Scientific studies show CoVID-19 has HIV inserts. Full damage to show YEARS after infection like HIV

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BREAKING! LatestCoronavirus Research Reveals That The Virus Has Mutated Gene Similar To HIV and Is 1,000 Times More Potent.

Source: Coronavirus Research News Feb 29, 2020

Latest coronavirus research by a team of researchers from Nankai University in Tianjin lead by Professor Ruan Jishou, a prominent virologists and genomicist have discovered that the new SARS-Cov-2 coronavirus that causes the Covid-19 disease has a mutated gene that is found in HIV virus. It is this unique feature that sets it aside from the rest of the known coronaviruses.

The study is published this week on Chinaxiv.org, a platform used by the Chinese Academy of Sciences to release scientific research papers before they have been peer-reviewed
http://www.chinaxiv.org/abs/202002.00082 (ChinaXiv.org 中国科学院科技论文预发布平台)

These findings have huge implications on the potency of the coronavirus and also what it can cause in humans, not just the Covid-19 disease. Furthermore, the Covid-19 disease should never be compared to like the common cold or influenza virus as this new coronavirus is in a separate league of its own.

Though it has not been peer reviewed, two other studies including one in Europe has confirmed the findings.

The combined findings from the three studies indicates that because of the HIV-like mutations, its ability to bind with human cells could be as much as 1,000 times more potent that the initial SARS virus of 2003.

The findings also indicate that the new SARS-CoV-2 has a ‘dual attack’ approach of binding to human cells.

The first is via the ACE2 receptors found on human cell membranes and it’s a typical mode of most coronaviruses. (The new SARS-CoV-2 coronavirus has a plus 80 percent genomic matching to the previous SARS virus, hence it explains this property that it possesses)

However it must be noted that the ACE2 protein does not occur in large quantities in healthy people, and this partly helped to limit the scale of the SARS outbreak of 2002/2003 which infected close to 8,000 people globally.

As the findings of the new study indicates that the new SARS-CoV-2 coronavirus has a mutated gene similarly found on the HIV virus, it is also able to attack human cells via the target called furin, which is an enzyme that works as a protein activator in the human body. Typically many proteins are inactive or dormant when they are produced and have to be “cut” at specific points to activate their various functions which furin does in the human cellular pathways.

Professor Ruan Jishou and his team at Nankai University in Tianjin discovered this new property of the SARS-CoV-2 when they were doing genome sequencing of the new coronavirus found a section of mutated genes that did not exist in the original SARS virus, but were similar to those found in HIV.

Professor Ruan Jishou told Thailand Medical News via a phone interview, “This finding suggests that 2019-nCoV coronavirus may be significantly different from the SARS coronavirus in the infection pathway and has the added potency of using the packing mechanisms of other viruses such as HIV.”

The findings of the study reveal that the mutation can generate a structure known as a cleavage site in the new coronavirus’ spike protein.

Typically, a virus uses the outreaching spike protein to hook on to the host cell, but normally this protein is inactive. The cleavage site structure’s role is to trick the human furin protein, so it will cut and activate the spike protein and cause a “direct fusion” of the viral and cellular membranes.

The result findings show that when compared to the initial SARs mode of entry, this binding method is more than a 1,000 times efficient.

Another research conducted also this month, by 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.
http://www.chinaxiv.org/abs/202002.00062 (ChinaXiv.org 中国科学院科技论文预发布平台)

The study indicated that the HIV-like gene found on the new SARS-CoV-2 coronavirus was not detected on any of the other coronaviruses including the MERS, original SARS and even the Bat-CoVRaTG13, a bat coronavirus that was considered the original source of the new coronavirus with 96 per cent similarity in genes.

Professor Li told Thailand Medical News,” This is maybe why the SARS-CoV-2 is more infectious than the other known coronaviruses.”

A European a study by French scientist professor Dr Etienne Decroly at Aix-Marseille University in France, which was published in the scientific journal Antiviral Research , also found a “furin-like cleavage site” that is absent in similar coronaviruses, thus confirming the initial findings as well.
The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade. - PubMed - NCBI

The new findings is bringing scientists and researchers towards understanding how the new coronavirus behaves and how it makes us ill plus helps in developing treatment protocols. Experts’ perception of the new coronavirus has changed dramatically over the past few weeks.

The link to the furin enzyme could shed light on the coronavirus’ evolutionary history before it made the jump to humans. The mutation, which Professor Ruan’s team terms as an “unexpected insertion”, could come from many possible sources such as a coronavirus found in rats or even a species of avian flu.

Initially, the new coronavirus was not considered a major threat, with the Chinese Centres for Disease Control and Prevention saying there was no evidence off human-to-human transmission. But this was later invalidated. Then it was said that it was not airborne, this too has become invalidated. Also came expert claims that the virus only had a 14 day incubation period and that it could only survive on surfaces for a few hours, all this have become invalidated.

As of today, Saturday 29 February 2020 we have almost close 90,000 infected cases worldwide, almost 3,000 deaths and more than a million suspected cases in a time span of about 9 weeks since the coronavirus was first detected.

Thailand Medical has been carefully studying and monitoring reports on various genomic sequencing studies to monitor the mutations of the coronavirus and almost all are proving that while the coronavirus is evolving with certain codon changes (no genetic or genomic expert knows what is these significance of these minute codon changes taking place as it passes from human to human, but we can safely assume that the virus is learning and adapting smartly).

However no major mutations have taken place as in the case of most typical coronaviruses when they replicate and lead to their inefficiency and eventual demise as in the case of the original SARS, these new coronavirus is extremely stable in transmissions and replications and is in fact becoming more virulent, indicating we are dealing with a strain that is going to be with us for a longtime.

It is also important for all experts to note that the coronavirus has a 96 percent match to the Bat-CoVRaTG13 coronavirus versus an approximate 82 per cent match to the original SARS coronavirus. Shifting a focus from the original SARS coronavirus which many experts tend to focus on when making doing studies and comparisons to instead the Bat-CoVRaTG13 coronavirus might also reveal more details about the new SARS-CoV-2 as these bat viruses have evolved over time and possess many unique properties that we have yet to understand.

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.

https://www.thailandmedical.news/news/breaking-latestcoronavirus-research-reveals-that-the-virus-has-mutated-gene-similar-to-hiv-and-is-1,000-times-more-potent- (BREAKING! LatestCoronavirus Research Reveals That The Virus Has Mutated Gene Similar To HIV and Is 1,000 Times More Potent. - Thailand Medical News)
 
Where are you getting "Full damage to show YEARS after infection like HIV" in your thread title? From the second article you posted? I didn't see anything in the first study suggesting this. Maybe I missed it?
 
This article makes it easier to understand.
If you take some time to read the scientific studies in the references, you'll realize how scary this one is.

It's actually a NEUROVIRUS.
It attacks the CNS (Central Nervous System).
As such, many wonder if it never actually leaves the body, it just goes dormant again to reappear months or years later.
Scary.



4 Clues That SARS-CoV-2 Invades the Brain
[updated 26/3/20] “They’re just not thinking that the brain could be the site of the problem,” says a neuropathologist.

First appearing in Wuhan, China in December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) — that causes COVID-19 — is now a pandemic. As the name implies, SARS-CoV-2 is characterized as a lethal respiratory infection.

But “increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases,” Dr. Tsutomu Hashikawa from Riken Brain Science Institute, Japan, and his colleagues Dr. Yan‐Chao Li and Dr. Wan‐Zhu Bai from China, wrote in a 2020 review published in Medical Virology.
The paper was titled “The neuroinvasive potential of SARS‐CoV2 may be at least partially responsible for the respiratory failure of COVID‐19 patients.” And it hints at 3 reasons why SARS-CoV-2 can invade the nervous system or, more specifically, the brain.

Hint 1: Evolutionary Relatedness
Bioinformatics analyses show that SARS-Cov-2 belongs to the same evolutionary clade — βCoV — as SARS-CoV and MERS-CoV.

Evolutionarily-related microbes — or any organisms for that matter — always bear functional similarities. To illustrate, they are all lethal respiratory diseases that show similar clinical symptoms and mechanisms of infection — such as neuroinvasiveness.
Indeed, all previous types of coronaviruses — SARS‐CoV, MERS‐CoV, HCoV‐229E, HCoV‐OC43, mouse hepatitis virus, and porcine hemagglutinating encephalomyelitis coronavirus (HEV) — are known to be neuroinvasive.

So, chances are that SARS-CoV-2 can invade neurons as well.


Hint 2: Receptor Distribution
To infect a cell, the virus must first attach to a receptor on that cell surface. This is a basic requirement for all viruses; no exceptions exist as of now. Curious about why our cells have receptors for the entry of viruses?

SARS‐CoV-2 enters the host cell via a receptor called angiotensin-converting enzyme 2 (ACE2) — exactly like SARS-CoV. Obviously, ACE2 is expressed on the cell surface of the human respiratory tract. But ACE2 is also present in the brain at lower levels.

It should be noted that the presence of receptors doesn’t confirm an infection. The small intestinal cells, for instance, do have ACE2 receptors on their surface but SARS-CoV doesn’t infect them. Why? Nobody knows for sure; maybe the virus may not even travel that far or it can’t survive in the acidic conditions therein [thanks to Lanu Pitan who suggests the latter example].

Nonetheless, in the early 2000s, several research groups [1,2,3] have discovered the presence of SARS-CoV particles concentrated in the neurons of brain specimens from infected victims.

How did SARS-CoV enter their brains? A receptor must be involved as it’s a prerequisite for all viruses. And that receptor is most likely ACE2 — as it’s known to be expressed in the brain — that enables the entry of both SARS-CoV and SARS-CoV-2. Chances are that SARS-CoV-2 behave like SARS-CoV and might already be present in the brains of infected people.

Another 2020 review published in ACS Chemical Neuroscience written by a group of Pakistanian researchers — titled “Evidence of the COVID-19 Virus Targeting the CNS: Tissue Distribution, Host-Virus Interaction, and Proposed Neurotropic Mechanisms” — also emphasized on the significance of ACE2 receptors in the brain as a means for SARS-CoV-2 to establish a brain infection.

“In light of the high similarity between SARS‐CoV and SARS‐CoV-2, it is quite likely that SARS‐CoV‐2 also possesses a similar potential,” agreed the authors, Li and colleagues, of the other 2020 review in Medical Virology.


Hint 3: Animal Studies
In transgenic mice that have the ACE2 gene in their genome, inoculating SARS-CoV into their nose resulted in brain infection. The virus first spreads to the olfactory bulb — presumably via the olfactory nerves — and then reaches other brain areas such as the thalamus, cerebrum, and brainstem.
And other coronaviruses have also been found to invade the host brain:

MERS-CoV infected the lungs and brain — particularly the thalamus and brainstem — of transgenic mice when the virus was inhaled.
HEV 67N, another type of coronavirus, was found to invade the pig’s lungs, intestines, and brain — involving the cerebellum, cerebrum, and brainstem — via the nose and mouth.

Avian coronavirus, when inhaled by mice, infected the vagus nerve, brainstem, and lungs.

It’s not a coincidence why the brainstem is targeted. The brainstem harbours the nucleus of the solitary tract that receives sensory information from the lungs and respiratory tracts. This nucleus also sends neuronal information to the smooth muscles, glands and blood vessels in the respiratory tract.

“Such neuroanatomic interconnections indicate that the death of infected animals or patients may be due to the dysfunction of the cardiorespiratory centre in the brainstem,” Li et al. said.

And based on data on the latency time of SARS-CoV-2, it’s “enough for the virus to enter and destroy the medullary [part of the brainstem] neurons,” the authors said. “As a matter of fact, it has been reported that some patients infected with SARS‐CoV‐2 did show neurologic signs, such as headache (about 8%), nausea, and vomiting (1%).”


Hint 4: Loss of Smell [26/3/2020 update]
Throughout the world, many patients suffering from COVID-19 had reported a loss of sense of smell, that is, anosmia — as Robert Roy Britt has written in Elemental. This can either be a symptom of inflamed nasal lining or neurological damage of the olfactory system.

The possibility of the latter “is something to keep a careful eye on,” the neuropathologist, Professor Matthew Anderson at Beth Israel Deaconess Medical Center, Boston opined.

“There’s been some intriguing observations in previous studies on viruses, including coronaviruses, to show that they have the capacity to enter the nervous system.”
Further, the proposition that SARS-CoV-2 cause neurological damage to the olfactory system is consistent with how other known coronaviruses infect the brain via olfactory neurons (as discussed above).
The olfactory neurons are “connected to the olfactory bulb, via small, sieve-like, tiny openings called the cribriform plate that is located at the base of the frontal lobes of the brain,” says the senior Pakistanian researcher, Abdul Mannan Baig at Aga Khan University. This direct neuronal connection of the olfactory system bypasses the blood-brain-barrier.


What it means for us now [also see author’s note below]
[1]
If SARS-CoV-2 does infect the brain, then antiviral treatment targeting the airways should be made urgent to inhibit virus replication before it spreads to the brain during its latency period, Li and colleagues recommended.

[2] If SARS-CoV-2 spreads to the brain via the nose, like SARS-CoV, then face mask or any nasal protection for that matter, is more crucial than ever, they emphasized.

[3] If SARS-CoV-2 behaves like a typical brain virus in its ability to lie dormant in the neuronal genome, then it likely stays for life with the possibility of reactivation in the future under conditions of immunosuppression and cellular stress. “Since SARS‐CoV-2 may conceal itself in the neurons from the immune recognition, complete clearance of the virus may not be guaranteed even the patients have recovered from the acute infection,” Li et al. explained.

[4] “It is important to screen the patients for neurological signs early and late in the course of COVID-19,” Manna remarks, “as this could be life-saving in our fight against COVID-19 pandemic.” Autopsies should also be conducted to examine any signs of brain damage of COVID-19 victims. But autopsies to date only look at the lungs and not the brain.

[27/3/2020 update]
And Professor Anderson was right. There’s a new case of Covid-19 encephalitis (i.e., brain inflammation) with SARS-CoV-2 being identified as the causative agent. In brief, researchers have detected the presence of SARS-CoV-2 genes in the cerebrospinal fluid of a Covid-19 patient. This shows, for the first time, that SARS-CoV-2 has directly attacked the brain.

Author’s Note
Thanks to a kind email, it seems that the online Li et al. paper stated that “Correction added on March 17, 2020, after first online publication: Manuscript has been revised with author’s latest changes.”
Upon reading the online full text again, they deleted an entire section called “The implications of the potential neuroinvasion of SARS-CoV-2” from which the first three abovementioned points were derived. Perhaps the authors were criticized for suggesting precautions based on theoretical evidence.
I have the original full-text pdf saved. Any interested reader please feel free to email me. And thanks to those who have done so :)

 
If you read the scientific studies cited, you'll realize how scary this virus is.

Lost Smell and Taste Hint COVID-19 Can Target the Nervous System


The symptoms suggest SARS-CoV-2 might infect neurons, raising questions about whether there could be effects on the brain that play a role in patients’ deaths, but the data are preliminary.

Nearly two weeks ago, Alessandro Laurenzi, a biologist working as a consultant in Bologna, Italy, was mowing the grass in his garden when a friend stopped him and said the mower reeked of fuel. “I couldn’t smell anything at all,” he tells The Scientist. That was in the morning. A few hours later, he went to have lunch and realized he couldn’t smell the food he was about to eat and when he took a bite, he couldn’t taste it either. Within a few days, he developed symptoms of COVID-19 and called his doctor to ask if he could get tested. Because his symptoms were mild, Laurenzi says, his doctor said no.

Laurenzi had heard anecdotally that many COVID-19 patients in Italy suffered from a loss of smell, so he started reading all the scientific papers he could find to see if his anosmia and ageusia would ever abate. One of the papers, a review published March 13, mentioned that SARS-CoV-2, like other coronaviruses such as SARS-CoV and MERS-CoV, could target the central nervous system, possibly infecting neurons in the nasal passage and disrupting the senses of smell and taste.

Some of the purely respiratory symptoms that you might attribute to the disease, the inability to get air into the lungs, might actually be defects in respiration controlled by the nervous system.
—Matthew Anderson, Beth Israel Deaconess Medical Center


Reading this, Laurenzi immediately reached out to the corresponding author, Abdul Mannan Baig, a researcher at Aga Khan University in Pakistan, and asked if his symptoms were reversible. The evidence, Mannan told Laurenzi and reiterated to The Scientist, indicates they will abate, possibly because the loss of sense is caused by inflammation in the area as the body fights the virus, so those symptoms could disappear in seven to 14 days. “Let’s hope so,” Laurenzi tells The Scientist.

Documenting such peculiar symptoms is important, Mannan tells The Scientist, because the loss of smell and taste could be an early warning sign of SARS-CoV-2 infection. Based on the literature, British ear, nose, and throat doctors have now called for adults who lost those senses to quarantine themselves in an attempt to tamp down the spread of the disease, The New York Times reports. The symptoms, Mannan adds, also suggest that the virus has the ability to invade the central nervous system, which could cause neurological damage and possibly play a role in patients dying from COVID-19.

“This is something to keep a careful eye on,” says Matthew Anderson, a neuropathologist at Beth Israel Deaconess Medical Center in Boston. “There’s been some intriguing observations in previous studies on viruses, including coronaviruses, to show that they have the capacity to enter the nervous system.” It’s important that this be considered for SARS-CoV-2 and for “people to do the experiments, including autopsies, to look for signs of this damage.”

How SARS-CoV-2 might infect nerve cells
Because COVID-19 has symptoms similar to the flu, “much of the attention could get diverted towards the pulmonary aspect of SARS-CoV-2, while neural involvement may remain covert,” Mannan says. When a patient begins to exhibit severe neurological symptoms, such as a loss of involuntary breathing, it may be “too late to prevent fatalities.”

In a review article first published February 27, Yan-Chao Li of Jilin University in China and colleagues argue that if SARS-CoV-2 infects nerve cells, particularly neurons in the medulla oblongata, which is part of the brain stem that serves as the control center for the heart and the lungs, the damage could contribute to “acute respiratory failure of patients with COVID-19.”

The epidemiological evidence supports the hypothesis that neurons in the medulla can become infected with SARS-CoV-2 and contribute to a patient’s breathing problems and potential death. Li and colleagues explain that the time it takes for COVID-19 to progress from first symptoms to difficulty breathing is typically five days; patients are then admitted to the hospital roughly two days later, and a day after that put into intensive care. “The latency period is enough for the virus to enter and destroy the medullary neurons,” they write.

See “Can the Flu and Other Viruses Cause Neurodegeneration?”

SARS-CoV-2 enters human cells using a receptor called ACE2. Researchers have reported that ACE2 regulates cardiovascular function, and according to a search of protein databases, many human cell types express ACE2, including lung, heart, kidney, intestine, and brain tissue, Mannan says. There are also multiple ways that the virus could invade the central nervous system, he explains. It might circulate through the blood and then attack ACE2 receptors in the endothelia that lines blood capillaries in the brain, breaching the blood-brain barrier and invading neurons through that route. A breached blood-brain barrier could also cause brain swelling, compressing the brain stem and affecting respiration, Mannan says. The cells innervating the lungs could also become infected, making involuntary respiration more difficult.

Evidence from experiments in mice also suggest that the virus might target the nervous system through the olfactory bulb. In a 2008 study, immunologist Stanley Perlman of the University of Iowa and colleagues showed that SARS-CoV—the virus that caused the SARS outbreak that killed more than 770 people in 2003—entered the brains of transgenic mice expressing human ACE2 through neurons in the nose. The virus then rapidly spread to connecting nerve cells. The extensive nerve damage was the major cause of death, the team reported, even though low levels of the virus were detected in the animals’ lungs.


Although this has not been demonstrated, SARS-CoV-2 could potentially enter the nervous system through the olfactory bulb, as SARS-CoV does in mice.
WIKIMEDIA, PETER J. LYNCH
“Death of the animal likely results from dysfunction and/or death of infected neurons, especially those located in cardiorespiratory centers in the medulla,” the team wrote. A study with the MERS virus in mice expressing ACE2 showed a similar result, Perlman tells The Scientist. “The brain certainly can be readily infected in mice,” he notes. “Whether this occurs in humans to any great extent is really unknown, but not very likely at this point,” given how much larger rodents’ olfactory bulbs are relative to the overall size of their brains compared with humans’ and the paucity of evidence in humans.

Still, he says, the fact that COVID-19 patients have lost their sense of smell or taste is interesting because, if the virus infects the nose, it would use the exact same neurons as in the mouse studies to enter the brain. If taking this path, SARS-CoV-2 could work its way up to the olfactory mucosa, which consists of epithelium cells, blood vessels, and the axons from olfactory neurons. “This area is connected to the olfactory bulb, via small, sieve-like, tiny openings called the cribriform plate that is located at the base of the frontal lobes of the brain,” Mannan explains. Because the brain’s frontal lobes are close to the olfactory bulb where neurons may be infected, the tissue deeper in the brain could be endangered too.

Infection of the brainstem could cause changes that would affect involuntary respiration, which suggests “some of the purely respiratory symptoms that you might attribute to the disease, the inability to get air into the lungs, might actually be defects in respiration controlled by the nervous system,” Anderson says.

Implications of neurological infection by SARS-CoV-2
Mannan emphasizes that the neurological data on SARS-CoV-2, though preliminary, could be important for doctors deciding how to treat patients. Asking about neurological symptoms—loss of taste or smell, twitching, seizures—could factor into who might go into acute respiratory failure, or at least who might suffer from it soonest, and allow for more efficient triaging of patients, with a close eye kept on those with neurological symptoms. “It is important to screen the patients for neurological signs early and late in the course of COVID-19,” he says, “as this could be life-saving in our fight against COVID-19 pandemic.”

Anderson and Perlman add that postmortem examinations of the brains of patients who died from COVID-19 are essential to understanding the role nerve damage might play in the progression of the disease. Few, if any, autopsies of these patients are being done because of fear of contracting the disease, and if the autopsies are being done, it’s not likely that examiners are looking at the brain, only the lungs. “They’re just not thinking that the brain could be the site of the problem,” Anderson says, “and so that’s the really important aspect of these reviews, getting that idea out there.”

Ashley Yeager is an associate editor at The Scientist. Email her at ayeager@the-scientist.com. Follow her on Twitter @AshleyJYeager.

Lost Smell and Taste Hint COVID-19 Can Target the Nervous System
 
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