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|Michael Novakhov - SharedNewsLinksâ|
|Popova called a singular coronavirus vaccine impossible [Russia's chief epidemiologist]|
There will not be a single coronavirus vaccine in Russia, and several treatments for various population groups will be used instead. This was stated by ...
|Popova called a singular coronavirus vaccine impossible [Russia's chief epidemiologist] : Coronavirus|
|12:16 PM 6/4/2020 - Is there a connection between Covid -19 and the present "civil unrest"£ Of course, it is. These are the two consecutive parts of the same Intelligence Operation. Rightists Trump and white nationalists , and the leftist Antifa are just the covers behind which is the New Abwehr.|
Pentagon chief breaks with Trump, opposes invoking Insurrection Act hill.cm/aovwuii
Is there a connection between Covid -19 and the present "civil unrest"£ Of course, it is.These are the two planned and consecutive parts of the same Intelligence Operation. Both rightist Trump and white nationalists on the one hand, and the leftist Antifa on another are just the covers behind which is the New Abwehr.
|Antifa planned anti-government insurgency before George Floyd protests: law enforcement official|
Activists of the far-left Antifa movement began planning to foment a nationwide anti-government insurgency as early as November as the U.S. presidential campaign season kicked off in earnest, according to a law enforcement official with access to intelligence behind the shadowy group.
The radical movement has emerged as a key focus for investigators in the wake of violent protests and looting across the country after the death of George Floyd in police custody in Minneapolis, according to U.S. law enforcement officials and private security experts.
The law enforcement official would not speak on the record about Antifa’s plans as the election season heats up, but longtime analysts of the group say such a move would be entirely in character.
“Antifa’s actions represent a hard break with the long tradition of a peaceful political process in the United States,” said former National Security Council staff member Rich Higgins. “Their Marxist ideology seeks not only to influence elections in the short term but to destroy the use of elections as the determining factor in political legitimacy.”
Added Joe Myers, a former Defense Intelligence Agency official and counterinsurgency expert, “President Trump’s election and revitalization of America are a threat to Antifa’s nihilist goals. They are fomenting this violence to create havoc, despair and to target the Trump campaign for defeat in 2020.”
More generally, senior Trump administration officials and private analysts are warning that the radicals have rushed to exploit recent anti-police protests to set into motion a program of widespread civil unrest, a program that involves using the protests for looting and burning inner cities with the help of criminals and street gangs.
Far from a centrally organized movement, Antifa is a shadowy “anti-fascist” political front of loosely organized, quasi-underground activists known for wearing black-clad outfits and masks who see destructive street violence as a political tool.
In recent days, the group interspersed its operatives among protests set off by the police killing of a handcuffed Mr. Floyd.
Mr. Trump has singled out Antifa for the violent protests. The president said Monday that “in recent days, our nation has been gripped by professional anarchists, violent mobs, arsonists, looters, criminals, rioters, Antifa and others.”
White House National Security Adviser Robert O’Brien said U.S. officials are pressing for more intelligence on the group’s activities in light of the events of recent days.
“The president and the attorney general want to know from [FBI] Director [Christopher] Wray what the FBI has been doing to track and dismantle and surveil and prosecute Antifa,” Mr. O’Brien said. “And if that hasn’t been happening, we want to know what the plan is going forward.”
Mr. Myers argued that Antifa clearly meets the criteria for being labeled a terrorist and insurgent movement.
“It is employing organized violence for political ends: destruction of the constitutional order,” he said.
What makes the shadowy group unique is its willingness to use of violence, what Antifa organizers and sympathizers call “direct” action in support of the anarchist and Marxist-Leninist agenda. That often involves setting fires, looting, throwing bricks and bottles at police, and in one case the apparent use of a milkshake laced with quick-dry cement in attacking an opponent in the face.
Antifa initially was focused in West Coast cities such as Portland, Oregon, and Berkeley, California. Antifa supporters later took part in demonstrations during the inauguration of Mr. Trump in January 2017.
However, security officials said the coordinated, national-level riots inspired by Antifa in recent days are unprecedented.
In New York, a senior police official provided the first details of how radical anarchists like those with Antifa came from outside the city and intentionally incited protesters to violence.
John Miller, deputy police commissioner for intelligence and counterterrorism, told NBC New York that the radicals’ operations included organized scouts, medical teams and an arsenal of rocks, bottles and accelerants.
The material was used by hard-core activists interspersed among the protesters who would break away from larger demonstrations to commit acts of violence and vandalism.
Mr. Miller, who did not mention Antifa by name, said he has high confidence in intelligence assessment of the activities. They included strong indicators that the violent protesters had made preparations. Antifa also used encrypted communications as part of the planning.
“Before the protests began, organizers of certain anarchist groups set out to raise bail money, and people who would be responsible to be raising bail money, they set out to recruit medics and medical teams with gear to deploy in anticipation of violent interactions with police,” Mr. Miller said.
“They prepared to commit property damage and directed people who were following them that this should be done selectively and only in wealthier areas or at high-end stores run by corporate entities,” he added.
A New York City police spokeswoman confirmed Mr. Miller’s information and said the operations of the rioters included a complex network of scouts on bicycles who would move ahead of demonstrators and identify locations with minimal police presence. At those locations, extremists were able to easily vandalize or burn vehicles using Molotov cocktails.
Antifa’s leftist agenda calls for supporting so-called social justice movements. Among the liberal-left causes espoused by the group are issues of racism and police misconduct, support for Muslim minorities and backing the transgender rights movement.
“Groups of outside radicals and agitators are exploiting the situation to pursue their own separate, violent and extremist agenda,” Mr. Barr said on Sunday.
FBI counterterrorism officials have been monitoring Antifa and similar violent groups for years. In a bid to obscure its actions, Antifa has begun using cover names such as Black Lives Matter, Smash Racism, Abolish ICE and others.
The name Antifa is derived from the Moscow-based Communist International that in 1933 directed the Soviet-led Communist Party USA to form the American League Against War and Fascism. That group was patterned after Germany’s Antifascist Action — or Antifa — formed in 1932.
CPUSA leader Manning Johnson testified to Congress in 1953 that the goal of the front group was never the abolishment of fascism, but rather “the subversion and subsequent overthrow of the United States.”
“They’re organized and use Molotov cocktails and fireworks and gas to burn down our cities, especially businesses in minority neighborhoods. It’s got to be stopped,” he said.
“Antifa’s goal is nothing less than fomenting revolution, civil war and silencing America’s anti-communists,” said Mr. Higgins, a former Pentagon irregular warfare expert. “Their labeling of Trump supporters and patriots as Nazis and racists is standard fare for left-wing communist groups.”
The ideology of Antifa is at its center Marxism-Leninism, he said.
“Antifa is currently functioning as the command and control of the riots, which are themselves the overt utilization of targeted violence against targets such as stores — capitalism; monuments — history; and churches — God,” he said.
Until the riots, the FBI paid little attention to left-wing radical groups and other subversive organizations because of the overwhelming focus of people and investigative resources on the Islamic State and al Qaeda terrorist groups. Social media sites such as Facebook also say they have taken down some provocative posts by right-wing groups posing as Antifa members.
Senate Judiciary Committee Chairman Lindsey Graham, South Carolina Republican, said he is skeptical about the prominence of Antifa’s role in the recent unrest despite the administration’s concerns.
“We will try to find out how organized this violence is,” Mr. Graham said. “But I am old enough to remember 1968, and Antifa was not around in 1968, that I know of.”
Antifa also gets support from some academics. Walter F. Heinecke, a University of Virginia associate professor of education, helped secure permits for counterprotests that included Antifa and other groups in 2017 against the Unite the Right political rally for white nationalists, although Mr. Heinecke asserted that he did not knowingly back the anarchist group’s participation.
Asked whether he supports the movement, Mr. Heinecke said, “I am against fascism, so if Antifa means against fascism, then generally, yes.”
“I like to think all Americans are against fascism, and if so they are anti-fascists,” he said.
Mr. Heinecke said Mr. Trump and Mr. Barr have made no mention of white nationalists taking action against a black church.
“We don’t hear the equivalent cries from Trump and Barr about extreme right-wing agitators attempting to turn this into a race war,” he said.
“They are opportunistically looking for the Antifa as boogeyman to deflect the real issue: There is an insurrection going on in this country against the racist culture and structure.”
Harvard Divinity School Professor Cornel R. West has praised Antifa for protecting him and other protesters in Charlottesville, Virginia, in 2017.
Antifa and its supporters call its operating methods direct action.
Mark Bray, author of “Antifa: The Anti-Fascist Handbook,” argues that “militant anti-fascism” is a reasonable response to what he sees as the rise of right-wing politics.
“It is an unabashedly partisan call to arms that aims to equip a new generation of anti-fascists with the history and theory necessary to defeat the resurgent Far Right,” Mr. Bray said.
Andy Ngo, a journalist who was beaten by Antifa activists last year, has closely monitored the activities of the group. He recently wrote that the riots around the country are “glimmers of the full insurrection the far left has been working toward for decades.”
Mobilization and disinformation
The death of Mr. Floyd in Minneapolis was a pretext for launching the Antifa insurgency, he said. “In a matter of hours after the video of Floyd began circulating the internet, militant Antifa cells across the country mobilized to Minnesota to aid Black Lives Matter rioters,” he said.
Mr. Ngo said Antifa supporters have spread disinformation that it is white supremacists and nationalists who are to blame for the rioting. So far, no evidence has emerged linking right-wing extremists to the violence.
Antifa has been operating relatively unimpeded by law enforcement in recent years despite its use of violence, and many analysts credit the movement’s support and sympathy from the liberal left of American political and media establishment.
“One reason is that so many Democrat leaders have children and family members who are active participants in the Marxist movement, with many of them being members of Antifa, insofar as one can be a member,” said Mr. Higgins, the former NSC official.
Jeremiah Ellison, son of Minnesota Attorney General Keith Ellison, tweeted his support for Antifa on Sunday. New York Mayor Bill de Blasio had his daughter arrested in New York with protesters, and Sen. Tim Kaine’s son Woody also was affiliated with Antifa, Mr. Higgins said.
House Speaker Nancy Pelosi, California Democrat, condemned Antifa after its activists sparked riots in Berkeley several years ago.
But in a now-deleted 2018 tweet, Mr. Ellison, then-deputy chairman of the Democratic National Committee, posted a photograph of an Antifa handbook with the statement that the manual should “strike fear in the heart of @realDonaldTrump.”
Asked about the tweet Sunday, Mr. Ellison told reporters that the tweet about Antifa was meaningless.
“It means nothing. Look, I was at a bookstore, and I saw a book,” said Mr. Ellison. “It means nothing.”
The FBI, which is in charge of countering domestic security threats posed by foreign intelligence services or domestic terrorists, has largely avoided focusing on Antifa. A search of the FBI website produces no results for Antifa.
Kenneth deGraffenreid, who was deputy national counterintelligence executive during the George W. Bush administration, said the FBI has not been engaged in effective domestic counterintelligence for years.
“The FBI has not had a meaningful domestic counterintelligence capability for many years,” Mr. deGraffenreid said. “They’ve been distracted or politically corrupted.”
An FBI spokeswoman declined to comment.
• Rowan Scarborough, Jeff Mordock and Valerie Richardson contributed to this report.
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|Antifa planned anti-government insurgency before George Floyd protests: law enforcement official|
Activists of the far-left Antifa movement began planning to foment a nationwide anti-government insurgency as early as November as the U.S. presidential campaign season kicked off in earnest, according to a law enforcement official with access to intelligence behind the shadowy group.
The radical movement has emerged as a key ...
|Former Defense Secretary Mattis Issues Stunning Rebuke Of Trump - NPR|
|Shining Light In A Black Box: Can The U.S. Slow The Flow Of Dirty Money From The Ex-U.S.S.R.£|
The United States may follow in Europe’s footsteps and create a register of beneficial owners of shell companies – putting names on massive, murky investments. Will it have an impact on illegal money flowing in from the former Soviet Union and elsewhere£
|Russia’s Putin declares state of emergency over Siberian fuel spill|
Russian President Vladimir Putin has declared a state of emergency over the spill of more than 2,000 tons of diesel fuel into a Siberian river. After a reservoir collapsed at a powerplant in the Arctic circle on Friday, a clean-up operation and a criminal investigation have been launched to unveil the circumstances over what could become the second worst environmental disaster in Russia’s history.
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|» mikenov on Twitter: Both health and law enforcement officials should be aware of the possibility for use of more than one biological agent or a combination of agents. - Medical Aspects of Biological Warfare covid-19-review.blogspot.com|
Michael Novakhov - Posts on Twitter - 250 | Page
|1:01 PM 6/3/2020 - Both health and law enforcement officials should be aware of the possibility for use of more than one biological agent or a combination of agents. - Medical Aspects of Biological Warfare|
Which Species Transmit COVID-19 to Humans£ We're Still Not Sure. | The Scientist Magazine®
|Coronavirus: Italian doctors say samples of virus getting weaker|
Italian medics say the infection - which has killed 370,000 worldwide - is much less lethal than it was and 'no longer clinically exists'.
Patients are showing much smaller amounts of the virus in their system, compared to samples taken during the peak of the crisis in March and April, they said.
Infections and deaths caused by Covid-19 have been falling in Italy for weeks. It was, at one point, the centre of Europe's escalating outbreak.
Scientific theory suggests viruses may become weaker over time in a bid to survive - if they kill or cripple all their human hosts they will run out of road.
But virologists have today cast doubt on the Italian doctors' claims, saying there is no evidence the virus is losing potency anywhere. One called them 'bulls***'.
Viruses known to have mutated in this way, such as HIV and the common cold, have been around for decades and thousands of years, respectively, while the coronavirus was only spotted in humans in December last year.
Another scientist said it was possible that the coronavirus would mutate in this way but it was dangerous to assume it was happening simply from swab samples.
The coronavirus is thought to kill around one in every 100 people who catch it and more than six million people have been diagnosed with it since January, with considerably more known to have had it but never been tested (Pictured: Medical workers process a test sample in Beijing, China)
Doctors in Italy, which has been one of the countries hit hardest by the coronavirus, say the virus has changed in the past couple of months and appears in much smaller quantities in patients' bodies (Pictured: Staff outside the Colosseum wearing protective gear)
Professor Alberto Zangrillo, head of the San Raffaele Hospital in Milan in the northern region of Lombardy, made the claim to the RAI TV channel.
Calling on politicians to get Italy back to being a normal country, he said: 'In reality, the virus clinically no longer exists in Italy.'
He said that swabs taken from patients during the last 10 days have an 'infinitesimal' - extremely small - viral load, compared to ones carried out a month ago.
The viral load is the quantity of virus that is detected in someone's swab sample - a greater load has been associated with worse symptoms.
The Italian government urged caution over the claims, warning it was far too soon to claim victory in the absence of scientific evidence.
But the head of the infectious diseases clinic at the San Martino Hospital in Genoa told reporters that he was also seeing the virus weaken.
Matteo Bassetti told the ANSA news agency: 'The strength the virus had two months ago is not the same strength it has today.
'It is clear that today the COVID-19 disease is different.'
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But leading academics today questioned the claims, which has sparked hope among thousands of people longing for an end to the pandemic.
Dr Gideon Meyerowitz-Katz, from the University of Wollongong in Australia, told MailOnline that the idea the virus has disappeared 'seems dubious'.
The epidemiologist warned Italy - which was the centre of Europe's coronavirus crisis in March - is still recording new Covid-19 cases and deaths, showing it is still a danger.
Coronaviruses are so named because their structure has jagged edges which look like a royal crown – corona is crown in Latin (Pictured, an illustration of the SARS-CoV-2 virus released by the US Centers for Disease Control and Prevention)
Italian health chiefs yesterday recorded just 355 cases, a fraction of the 6,000-plus that were being declared daily at the peak of the outbreak.
And officials announced 75 more Covid-19 deaths - significantly fewer than the 919 recorded on March 27, the darkest day in Italy's crisis.
Other experts slammed the report, with one virologist saying the SARS-CoV-2 virus has not attenuated and saying the claim was 'awful'.
HOW AND WHY CAN VIRUSES LOSE POTENCY OVER TIME£
Viruses are known to change over time because they are subject to random genetic mutations in the same way that all living things are.
These mutations can have various effects and many will only happen briefly and not become a permanent change as newer generations of viruses replace the mutated ones.
However, some of the mutations might turn out to be advantageous to the virus, and get carried forward into future generations.
For example, if a virus becomes less dangerous to its host - that is, it causes fewer symptoms or less death - it may find that it is able to live longer and reproduce more.
As a result, more of these less dangerous viruses are produced and they may go on to spread more effectively than the more dangerous versions, which could be stamped out by medication because more people realise they are ill, for example.
The mutation may then be taken forward in the stronger generations and become the dominant version of the virus.
In an explanation of an scientific study about HIV, the NHS said in 2014: 'The optimal evolutionary strategy for a virus is to be infectious (so it creates more copies of itself) but non-lethal (so its host population doesn’t die out).
'The "poster boy" for successful long-living viruses is, arguably, the family of viruses that cause the, which has existed for thousands of years.'
Dr Angela Rasmussen, based at Columbia University, tweeted: 'There is no evidence that the virus is losing potency anywhere.'
She added less transmission means fewer hospitalisations and deaths - but warned: 'That doesn't mean less virulence.'
The virulence of a virus is how dangerous the illness is but may not directly relate to how contagious it is.
Dr Seema Yasmin, an epidemiologist from Stanford University, called for the original report to be deleted, saying it was 'bulls***'.
Dr Oscar MacLean, of the University of Glasgow, said: 'These claims are not supported by anything in the scientific literature, and also seem fairly implausible on genetic grounds.
'The vast majority of SARS-CoV-2 mutations are extremely rare, and so whilst some infections may be attenuated by certain mutations, they are highly unlikely to be common enough to alter the nature of the virus at a national or global level.
'As testing efforts are scaled up across the globe, asymptomatic and mild infections which previously would not have been detected, are now much more likely to be identified. It's important not to confuse this with any weakening on the virus's part.
'Making these claims on the basis of anecdotal observations from swab tests is dangerous. Whilst weakening of the virus through mutations is theoretically possible, it is not something we should expect, and any claims of this nature would need to be verified in a more systematic way.
'Without significantly stronger evidence, no one should unnecessarily downplay the danger this highly virulent virus poses, and risk the ongoing society-wide response.'
New cases and deaths have fallen steadily in Italy, and officials are finally unwinding strict lockdown restrictions imposed to control the outbreak.
A decline in cases and deaths, however, is not proof that the virus is becoming less dangerous, but proof that the social distancing and lockdown measures have worked.
No matter how virulent a virus is, if people act to stop it spreading between them, the scale of the effect it can have on the population will be dramatically reduced.
Less human contact will automatically lead to fewer infections which will in turn result in fewer deaths.
Some viruses do lose their virulence over time, though, meaning the Italian doctors' claims are not without scientific basis.
Some viruses may do this in a bid to survive by becoming less deadly so they do not run out of people to infect.
Tourists return to Venice as lockdown eases in Italy
Viruses can only continue to spread if they have an unprotected population of people - or other hosts if they infect animals - to move through and reproduce.
An extremely deadly virus which killed everyone who caught it would run out of road because the patient would likely not infect many others if they died quickly.
All viruses change the longer they exist because of random genetic mutations which happen to all living things.
If a mutation turns out to be of benefit to the virus - for example, if being less dangerous means it can survive for longer and reproduce more - it may be that this mutated strain becomes more widespread and eventually the dominant type.
A study of HIV in 2014 found that HIV samples in Botswana seemed to show that patients had less of the virus in their blood when infected, even though the disease was more common.
In an explanation of an article about HIV, the NHS said in 2014: 'The optimal evolutionary strategy for a virus is to be infectious (so it creates more copies of itself) but non-lethal (so its host population doesn’t die out).
'The "poster boy" for successful long-living viruses is, arguably, the family of viruses that cause the, which has existed for thousands of years.'
A study published last month suggested that the coronavirus (SARS-CoV-2), which has only been known about for six months, is changing but does not appear to be getting weaker.
Dr Fang Li, from the University of Minnesota, said: 'Typically when a virus develops mechanisms to evade immune responses, it loses its potency to infect people.
'However, SARS-CoV-2 maintains its infectivity using two mechanisms.
'First, during its limited exposure time, the tip of the viral key grabs a receptor protein on human cells quickly and firmly. Second, the pre-activation of the viral key allows the virus to more effectively infect human cells.'
|German spy agency doubts US ‘China lab’ coronavirus accusations, report says|
German Chancellor Angela Merkel and U.S. President Donald Trump are seen as they pose for a family photo at the start of the NATO summit in Brussels, Belgium July 11, 2018.
Reinhard Krause | Reuters
A German intelligence report casts doubts on U.S. allegations that COVID-19 originated in a Chinese laboratory and says the accusations are an attempt to divert attention from U.S. failure to rein in the disease, Der Spiegel magazine reported on Friday.
U.S. Secretary of State Mike Pompeo said on Sunday there was “a significant amount of evidence” that the coronavirus had emerged from a Chinese laboratory, but did not dispute U.S. intelligence agencies’ conclusion that it was not man-made.
Spiegel said Germany’s BND spy agency had asked members of the U.S.-led “Five Eyes” intelligence alliance for evidence to support the accusation. None of the alliance’s members, the United States, Britain, Canada, Australia and New Zealand, wanted to support Pompeo’s claim, it said.
An intelligence report prepared for German Defense Minister Annegret Kramp-Karrenbauer concluded that the U.S. accusations were a deliberate attempt to divert public attention away from President Donald Trump’s “own failures”.
A German government spokesman was not immediately available for comment. Trump has said he has evidence the virus could have originated in a Chinese lab, but he has declined to elaborate.
U.S. deaths from the coronavirus exceeded 75,000 on Thursday, according to a Reuters tally, with mixed messages from the White House and state governments on how to slow the rate of infection.
Deaths in the United States, the epicenter of the pandemic, have averaged 2,000 a day since mid-April.
|Emergence of SARS-CoV-2 through recombination and strong purifying selection|
COVID-19 has become a global pandemic caused by the novel coronavirus SARS-CoV-2. Understanding the origins of SARS-CoV-2 is critical for deterring future zoonosis, discovering new drugs, and developing a vaccine. We show evidence of strong purifying selection around the receptor binding motif (RBM) in the spike and other genes among bat, pangolin, and human coronaviruses, suggesting similar evolutionary constraints in different host species. We also demonstrate that SARS-CoV-2’s entire RBM was introduced through recombination with coronaviruses from pangolins, possibly a critical step in the evolution of SARS-CoV-2’s ability to infect humans. Similar purifying selection in different host species, together with frequent recombination among coronaviruses, suggest a common evolutionary mechanism that could lead to new emerging human coronaviruses.
The severe respiratory disease COVID-19 was first noticed in late December 2019 (1). It rapidly became epidemic in China, devastating public health and economy. At the beginning of May, COVID-19 had spread to ~150 countries and infected over 3.3 million people (2). On March 11, 2020, the World Health Organization (WHO) officially declared it a pandemic.
The etiological agent of COVID-19 (3), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (4), was identified as a new member of the genus Betacoronavirus, which includes a diverse reservoir of coronaviruses (CoVs) isolated from bats (5–7). While genetically distinct from the betacoronaviruses that cause SARS and MERS in humans (8, 9), SARS-CoV-2 shares the highest level of genetic similarity (96.3%) with CoV RaTG13, sampled from a bat in Yunnan in 2013 (8). Recently, CoV sequences closely related to SARS-CoV-2 were obtained from confiscated Malaya pangolins in two separate studies (10, 11). These pangolin SARS-like CoVs (Pan_SL-CoV) form two distinct clades corresponding to their locations of origin: the first clade, Pan_SL-CoV_GD, sampled from Guangdong (GD) province in China, is genetically more similar to SARS-CoV-2 (91.2%) than the second clade, Pan_SL-CoV_GX, sampled from Guangxi (GX) province (85.4%).
Understanding the origin of SARS-CoV-2 may help develop strategies to deter future cross-species transmissions and to establish appropriate animal models. Recombination plays an important role in the evolution of coronaviruses (12, 13). Viral sequences nearly identical to SARS and MERS viruses were found in civets and domestic camels, respectively (14, 15), demonstrating that they originated from zoonotic transmissions with intermediate host species between the bat reservoirs and humans—a common pattern leading to CoV zoonosis (5–7). However, non-human viruses nearly identical to SARS-CoV-2 have not yet been found. In this paper we demonstrate, through localized genomic analysis, a complex pattern of evolutionary recombination and strong purifying selection between CoVs from distinct host species and that cross-species infections that likely originated SARS-CoV-2.
Acquisition of receptor binding motif through recombination
Phylogenetic analysis of 43 complete genome sequences from three clades (SARS-CoVs and bat_SL-CoVs in clade 3; SARS-CoV-2, bat_SL-CoVs and pan_SL-CoVs in clade 2; and two divergent bat_SL-CoVs in clade 1) within the Sarbecovirus group (9) confirms that RaTG13 is overall the closest sequence to SARS-CoV-2 (Fig. S1). Pan_SL-CoV_GD are the next closest viruses, followed by Pan_SL-CoV_GX. Among the bat-CoV sequences in clade 2 (Fig. S1), ZXC21 and ZC45, sampled from bats in 2005 in Zhoushan, Zhejiang, China, are the most divergent, with the exception of the beginning of the ORF1a gene (region 1, Fig. 1A). All other Bat_SL-CoV and SARS-CoV sequences form a separate clade 3, while clade 1 comprises BtKY72 and BM48-31, the two most divergent Bat_SL-CoV sequences in the Sarbecovirus group (Fig. S1). Recombination in the first SARS-CoV-2 sequence (Wuhan-Hu-1) with other divergent CoVs has been previously noted (3). Here, to better understand the role of recombination in the origin of SARS-CoV-2 among these genetically similar CoVs, we compare Wuhan-Hu-1 to six representative Bat_SL-CoVs, one SARS-CoV, and the two Pan_SL-CoV_GD sequences using SimPlot analysis (16). RaTG13 has the highest similarity across the genome (8), with two notable exceptions where a switch occurs (Fig. 1A). In phylogenetic reconstructions, SARS-CoV-2 clusters closer to ZXC21 and ZC45 than RaTG13 at the beginning of the ORF1a gene (region 1, Fig. 1B), and, as previously reported (10, 17), to a Pan_SL-CoV_GD in region 2 (Figs. 1C and S2), which spans the receptor angiotensin-converting enzyme 2 (ACE2) binding site in the spike (S) glycoprotein gene. When comparing Wuhan-Hu-1 to Pan_SL-CoV_GD and RaTG13, as representative of distinct host-species branches in the evolutionary history of SARS-CoV-2, using the recombination detection tool RIP (18), we find significant recombination breakpoints before and after the ACE2 receptor binding mortif (RBM) (19, 20) (Fig. S2A). This suggests that SARS-CoV-2 carries a history of cross-species recombination between the bat and the pangolin CoVs.
Pan_SL-CoV sequences are generally more similar to SARS-CoV-2 than other CoV sequences, with the exception of RaTG13 and ZXC21, but are more divergent from SARS-CoV-2 at two regions in particular: the beginning of the ORF1b gene and the highly divergent N terminus of the S gene (regions 3 and 4, respectively, Fig. 1A). Within-region phylogenetic reconstructions show that Pan_SL-CoV sequences become as divergent as BtKY72 and BM48-31 in region 3 (Fig. 1D), while less divergent in region 4, where Pan_SL-CoV_GD clusters with ZXC21 and ZC45 (Fig. 1E). Together, these observations suggest ancestral cross-species recombination between pangolin and bat CoVs in the evolution of SARS-CoV-2 at the ORF1a and S genes. Furthermore, the discordant phylogenetic clustering at various regions of the genome among clade 2 CoVs also supports extensive recombination among these viruses isolated from bats and pangolins.
The SARS-CoV-2 S glycoprotein mediates viral entry into host cells and therefore represents a prime target for drug and vaccine development (12, 19). While SARS-CoV-2 sequences share the greatest overall genetic similarity with RaTG13, this is no longer the case in parts of the S gene. Specifically, amino acid sequences of RBM in the S1 subunit are nearly identical to those in two Pan_SL-CoV_GD viruses, with only one amino acid difference (Q498H)—although the RBM region has not been fully sequenced in one of Guangdong pangolin virus (Pan_SL-CoV_GD/P2S) (Fig. 2A). Pangolin CoVs from Guangxi are much more divergent. Phylogenetic analysis based on the amino acid sequences of this region shows three distinct clusters of SARS-CoV, SARS-CoV-2 and bat-CoV only viruses, respectively (Fig. 2B). Interestingly, while SARS-CoV and SARS-CoV-2 viruses use ACE2 for viral entry, all CoVs in the third cluster have a 5-aa deletion and a 13-14-aa deletion in RBM (Fig. 2A) and do not infect human target cells (5, 21, 22).
Although both SARS-CoV and SARS-CoV-2 use the human ACE2 as their receptors (8, 23), they show a high level of genetic divergence (Figs. 1 and S1). However, structures of the S1 unit of the S protein from both viruses are highly similar (20, 24–26), with the exception of a loop that bends differently (Fig. 3A). The root-mean-square deviation (RMSD) between the two S proteins are 1.2Å over 174 Cα residues (24). This suggests that conformational similarity of the binding motif enables viral entry through molecular recognition of ACE2. These structural studies also thoroughly analyzed the contact residues between the S protein and human ACE2 (20, 24). Previously structural and mutagenesis studies have identified two hot-spots, K31 and K353, at the S/ACE2 interface in SARS-CoV. In SARS-CoV-2, these two hot-spots were slightly weakened due to different residues on its S protein but the loop that takes different conformations from SARS-CoV provides additional interaction that strengthens the interaction (26). Among 17 distinct amino acids between SARS-CoV-2 and RaTG13 in the RBM region (Fig. 2A), five contact sites based on the structural studies (24) are different, likely impacting RaTG13’s binding to ACE2 (Fig. 3B and Table S1). The single amino acid difference at position 498 (Q or H) between SARS-CoV-2 and Pan_SL-CoV_GD is at the edge of the ACE2 contact interface; neither Q or H at this position form hydrogen bonds with ACE2 residues (Fig. 3C). Thus, a functional RBM nearly identical to the one in SARS-CoV-2 is naturally present in Pan_SL-CoV_GD viruses. The very distinctive RaTG13 RBM suggests that this virus will not likely infect human cells efficiently. Indeed, a recent study showed that the RaTG13 pseudovirus is much less efficient than SARS-CoV-2 pseudoviruses in using ACE2 to infect cells, and this is most likely due to the L486F and Y493Q substitutions, which result in lower ACE2 binding in RaTG13 (26). Therefore, it is likely that the acquisition of a complete functional RBM by a RaTG13-like CoV through a recombination event with a Pan_SL-CoV_GD-like virus enabled it to more efficiently use ACE2 for human infection.
Three small insertions are identical in SARS-CoV-2 and RaTG13 but not found in other CoVs in the Sarbecovirus group (27, 28). The RaTG13 sequence was sampled in 2013, years before SARS-CoV-2 was first identified. It is unlikely that both SARS-CoV-2 and RaTG13 independently acquired identical insertions at three different locations in the S gene. Thus, it is plausible that a RaTG13-like virus served as a progenitor to generate SARS-CoV-2 by gaining a complete human ACE2 binding RBM from Pan_SL-CoV_GD-like viruses through recombination. Genetic divergence at the nucleic acid level between Wuhan-Hu-1 and Pan_SL-CoV_GD viruses is significantly reduced from 13.9% (Fig. 1E) to 1.4% at the amino acid level (Fig. 2B) in the RBM region, indicating recombination between RaTG13-like CoVs and Pan_SL-CoV_GD-like CoVs. Furthermore, SARS-CoV-2 has a unique furin cleavage site insertion (PRRA) not found in any other CoVs in the Sarbecovirus group (Fig. S3) (27), although similar motifs are also found in MERS and more divergent bat CoVs (29). This PRRA motif makes the S1/S2 cleavage in SARS-CoV-2 much more efficient than in SARS-CoV and may expand its tropism and/or enhance its transmissibility (20). A recent study of bat CoVs in Yunnan, China, identified a three-amino acid insertion (PAA) at the same site (30). Although it is not known if this PAA motif can function like the PRRA motif, the presence of a similar insertion at the same site indicates that such insertion may already be present in the wild bat CoVs. The more efficient cleavage of S1 and S2 subunits of the spike glycoprotein (29) and efficient binding to ACE2 by SARS-CoV-2 (20, 25) may have allowed SARS-CoV-2 to jump to humans, leading to the rapid spread of SARS-CoV-2 in China and the rest of the world.
Strong purifying selection among SARS-CoV-2 and closely related viruses
Recombination from Pan_SL-CoV_GD at the RBM and at the unique furin cleavage site insertion prompted us to examine the SARS-CoV-2 sequences within these regions. Amino acid sequences from SARS-CoV-2, RaTG13, and all Pan_SL-CoV viruses (group A) are identical or nearly identical in the region before and after the RBM and at the region after the furin cleavage site (S2 subunit), while all other CoVs (group B) are very distinctive (Fig. 4A and S4). The average of all pairwise dN/dS ratios, defined as ω, among SARS-CoV-2, RaTG13, and Pan_SL-CoV viruses at the S2 subunit is ω = 0.013, compared to the much higher values ω =0.053 in the S1 region preceding the furin cleavage site, and ω = 0.042 at the S2 subunit for all other CoVs (Fig. 4B). The much lower ω value at the S2 subunit among the SARS-CoV-2, RaTG13, and Pan_SL-CoV viruses indicates that this region is under strong purifying selection within these sequences. A plot of synonymous and nonsynonymous substitutions relative to Wuhan-Hu-1 highlights the regional differences across the region before and after the furin cleavage site (Fig. 4A): the S2 subunit is highly conserved among the SARS-CoV-2, RaTG13, and Pan_SL-CoV viruses (group A), while far more nonsynonymous mutations are observed in the rest of the CoV sequences (group B). The shift in selective pressure at the S1/S2 cleaveage site among these related viruses versus other CoVs begins near codon 368 (Fig. 4B): the two graphs show the cumulative plots of the average behavior of each codon for all pairwise comparisons in the input data, for synonymous mutations, non-synonymous mutations and indels of group A sequences and group B sequences. The non-synonymous plot shows a marked change in slope (vertical step) in the group A sequences at codon 368, but not in group B sequences. Similarly, when looking at all the dS/dN ratios (ω) for each group A sequence compared to the Wuhan-Hu-1 sequence, we see that these ratios are much lower in the 5′-end of the region, before codon 368 (nucleic acid position 1104), compared to the 3′-end, and no such difference is observed in the group B sequences (Fig. 4C).
This strong purifying selection observed in the S2 subunit of the S gene is not surprising given its role in cell entry by fusing the viral and host cell membranes (5, 19). Following the binding of RBD to the ACE2 receptor, heptad repeat regions 1 (HR1) and 2 (HR2) within the S2 subunit rearrange to form the fusion core, bringing together the viral and cell membranes for fusion and infection (Fig. S5A). Due to the mechanistic constraints for this assembly for fusion, the protein segments that take part in this assembly are well preserved (20, 31). Furthermore, some regions of the S2 subunit are covered by S1 in the trimer conformation of the spike protein (Fig. S5B). Based on the currently available, but incomplete, cryo-EM structure of the spike trimer, we estimate that 60%-65% of S2 amino acids are buried. This adds further structural constraints on changing amino acids in S2.
While hundreds of new SARS-CoV-2 sequences are added to the GISAID repertoire every day (32), we note that the RBM region currently remains highly conserved. No amino acid within 6 Angstroms of the ACE2 binding site has repeated variations, with the exception of G476S, a very rare mutation found in 8 sequences from a local cluster in Washington state, out of 6,400 total sequences from GISAID (April 13, 2020). In addition, we observe similar patterns of purifying selection pressure in other parts of the genome, including the E and M genes, as well as the partial ORF1a and ORF1b genes (Fig. S6 and S7). Interestingly, the viruses affected by purifying selection pressure varies depending on which genes are analyzed. SARS-CoV-2, RaTG13, all Pan_SL-CoV and the two bat CoVs (ZXC21 and ZC45) are under the similar purifying selection in both the E and M genes (Figs. 5A and S6). In the S2 subunit, similar purifying selection are only observed for SARS-CoV-2, RaTG13, and all Pan_SL-CoV (Fig. 5B). A few viruses including only SARS-CoV-2, RaTG13, and pangolin CoVs from Guangdong are under similar purifying selection in the partial regions of ORF1a and ORF1b (Figs. 5C and S7). Strong purifying selection pressure on SARS-CoV-2, RaTG13 and Pan_SL-CoV_GD viruses, as indicated by consistently low ω values, suggests that these complete and partial genes are under similar functional/structural constraints among the different host species. In two extreme cases, amino acid sequences of the E gene and the 3′ end of ORF1a are identical among the compared CoV sequences, although genetic distances are quite large among these viruses at the nucleic acid level (Fig. 5A and 5C). Such evolutionary constraints in many parts of the viral genome, especially at functional domains in the S gene which plays an important role in cross-species transmission (5, 12), coupled with frequent recombination, may facilitate cross-species transmissions between RaTG13-like bat and/or Pan_SL-CoV_GD-like viruses.
Frequent recombination between SARS-CoVs and bat_SL-CoVs
Previous studies using more limited sequence sets found that SARS-CoVs originated through multiple recombination events between different bat-CoVs (10, 12, 21, 33, 34). Our phylogenetic analyses of individual genes confirm this and show that SARS-CoV sequences tend to cluster with YN2018B, Rs9401, Rs7327, WIV16 and Rs4231 (group A) for some genes and Rf4092, YN2013, Anlong-112 and GX2013 (group B) for others (Fig. S8). SimPlot analysis using both groups of bat_SL-CoVs and the closely related bat CoV YNLF-34C (34) shows that SARS-CoV GZ02 shifts in similarity among different bat SL-CoVs at various regions of the genome (Fig. 6A). In particular, phylogenetic reconstruction of the beginning of ORF1a (region 1) confirms that SARS-CoVs cluster with YNLF-34C (34), and this cluster is distinctive comparing to all other CoVs (Fig. 6B). YNLF-34C is more divergent from SARS-CoV than other bat-CoV viruses before and after this region, confirming the previously reported complex recombinant nature of YNLF-34C (34) (Fig. 5A). At the end of the S gene (region 2), SARS-CoVs cluster with group A CoVs, forming a highly divergent clade (Fig. 6C). In region 3 (ORF8), SARS-CoVs and group B CoVs, together with YNLF-34C, form a very divergent and distinctive cluster (Fig. 6D). To further explore the recombinant nature of SARS-CoVs, we compared GZ02 to representative bat CoV sequences using the RIP recombination detection tool (18). We identified four significant breakpoints (at 99% confidence) between the two parental lineages (Fig. S9A), further supported by phylogenetic analysis (Fig. S9B-S9D). In addition, the two aforementioned groups of bat CoVs (shown in light brown and light blue in the trees) show similar cluster changes across the five recombinant regions, suggesting multiple events of historic recombination among bat SL-CoVs. These results demonstrate that SARS-CoV shares a recombinant history with at least three different groups of bat-CoVs and confirms the major role of recombination in the evolution of these viruses.
Of the bat SL-CoVs that contributed to the recombinant origin of SARS-CoV, only group A viruses bind to ACE2. Group B bat SL-CoVs do not infect human cells (5, 21, 22) and have two deletions in the RBM (Figs. 1E and 2A). The short deletion between residues 445 and 449, and in particular the loss of Y449, which forms three hydrogen bonds with ACE2, will significantly affect the overall structure of the RBM (Figs. 3C and 3D). The region encompassing the large deletion between residues 473 and 486 contains the loop structure that accounts for the major differences between the S protein of SARS-CoV and SARS-CoV-2 (Fig. 3A) and strengthen the interaction of the latter to ACE2 (26). This deletion causes the loss of contact site F486 and affects the conserved residue F498’s hydrophobic interaction with residue M82 on ACE2 (Fig. 3D). These two deletions will render RBM in those CoVs incapable of binding human ACE2. Therefore, recombination may play a role in enabling cross-species transmission in SARS-CoVs through the acquisition of an S gene type that can efficiently bind to the human ACE2 receptor.
ORF8 is one of the highly variable genes in coronaviruses and its function has not yet been well elucidated (5, 12, 35). Recombination breakpoints within this region show that recombination occurred at the beginning and the end of ORF8 (Fig. S10), where nucleic acid sequences are nearly identical among both SARS-CoVs and group B bat CoVs. Moreover, all compared viruses form three highly distinct clusters (Fig. 6D), suggesting that the ORF8 gene may be biologically constrained and evolves through modular recombination. The third recombination region at the beginning of ORF1a is near where SARS-CoV-2 also recombined with other bat CoVs (region 1 in Fig. 1A). This region is highly variable (5, 12) and recombination within this part of the genome was also found in other CoVs, suggesting that it may be a recombination hotspot and may factor into cross-species transmission.
There are three important aspects to betacoronavirus evolution that should be carefully considered in phylogenetic reconstructions among more distant coronaviruses. First, there is extensive recombination among all of these viruses (10, 12, 21, 33, 34) (Figs. 1 and 5), making standard phylogenetic reconstructions based on full genomes problematic, as different regions of the genome have distinct ancestral relationships. Second, between more distant sequences, synonymous substitutions are often fully saturated, which can confound analyses of selective pressure and adds noise to phylogenetic analysis. Finally, there are different selective pressures at work in different lineages, which is worth consideration when interpreting trees.
The currently sampled pangolin CoVs are too divergent from SARS-CoV-2 to be its recent progenitors, but it is noteworthy that these sequences contain an RBM that can most likely bind to human ACE2. While RaTG13 is the most closely related CoV sequence to SARS-CoV-2, it has a distinctive RBM. In addition, a recent study showed that the RaTG13 pseudovirus is much less efficient than the SARS-CoV-2 pseudovirus in using ACE2 to infect cells (26). SARS-CoV-2 has a nearly identical RBM to the one found in the pangolin CoVs from Guangdong. Thus, it is plausible that RaTG13-like bat-CoV viruses may have obtained the RBM sequence binding to human ACE2 through recombination with Pan_SL-CoV_GD-like viruses. We hypothesize that this, and/or other ancestral recombination events between viruses infecting bats and pangolins, may have played a key role in the evolution of the strain that lead to the introduction of SARS-CoV-2 into humans. It is also possible that other not yet identified hosts infected with CoVs that can jump to human populations through cross-species transmission if they can successfully infect human cells through ACE2 or other receptors. Interestingly, an analysis of 6,400 SARS-CoV-2 sequences from GISAID (Global Initiative on Sharing All Influenza Data) (36, 37) identifies only one very rare mutation, G476S that is directly in a ACE2 contact residue. It was found in a local cluster of sequences from Washington state. However, it is at the periphery of the receptor contact surface, and so may not significantly impact the virus’s receptor binding affinity.
All three human CoVs (SARS, MERS and SARS-2) are the result of recombination among CoVs. Recombination in all three viruses involved the S gene, likely a precondition to zoonosis that enabled efficient binding to human receptors (5, 12). Extensive recombination among bat coronaviruses and strong purifying selection pressure among viruses from humans, bats and pangolins may allow such closely related viruses to readily jump between species and adapt to the new hosts. Many bat CoVs have been found able to bind to human ACE2 and replicate in human cells (10, 21, 22, 38–40). Serological evidence has revealed that additional otherwise undetected spillovers have occurred in people in China living in proximity to wild bat populations (41). Continuous surveillance of coronaviruses in their natural hosts and in humans will be key to rapid control of new coronavirus outbreaks.
While the SARS and MERS originating strains have been found in civets and dromedary camels respectively (14, 15), so far, efforts to identify a similarly close link in the original pathway of SARS-CoV-2 into humans have failed. If the new SARS-CoV-2 strain did not cause widespread infections in its natural or intermediate hosts, such a strain may never be identified. The close proximity of animals of different species in a wet market setting may increase the potential for cross-species spillover infections, by enabling recombination between more distant coronaviruses and the emergence of recombinants with novel phenotypes. While the direct reservoir of SARS-CoV-2 is still being sought, one thing is clear: reducing or eliminating direct human contact with wild animals is critical to preventing new coronavirus zoonosis in the future.
Materials and Methods
All 43 CoV complete genome sequences were obtained from GenBank and GISAID (Global Initiative on Sharing All Influenza Data) (36, 37), and were selected to be representative of the diversity (Tables S2 and S3). Pan_SL-CoV_GD/P1La sequence was generated by combining Pan_SL-CoV_GD/P1L (10) with some additional sequences from the NCBI BioProject database PRJNA5732983 (11, 42) to have a maximal coverage of the complete genome sequence for analysis. A new CoV sequence from pangolin (EPI_ISL_410721) (43) was not included here as it became available after we had already completed the analyses in this study. Once it became available, we observed that it was as close to SARS-CoV-2 as the sequences we had already used and hence did not change the interpretation of our results. Whole genome sequences were first aligned using Clustal X2 (44). The alignments for all coding regions were manually optimized based on the amino acid sequence alignment using SeaView 5.0.1.
SimPlot 3.5.15 (16) was used to determine the percent identity of the query sequence to reference sequences. Potential recombinant regions among analyzed sequences were identified by sliding a 400bp-window at a 50bp-step across the alignment using the Kimura 2-parameter model. Phylogenetic trees were constructed by the maximum likelihood method using the GTR model (45), and their reliability was estimated from 1,000 bootstrap replicates. The positions of analyzed sequence regions were based on those in the reference SARS-CoV-2 Wuhan-Hu-1 (MN908947). Recombination regions and breakpoints were also analyzed using the LANL database (46) tool RIP (18) with a 400bp window. Regions between breakpoints were identified using a 99% confidence threshold.
Cumulative plots of the average behavior of each codon for all pairwise comparisons in the input data, for insertions and deletions (indels), synonymous (syn), and nonsynonymous (nonsyn) mutations and values of the ratios of the rate of synonymous nucleotide substitutions per synonymous site and nonsynonymous substitutions per nonsynonymous site (dN/dS, or ω) were obtained using the LANL database tool SNAP (47). In order to avoid counting instances where synonymous mutations were saturated, averages of all pairwise dN/dS ratios were calculated excluding pairs that yielded dS values greater than 1.
Structure modeling of receptor binding
To investigate the single mutation Q498H in RBM between SARS-CoV-2 and Pan_SL-CoV_GD, Q498 in the crystal structure of S/ACE2 complex was mutated to H498 using Chimera (48). Local energy minimization (only H498 was allowed to move) was computed using Chimera’s built-in functions. To investigate the impact of the deletion between residue 473 to 486 to the binding interface between SARS-CoV-2 and human ACE2, a homology model with the deletion was generated using I-TASSER (49). The top five best models provided by the server have Confidence Score (C-score) of 0.86, -2.33, -4.01, -4.17, and -4.49. The C-score was used to estimate the quality of the models, which should be between -5.0 to 2; the higher the value, the higher the confidence in the model (49). Based on the C-score, model 1 was used in Fig. 3D. The interaction of the RBD of RaTG13 and ACE2 was modeled on PDB 6M0J, a structure of RBD of SARS-CoV-2 in complex with human ACE2 (24) using ICM software package (50), and the mutational differences of the Gibbs free energy (Table S1) were calculated with the built-in algorithm.
This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license, which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited.
References and Notes
We thank all those who have contributed SARS-CoV-2 genome sequences to the GISAID database (https://www.gisaid.org
). We also thank Dr. Xinquan Wang from Tsinghua University for sharing the PDB 6M0J structure with us before its official release date.Funding:
EEG, BK, SG and BF acknowledge support by the Laboratory Directed Research and Development program of Los Alamos National Laboratory under project number 20200554ECR.Author contributions:
Project conceptualization: F.G., B.K., E.E.G; Structure analysis: C.X., X-P.K., S.G.; Sequence analysis: F.G., B.K., X.L., E.E.G., M.H.M., Y.C., B.F; Phylogenetic analysis: F.G., B.K., X.L., E.E.G., M.H.M., Y.C.; Recombination analysis: F.G., E.E.G., B.K., X.L., M.H.M., B.F.; Manuscript writing: F.G., B.K., E.E.G. Manuscript editing: F.G., B.K., E.E.G., X.L., C.X., X-P.K.; F.G. and B.F. supervised the project.Competing interests:
All authors declare no competing interests. All data are available in the main text or the supplementary materials.Data and materials availability:
All data needed to evaluate the conclusions in the paper are present in the paper and/or the Supplementary Materials. Additional data related to this paper may be requested from the authors.
|SARS-CoV-2 looks like a hybrid of viruses from two different species|
One of the longest-running questions about this pandemic is a simple one: where did it come from£ How did a virus that had seemingly never infected a human before make a sudden appearance in our species, equipped with what it needed to sweep from China through the globe in a matter of months£
Analysis of the virus's genome was ambiguous. Some analyses placed its origin within the local bat population. Others highlighted similarities to pangolins, which might have been brought to the area by the wildlife trade. Less evidence-based ideas included an escape from a research lab or a misplaced bioweapon. Now, a US-based research team has done a detailed analysis of a large collection of viral genomes, and it finds that evolution pieced together the virus from multiple parts—most from bats, but with a key contribution from pangolins.
How do pieces of virus from different species end up being mashed together£ The underlying biology is a uniquely viral twist on a common biological process: recombination.
In cells, recombination is a normal part of genetics. Any time two DNA molecules share extensive similarities, it's possible for them to exchange pieces. The result is a hybrid molecule: a stretch of DNA from one parental piece of DNA, followed by a stretch from the other. As a result, some of the differences between the two parent molecules get scrambled—some from each parent will end up on the final molecule.
Recombination is a normal part of the reproduction of complicated cells. If you happen to have an offspring, you've given that child a set of chromosomes that are a mix of pieces from the ones you were given by your mother and father. Recombination can also take place in simpler cells, where it has been the primary tool that we've used to engineer new or altered genes into the genome of bacteria. And, since the molecules that perform the recombination aren't especially picky about which DNA molecules they work with, DNA viruses that infect cells can sometimes recombine if more than one strain of virus infects a single cell.
Those of you who have followed the virus closely, however, may be wondering what's going on here. All of this recombination takes place between DNA molecules. But the coronavirus genome is composed of RNA. So why would any of it work there£
The answer is that it doesn't. But other processes essentially perform the same function, mixing up pieces of RNA to form distinct genetic combinations. For example, the influenza virus spreads its genome across eight different molecules, allowing cells infected by more than one strain of flu virus to produce viral particles that have a random assortment of molecules from the two strains.
Coronavirus's genome is a single, long RNA molecule, so that sort of recombination doesn't work there. But it still can recombine. The enzyme that copies the RNA genome moves down it from one end to the other, making a copy as it goes. Sometimes, however, it can stall and fall off the molecule it's copying, while still hanging on to its partially complete copy. In many cases, the copying will just be aborted. But in others, it can latch on to a new genome and use the copy to pick up where it left off.
Critically, the new molecule with which it restarts the copying doesn't have to be the one it was copying originally. It just has to be similar to the first one it copied—it doesn't have to be identical. As a result, this process can allow recombination among viruses that are relatively distantly related from an evolutionary perspective. All they have to do is infect the same host.
Now that we know recombination can take place, how would we go about looking for it£ The key here is that we now have a lot of coronavirus sequences from a lot of different hosts available in public databases. Dedicated public health researchers have even gone in and sampled dozens of bat sources to look for strains that might be capable of starting a pandemic. So, for the new analysis, the research team started with a collection of 43 different coronaviruses from a variety of species, including humans, bats, and the pangolin sequences known to be similar to SARS-CoV-2.
The basic genome analysis confirmed that SARS-CoV-2 is most closely related to a number of viruses that had been isolated from bats. But different areas of the virus were more or less related to different bat viruses. In other words, you'd see a long stretch of RNA that's most similar to one virus from bats, but it would then switch suddenly to look most similar to a different bat virus.
This sort of pattern is exactly what you'd expect from recombination, where the switch between two different molecules would cause a sudden change in the sequence at the point where the exchange took place. (You'd see this rather than differences from both parent molecules being spread evenly throughout the genome.)
But there was a notable exception to this mixing of bat viruses: the spike protein that sits on the virus's surface and latches on to human cells. Here, the researchers found exactly what the earlier studies had suggested: a key stretch of the spike protein, the one that determines which proteins on human cells it interacts with, came from a pangolin version of the virus through recombination.
In other words, both of the ideas from earlier work were right. SARS-CoV-2 is most closely related to bat viruses and most closely related to pangolin viruses. It just depends on where in the genome you look.
The other bit of information to come out of this study is an indication of where changes in the virus's proteins are tolerated. This inability to tolerate changes in an area of the genome tends to be an indication that the protein encoded by that part of the genome has an essential function. The researchers identified a number of these, one of which is the part of the spike protein that came from the pangolin virus. Of all 6,400 of the SARS-CoV-2 genomes isolated during the pandemic, only eight from a single cluster of cases had any changes in this region. So, it's looking likely that the pangolin sequence is essential for the virus's ability to target humans.
There's some good news in all of this: rumors about this being an escaped weapons experiment make little sense in terms of what the genome sequences tell us about biology. Less reassuring, however, is what the sequences tell us about the giant natural experiment that may be going on around us. And that tells us there appears to be a large number of coronaviruses that are regularly exchanging genetic information. And, while exchanges are more common among viruses that infect the same species, it's entirely possible that contributions can come from much more distantly related ones.
The authors find evidence that the viruses from different species may experience distinct selective pressure, which isn't really surprising. But that also can produce difficult-to-predict results when those viruses hop to a new species—and the difficulty will rise if they then exchange information with other viruses native to that species.
Summing this up, there seem to be myriad coronaviruses out there (including plenty we don't know about), and some species are serving as labs in which new genetic combinations are created. And, right now, we only have a very partial window into the sort of potential out there in species that have frequent contacts with humans. And some research cited by the authors suggests that humans have been exposed to at least some of these viruses (based on antibodies to them)—fortunately without a major outbreak occurring.
All of which suggests that additional pandemics are a question of when, rather than if. But, of course, that had already been suggested in the aftermath of MERS and the original SARS, and the world as a whole did remarkably little to study the risk, work toward treatments, or plan for the pandemic's arrival. We can only hope that the more obvious example of COVID-19 will change that.
|Studies suggest even mild symptoms of COVID-19 can cause severe damage to lungs, heart and brain|
Studies suggest even mild symptoms of COVID-19 can cause severe damage to lungs, heart and brain
Since there are no medications for COVID-19 infection yet, the doctors are focusing on treating the patients at the acute stage to help them recover from the infection. But as more people recover, there is also a growing need to understand the possible damage caused by the disease. So far, it has been observed that a person with severe symptoms of COVID-19 may suffer from multiple organ damage. However, various studies have shown that people presenting with mild symptoms of COVID-19 may also suffer from irreversible damage to the vital organs of the body.
Permanent lung damage from COVID-19
Studies reveal that the people presenting with severe symptoms of COVID-19 usually suffer from pneumonia as their lungs become devoid of oxygen, thus allowing fluid to fill in.
As pneumonia keeps on progressing, it gets difficult for the person to breathe which can lead to a potentially fatal condition called acute respiratory distress syndrome (ARDS). In ARDS, the lungs become severely inflamed which can eventually lead to pulmonary fibrosis, also known as scarring of the lung tissue.
In the case of people with mild symptoms, SARS-CoV-2 virus impairs the lung capacity as the affected person tends to breathe faster when they feel breathless. This makes them use the top of their chest to breathe instead of the whole of the lungs. Moreover, researchers also found that some patients also developed silent hypoxia, where the oxygen levels of their body were plummeting without any noticeable symptoms. This made the patients collapse quickly and with no warning. Even after getting discharged, these people may need to undergo long-stretched therapy sessions to recover from this damage.
Even mild symptoms can affect the heart
It has been reported in many cases that COVID-19 infection damages the heart of the people with comorbidities or the ones who suffer from severe symptoms. However, a case of heart damage due to COVID-19 was seen in a 51-year-old, otherwise healthy journalist living in London.
She presented with mild symptoms of COVID-19 initially, such as mild body ache and sore throat, but on the eighth day, she complained of heaviness in her chest. On getting an electrocardiogram (ECG), it was reported that the virus caused inflammation of her heart which further lead to myocarditis. Myocarditis is a condition where the muscles of the heart get inflamed, which reduces the ability of the heart to pump.
COVID-19 causes brain abnormalities
So far, doctors stated that patients experiencing severe symptoms of COVID-19 or those who have been hospitalized for a long time are likely to suffer from brain damage. According to a French study, published in the New England Journal of Medicine on 15th April 2020, one-third of the COVID-19 patients who got discharged suffered from a dysexecutive syndrome. In this condition, the person suffers from disorientation and is unable to respond to commands.
However, now doctors have reported that patients with mild or moderate symptoms may also suffer from some sort of brain damage. A study published in Annals of Internal Medicine in May 2020 stated that 87% of patients with mild or moderate symptoms of COVID-19 lost their sense of smell. While some doctors believed that it could be due to some inflammation or nasal congestion, others said that it could be due to the interaction of coronavirus with the nerves of the brain that help in processing scent.
This claim was supported by another study published in the journal JAMA where the researchers did an MRI of the brain of a COVID-19 patient who lost her sense of smell. The study stated that the virus had invaded some parts of the brain.
For more information, read our article on COVID-19.
Health articles in Firstpost are written by <a href="http://myUpchar.com" rel="nofollow">myUpchar.com</a>, India’s first and biggest resource for verified medical information. At myUpchar, researchers and journalists work with doctors to bring you information on all things health.
Updated Date: Jun 02, 2020 16:42:54 IST
Tags : Acute Respiratory Distress Syndrome, ARDS, Brain Damage, Coronavirus, Coronavirus Mild Symptoms, Coronavirus Outbreak, COVID-19, COVID-19 Infection, covid19, Loss Of Smell, Myocarditis, Myupchar, NewsTracker, Pneumonia
|8:37 AM 6/2/2020 - Michael Novakhov - SharedNewsLinksâ|
Michael Novakhov - SharedNewsLinksâ | InBrief |
|1/06/20 15:32 from Michael Novakhov on Twitter: To date no hantavirus disease risk has been associated with rodents of the Sciuridae family (squirrels and chipmunks) or the groups of rodents used as food sources (guinea pigs, capybara, agouti, nutria, and tepisquintle). hantavirus in ...|
Michael Novakhov - Posts on Twitter - 250 | Page
|Introductions and Early Spread of SARS-CoV-2 in the New York City Area - PubMed|
New York City (NYC) has emerged as one of the epicenters of the current SARS-CoV-2 pandemic. To identify the early transmission events underlying the rapid spread of the virus in the NYC metropolitan area, we sequenced the virus causing COVID-19 in patients seeking care at the Mount Sinai Health System. Phylogenetic analysis of 84 distinct SARS-CoV2 genomes indicates multiple, independent but isolated introductions mainly from Europe and other parts of the United States. Moreover, we find evidence for community transmission of SARS-CoV-2 as suggested by clusters of related viruses found in patients living in different neighborhoods of the city.
|6 deadly bioweapons the US Army has faced since 1969|
Few things are more frightening as a weapon than infectious diseases. The idea of a creeping, invisible death that will probably make you bleed from places you'd rather not is much worse than the idea of getting shot.
In this veteran's opinion, anyway.
In any case, it's a good thing the US Army has its Medical Research Institute of Infectious Diseases to counteract the development or weaponization of superbugs and viruses for use against the United States.
Since the 1960s, USAMRIID has been on the front lines of disease research and testing in order to keep the communists, terrorists, Mother Nature or anyone else from using biological weapons against America and its allies.
It's one of the only places in America that can handle Biosafety Level 4 viruses, the highest levels of safety containment for some of the world's deadliest diseases and toxins.
Here are just a few of the menaces USAMRIID is helping to nip in the bud before they get out of hand — or into the wrong hands.
|Outbreak Of Hanta Is Unusual|
A hantavirus outbreak killed 11 people and sickened nine others in Argentina last year in the first known case in which the respiratory illness spread from person to person, United States health officials have reported.
Scientists had previously thought that hantavirus pulmonary syndrome could sicken people only if they inhaled microscopic bits of rodent urine or feces containing the virus.
No cases of person-to-person transmission have been documented in the United States, where the viral strain that causes respiratory illness was first identified in 1993. Virtually all cases in this country were linked to exposure to the feces or urine of infected deer mice.
''We are hoping physicians will be looking for this,'' said Dr. C. J. Peters, chief of the special pathogens branch at the Centers for Disease Control and Prevention in Atlanta. ''We also will be looking for this in our central registry of cases.''
Hantaviruses are a family of viruses named for the Hantaan River in Korea, where the first strain was discovered decades ago. That strain infected about 3,000 American soldiers during the Korean War, killing 190 by destroying their kidneys.
There are dozens of strains throughout the world, but none until now have shown that they could spread from person to person, Dr. Peters said.
Hantavirus pulmonary syndrome first emerged when it killed dozens of people in the Four Corners region, where Arizona, Colorado, New Mexico and Utah meet. Since then, hantavirus has sickened 162 people in 27 states, and 76 of them have died, the centers said.
The respiratory illness starts out with flulike symptoms that worsen and can become deadly. The lungs drown in fluid and the heart slows down, sending patients into shock. About half of people infected with hantavirus die.
In the coastal town of El Bolson in southern Argentina, 18 people became sick from September to December with hardly any rodents around. In addition, two more people who had contact with El Bolson residents but never went there became ill.
A 41-year-old man was the first to get sick. In three weeks, his mother and his doctor fell ill. Four weeks after that, the doctor's wife became sick, and it spread from there. The doctor's wife traveled to Buenos Aires for medical care, and then her doctor got sick. When the daughter of the first man's maid got sick after riding in a car with her, scientists knew this was no ordinary hantavirus outbreak.
''We first thought: could the rodents get into the car£'' Dr. Peters recalled. ''The Argentines took that car apart looking for rodent nests and couldn't find anything.''
Health officials put out traps for rodents in the area where the first patient lived and found only a few. The man had moved into a new, brick home from a wooden cabin several weeks before he got sick.
''We believe the virus ultimately came from a rodent, but it appears it may have been passed on through several persons,'' Dr. Peters said. Three of the ill were doctors who treated the hantavirus patients.
The agency in Atlanta has kept close tabs on health care workers in the United States since the disease first emerged. In 1993, blood tests of 396 workers, 266 of whom were exposed to hantavirus patients, found that none were sick. ''There is not a single case in the United States or Canada yet where there is a smoking gun,'' said Dr. Brian Hjelle, a molecular epidemiologist at the University of New Mexico.
The only case that came close in this country was in Crownpoint, N.M., in 1993 when four adults living in the same trailer got sick. But the trailer was overrun with rodents, said Dr. Fred Koster, who cared for the first hantavirus patients in whom the disease was diagnosed in New Mexico. ''We have to ask ourselves, why is Argentina's virus different from ours£'' Dr. Koster said. ''That simply remains a puzzle.''
|Wild rats, laboratory rats, pet rats: Global seoul hantavirus disease revisited — UTMB Health Research Expert Profiles|
Recent reports from Europe and the USA described Seoul orthohantavirus infection in pet rats and their breeders/owners, suggesting the potential emergence of a “new” public health problem. Wild and laboratory rat-induced Seoul infections have, however, been described since the early eighties, due to the omnipresence of the rodent reservoir, the brown rat Rattus norvegicus. Recent studies showed no fundamental differences between the pathogenicity and phylogeny of pet rat-induced Seoul orthohantaviruses and their formerly described wild or laboratory rat counterparts. The paucity of diagnosed Seoul virus-induced disease in the West is in striking contrast to the thousands of cases recorded since the 1980s in the Far East, particularly in China. This review of four continents (Asia, Europe, America, and Africa) puts this “emerging infection” into a historical perspective, concluding there is an urgent need for greater medical awareness of Seoul virus-induced human pathology in many parts of the world Given the mostly milder and atypical clinical presentation, sometimes even with preserved normal kidney function, the importance of simple but repeated urine examination is stressed, since initial but transient proteinuria and microhematuria are rarely lacking.
|Koreans rush to get rodent bile|
Koreans rush to get rodent bile
“It was to the point where we couldn’t get any other work done,” explained Jeon Hong-won, an official on the office’s Nutria Extermination Team. “Throughout the day, people were asking me how to trap the animal and whether their bile was up for sale.”
They had every reason.
In a joint study by Gyeongsang National University in Jinju, South Gyeongsang, and the Nakdong River Basin Environmental Office, the rodent’s bile was recently found to have a higher percentage of ursodeoxycholic acid (UDCA) than that of a bear’s, prompting what now seems to be a rush to get ahold of the species.
UDCA is known to be effective for treating liver ailments, especially primary biliary cholangitis (PBC).
According to the research, a nutria’s bile is 43.8 percent UDCA, higher than that of an American black bear (38.8 percent), a brown bear (18.6 percent) or a badger (4.5 percent).
What many seem to have overlooked, however, was that the substance is nowhere near being edible.
Prof. Yeon Seong-chan of Gyeongsang National University, who participated in the research, warned that consuming a nutria’s bile can cause serious parasitic infections.
The Korean government encourages nutria hunting with a 20,000 won (about $17) bounty for each catch, but said it would strictly prohibit nutria farming due to such health concerns. Anyone who violates the law prohibiting the trade, storage or breeding of nutria is subject to a maximum fine of 20 million won.
The national nutria control program is aimed at alleviating the damage they cause to wetlands.
According to descriptions from the Washington Department of Fish & Wildlife, nutria rodents are semi-aquatic, native to southern parts of South America and three times the size of muskrats. Adult nutria are about 24 inches long from nose to tail, with the tail itself being 12 to 16 inches long.
Rodents such as nutria, rabbits, hares, voles, muskrats and beavers are some of the species that can be infected with the bacterial disease tularemia. Tularemia may be transmitted to humans if they drink contaminated water, eat undercooked, infected meat, or allow an open cut to come into contact with an infected animal.
BY KANG CHAN-SU [[email protected]]
|9:11 AM 5/31/2020 - The Disease X-19 Hypothesis: Disease X-19, presently designated as "Covid-19" is the complex and long standing, about 2-3 years duration, combination of the biological and the informational warfare, conceived, operationalized, and managed by the New Abwehr, to commemorate the 75-th anniversary of the end of the WW2.|
The Hypothesis of the Disease X-19 as the New Abwehr Intelligence Operation and the new type of the combined Biological - Informational Warfare
Disease X-19, presently designated as "Covid-19" is the complex and long standing, about 2-3 years duration, combination of the biological and the informational warfare, conceived, operationalized, and managed by the New Abwehr, to commemorate the 75-th anniversary of the end of the WW2.
It started in 1917, and is the direct sequel of the Operation Trump: the managed and manipulated election of Donald Trump as the US President. The Russian Jewish Mafia are the foot soldiers and the immediate executors for the New Abwehr in both operations.
Disease X-19 is the combination biological weapon. The main and the most deadly part of it is the Hantavirus Infection, transmitted by rodents, with the "novel Coronavirus", Sars-Cov-2 as the second part and the cover, designed to facilitate the infectivity of the main Hantavirus part, and to make the attempts to arrive at the correct diagnosis confusing and more difficult.
The emergence of the Disease X-19 Pandemic was promoted by the unprecedented and orchestrated mass media campaign, controlled by the New Abwehr. The initial "legend", the explaining story, was constructed around the emergence of the epidemic in Wuhan, China, and reflects the today's geopolitical underpinnings and the ease of the manipulation of the Chinese medical thinking and the public opinion.
Apparently, the Chinese epidemic was first seeded in 2017-2018 by infecting the huge and commercially competitive livestock of the domestic pigs with the Coronavirus, Hantavirus, and the African/Classical Swine Fevers, with the latter served as the manifest pathological cover for the first two infections.
About half of the Chinese pigs livestock was culled, and most likely the carcasses were not disposed of properly, providing the abundant feeds for the rats and mice, and infecting them with the pathogens listed above. It is also quite possible, and even likely, that the significant part of the infected pork and pork products were sold at the discounted prices and shipped broadly worldwide, providing the operators and the executors of the Disease X-19 future pandemic with the ready made, natural and accessible infectious material in unlimited supply.
My assumption and the part of this hypothesis is, that this infectious pork was then broadly distributed and dispersed in the major capital cities around the world, by adding them discreetly, in the sealed bags, to the street garbage piles, thus infecting the rodents with these and possibly other infectious diseases.
The recent, last 2-3 years especially, explosions of the rodent populations, including the unusually large and possibly "transgenic" rats in the major world capitals and the other large cities is the well known fact. It is logical to assume that these explosions of rat and mice populations are due to the generous feedings of the infected pork as the part of this operation and the warfare.
It appears that the clinical presentations and manifestations of the Disease X-19 are quite diverse, polymorphous, multi-system and multi-organs, and they vary in severity from asymptomatic to lethal pulmonary, kidney, and other conditions. This complex clinical picture can represent several different illnesses.
The testing and evaluations for the infections other than presumed "novel Coronavirus", the Sars-Cov-2, are not performed in the hospital settings, and the clinical diagnostic tests for Hantavirus do not exist. That is why the main culprit can be easily missed. Furthermore, the clinical pictures of the Hantavirus infections and "Covid-19" appear to be very similar, practically the same.
The summary of the Disease X-19 Hypothesis is presented in this post as the brief, general and the somewhat schematic outline. The further details, the causes and mechanisms, both the medical-epidemiological and the forensic-investigative have to be researched and elucidated further.
Michael Novakhov | 9:11 AM 5/31/2020
|6:18 PM 5/30/2020 - It is not a BAT, it is a RAT! Most definitely! Test them, investigate them, and deal with them!|
Tehran giant rats
Michael Novakhov - SharedNewsLinksâ | InBrief |
|Renal Manifestations Of The Novel Coronavirus|
Within the last 48 hours, the United States reached the solemn milestone of surpassing 100,000 lives lost from Covid-19. Sadly, community spread of this novel coronavirus continues as cases and deaths in the U.S. relentlessly rise, now reaching 1.79 million and 104,000, respectively. Multiple clinical studies have also indicated that we’re dealing with more than just a “respiratory virus”: neurological, cardiac and clotting manifestations have been documented thus far. Here, I uncover the effects of COVID-19 on the renal system, gleaning insights from three of the nation’s kidney experts.
Outside the respiratory system, the kidneys are among the most common organs targeted by SARS-CoV-2. To illustrate the magnitude of the problem, among hospital ICUs in New York City – the epicenter of Covid-19 – approximately 20-40% of intubated patients had acute kidney injury (AKI) requiring dialysis (described later). Another study conducted by Northwell Health, New York state’s largest healthcare provider, found that among 5449 patients admitted with Covid-19, 36.6% developed AKI.
What Do the Kidneys Do£
We are born with two kidneys, each made up of a million nephrons which work together to perform multiple life-sustaining tasks. One major function is to act as the body’s filtration system: kidneys remove waste products and excess fluid through the urine. In addition, according to the National Kidney Foundation, kidneys play a critical role in regulating the body's salt, potassium and acid content. Kidneys also produce hormones such as erythropoietin which promotes red blood cell production as well as other hormones that regulate blood pressure and calcium metabolism.
How Does Covid-19 Affect the Kidneys£
Covid-19 has been shown to impair renal function in several ways, ranging from poor blood flow to the formation of tiny blood clots which can clog the kidneys and prevent urine formation.
“By far the most common injury is Acute Tubular Necrosis or ATN, which happens when the kidneys do not get enough blood flow because a Covid-19-infected patient goes into shock and has very low blood pressure,” explained Herbert Lin, MD, PhD, FASN, associate professor of medicine, Massachusetts General Hospital and Harvard Medical School. Direct infection of the kidneys is also a possibility.
“There is likely a small subset of patients that have direct viral infections of the kidney but this is likely a rare event,” said Matthew Sparks, MD, Assistant Professor of Medicine, Division of Nephrology, Duke Medical Center, citing an NEJM study with “superb methodology.” In a recent paper, Dr. Sparks and colleagues emphasized that AKI can be a severe complication of Covid-19.
Unfortunately, many patients infected with Covid-19 sustained renal injuries so severe that their kidneys almost shut down completely. Dialysis, or kidney replacement therapy, is a procedure where blood is filtered by a machine to clean out the urine that builds up in the blood when the kidneys do not work well, described Dr. Lin.
At the height of the pandemic, New York City hospitals were seeing no shortage of patients requiring dialysis, according to David S. Goldfarb, MD, Clinical Director, Division of Nephrology at the NYU Grossman School of Medicine.
“A surprisingly high proportion of the people who needed ventilators to help them breath also had kidney failure that required dialysis,” recalled Dr. Goldfarb. “In fact, when everyone was talking about running out of ventilators, the medical centers in New York were worried about running out of dialysis machines for that many people.” The NYU nephrologist went on to point out that the combination of lung and kidney failure was associated with a very high mortality rate, though a few people did recover. The good news is that when most of these very sick COVID-19 patients recover, so will their kidneys.
What Should We All Know About Kidney Health£
The optimal way to care for our kidneys is by controlling our blood pressure (healthy diet, low salt, regular exercise, quitting smoking) and staying hydrated with water, not sugary beverages or alcohol. There are other methods, too.
“Avoid taking medications such as NSAIDs (e.g. ibuprofen) that can harm the kidneys if taken in excess,” reminded Dr. Lin. “And if you have diabetes mellitus, control your blood sugar as much as possible” as hyperglycemia can also cause long-term renal damage.
Dr. Sparks’ message to physicians: “Be cognizant of kidney function and other parameters such as proteinuria and hematuria in patients with COVID-19.” He also acknowledged confusion about management of common blood pressure medications such as ACE inhibitors and ARBs (angiotensin II receptor blockers): “Currently, there is no evidence that these medications alter the clinical course or lead to an increased risk of infection.”
The most sensible way to protect our kidneys, according to Dr. Goldfarb – don’t get the virus!
“Social distancing will prove effective, and wearing a mask cannot be underestimated.” Wise words rooted in long-standing public health from Dr. Goldfarb.
Other renal health considerations: patients with pre-existing chronic kidney disease will be at increased risk for AKI. In addition, depending on location and status of local hospital staffing, individuals receiving peritoneal dialysis at home may encounter disruption in delivery of PD supplies and nursing support. Kidney transplant programs will also likely be on hold given the multiple resources required including staffing.
What’s become obvious by now is that this coronavirus has triggered multiorgan damage and has catalyzed the global medical research community to examine its plethora of effects. I remain humbled by this pathogen and by sickness in general. To quote the great Canadian physician and father of modern medicine, Sir William Osler: “Medicine is a science of uncertainty and an art of probability.”