific journal Antiviral Research, found a “furin-like cleavage site” that is not present in other coronaviruses.
It is well documented that SARS (severe acute respiratory syndrome) binds to human cells using a receptor protein called ACE2 (angiotensin-converting enzyme 2)present on cells membrane.
Since the 2019 coronavirus shares about 80% of the genetic structure of SARS some studies suggest it might use the same mechanism to bind to human cells.
Highly contagious viruses, like HIV and Ebola, target an enzyme called furin, it works like a protein activator. There are many inactive, or dormant proteins in our body, to activate their various functions they have to be severed in a specific way. (see video for more detailed explanation)
Professor Li Hua , another prominent virologist and genetic specialists, and his team from Huazhong University of Science and Technology in Wuhan, Hubei province, also confirmed Professor Ruan’s findings.
The findings so far indicate that the new SARS-CoV-2 has a ‘dual attack’ approach of binding to human cells: The first is via the ACE2 receptors and the second via the furin enzyme. This binding method makes it 1,000 times more efficient.
“The epidemiological observations showed the infectious capacity of SARS-CoV-2 is stronger than SARS-CoV, so there are likely to be other mechanisms to make the infection of SARS-CoV-2 easier. We suppose the main possibilities as follows, first, SARS-CoV-2 RBD combining with ACE2 may have other conformations; second, the SARS-CoV-2 Spike protein can also bind to other receptors besides ACE2; third, Spike is more easily cleaved by host enzymes and easily fuses with host cell membrane. We compared the Spike proteins from four sources, SARS-CoV-2, SARS-CoV, MERS-CoV and Bat-CoVRaTG13, and found that the SARS-CoV-2 virus sequence had redundant PRRA sequences. Through a series of analyses, this study propose that one of the important reasons for the high infectivity of SARS-CoV-2 is a redundant furin cut site in its Spike protein.And through structure based virtual ligand screening, we proposed possible furin inhibitors, which might be potentially used in the treatment of COVID-19.” Furin, a potential therapeutic target for COVID-19
Young and Old react differently to infection of SARS-CoV-2
In the SARS outbreak of 2003 kids were largely unaffected. In Hong Kong, no one under the age of 24 years died, while more than 50% of patients over 65 succumbed to the infection. Globally, less than 10% were children.
A similar pattern been observed with the outbreak of COVID-19. In Wuhan, between November 2019 and the second week of January 2020 no children were tested positive. However elderly proved particularly vulnerable. In mid-February there were 44,672 confirmed cases of COVID-19, 86.6% were between 30 and 79 years old. 0.9 percent of confirmed cases were under the age of nine, while only 1.2 percent were between 10 and 19 years old according to the chinese CDC.
However it is now understood that although few children suffer severely from COVID-19, they do get infected, it is quite likely that children are an important source of the virus. says virologist Robin Shattock of Imperial College London.
“Infected children may harbor SARS-CoV-2 while showing less-severe symptoms than adults. Their young immune systems, ACE2 receptor levels, and even exposure to other coronaviruses might play a role in their resilience.”
Possible Biological Explanations for Kids’ Escape from COVID-19 | The new scientist
This view is echoed by other scientists Ralph Baric, from North Carolina University confirms mice studies show a similar pattern. Oh yes it is the same Ralph Baric who was involved in experiments done in North Carolina University in 2015: Encoding the SHC014 spike from a chinese bat to efficiently use multiple the SARS human receptor ACE2 (human angiotensin converting enzyme II) to replicate efficiently in primary human airway cells and achieve in vitro titers equivalent to epidemic strains of SARS-CoV.
Professor Francis A. Boyle explains: “This was a DNA genetic engineering of SARS, which is already a biological warfare agent, to give it gain-of-function activities.” And who else is involved and funded this study? Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Scientists propose possible explanations:
“As you age, your immune system undergoes senescence and loses its capacity to respond as effectively or be regulated as effectively,” Baric
“Another explanation, is aging lung environment. Aged lungs counter the usual immune reaction with some tamping down of inflammation. As a result, the lungs do not respond quickly enough to a viral infection.” Perlman.
“It is almost certain we need both an antibody- and T cell–response to do well… the young immune system and its efficient T cells do a superior job of responding to SARS-CoV-2.” Perlman.
…”the importance of CD4+ helper T cells, which stimulate B cells to make antibodies against pathogens, in controlling SARS-CoV infection” Subbarao
ACE2 receptor role in immunity
ACE2 receptor volume diminishes with age, although this may seem like a contradiction, this may place the elderly at a greater risk of severe illness.
Because the ACE2 enzyme is an important regulator of an immune response, particularly inflammation according to The new scientist.
In 2014 a study titled: Angiotensin-converting enzyme 2 protects from lethal avian influenza A H5N1 infections found that the ACE2 enzyme offers protection against lethal avian influenza.
The study looked at patients infected with H5N1 and found that those with better outcomes had higher levels of the ACE2 protein in their blood. Turning off the gene for ACE2 in infected mice led to severe lung damage but when treating infected mice with human ACE2 it diminished their lung injury.
So it is possible that reduced ACE2 receptors in older people could be the reason they are less able to cope with SARS-CoV-2.mic
Reinfection – The elephant in the room
QinGyuan suggested that those who have been infected with Covid-19 do develop a protective antibody – but it isn’t clear how long the protection lasts. However, in certain individuals, the antibody cannot last that long. He said:
“For many patients who have been cured, there is a likelihood of relapse.”
In children, it is currently believed that the virus causes the development of “at least short-term immunity”.
“The fact that reinfections are emerging and that we still do not know what latent viral loads in the body can do to us in the short term, midterm or long term as we have only been exposed to the new virus in the last 9 weeks or so makes it even more frightening.
One virologist from UK who says he wanted to remain anonymous as he might be accused of causing panic or misinformation warned that the new coronavirus can be described in basic terms as a “slow airborne killer that will never let its victim off, even if it loses the battle the first time”,implying that even in those so called recovered , they might face reinfections or that the existing viral loads in the body will eventually cause some other new chronic disease.”
