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Novel Coronavirus Defies Conspiracy Theories As Data Shows Its Coming Decline
There are first signs that the novel Cornoavirus (nCoV19) epidemic will come to an end within a month or so. An analysis from the Chinese media house Caixin provides the newest numbers (machine translated):
[O]n January 31, 2020, 2102 new cases of new coronavirus were diagnosed nationwide, 46 deaths were added, and 5019 suspected cases were added which increased by 6.1%, 7.0%, and 4.3% respectively compared with the previous day, and increased by 21.8%, 29.0%, and 23.3% respectively compared with the average of the previous three days.
There are some 12.000 recognized infected persons in total. More than 99.9% of all nCoV19 cases are in China. The growth per day is still strong but not exponential. With people now traveling less from, to and within China the epidemic will likely stay contained.
We had documented in an earlier post that neither the infectiousness nor the mortality of the novel Cornoavirus are especially severe. This New York Times graphic also explains that.
bigger
More from Caixin (machine translated):
As of January 31, the cumulative number of severe cases accounted for 15.8% of the confirmed cases, and the mortality rate (accumulated death cases accounted for the cumulative confirmed cases) has remained at the level of 2.2% for 3 consecutive days.
Both numbers are relatively low and here are the first signs that the epidemic is coming to a halt:
The current situation of the new coronavirus epidemic situation is still serious, the epidemic situation is still spreading and spreading throughout the country, and the number of newly diagnosed cases has increased. At the same time, the growth rate of confirmed cases nationwide has also shown signs of decline. The number of newly cured cases on the 30th and 31st days exceeded the number of new deaths.
The declining growth rate proves that the quite extreme quarantine measure China has taken are very effective.
New test kits for the novel coronavirus have been developed and were approved by the Chinese regulator NMPA (vid). These new kits allow new patients to be tested in just 30 minutes. People who have a normal flu can now be early on distinguished from those who have caught the virus.
The graph of new suspected cases per day (yellow) is flattening while the number of newly confirmed cases per day (red) is now linear and starts to show a slight decrease.
Source: Dxy - bigger
Unless something unforeseen happens we are now coming near to the top of the epidemic. The number of new infections per day may soon start to decrease.
All this is good news. The Global Times is already pushing for new economic measures to increase growth when the epidemic is over.
But there is also bad news in that some people use the epidemic to profit from it.
There have been a number of conspiracy stories which make totally unfounded claims that the virus is a bio weapon or that it escaped from a high security bio lab in Wuhan or was intentionally created or released by Chinese researchers. To use such fantasies to then dox a researcher is irresponsible.
The novel coronavirus is NOT a bioweapon. No military will develop a weapon that kills only 2% of those affected by it. A real bio weapon would also spread much faster.
The Wuhan Institute of Virology and the Wuhan National Biosafety Laboratory are first class medical research institutions with many global cooperation agreements. The laboratory was built after China had been hit by the SARS epidemic. It is the only one in China that has a Bio Safety Level of 4:
BSL-4 labs are rare. However some do exist in a small number of places in the US and around the world. As the highest level of biological safety, a BSL-4 lab consists of work with highly dangerous and exotic microbes. Infections caused by these types of microbes are frequently fatal, and come without treatment or vaccines. Two examples of such microbes include Ebola and Marburg viruses.
In addition to BSL-3 considerations, BSL-4 laboratories have the following containment requirements:
- Personnel are required to change clothing before entering, shower upon exiting
- Decontamination of all materials before exiting
- Personnel must wear appropriate personal protective equipment from prior BSL levels, as well as a full body, air-supplied, positive pressure suit
- A Class III biological safety cabinet
A BSL-4 laboratory is extremely isolated—often located in a separate building or in an isolated and restricted zone of the building. The laboratory also features a dedicated supply and exhaust air, as well as vacuum lines and decontamination systems.
The U.S. has at least 13 such labs. Some of those are used by the military and may be used for bio weapon research. But most are medical research facilities.
The laboratory in Wuhan is specialized on viruses that are typical for the larger area. Some of its leaders are researching why bats are not affected by the viruses that they carry and which can kill people. SARS is known to have emerged from bats. Knowing how a bat's protection mechanism works could help to create better vaccines.
To jump from those facts to unfounded speculations and to accusing the researchers of having developed the nCoV19 or of spreading it is truly nefarious.
Aside from conspiracy nutters there is one serious suggestion that the novel coronavirus may indeed be something special.
A number of Indian researchers have self-published a paper that claims that the 'building plan' of the novel coronavirus, its RNA, contains elements of the HIV-1 Aids virus RNA. The paper was NOT peer reviewed and two researchers in microbiology I have contacted have, like me, doubts about its conclusions.
The paper confirms that the novel coronavirus is related to the virus that caused the SARS epidemic:
Our phylogentic tree of full-length coronaviruses suggests that 2019-nCoV is closely related to SARS CoV [Fig 1]. In addition, other recent studies have linked the 2019-nCoV to SARS CoV.
The researchers then sequenced 6 strings which form a part of the RNA of the novel corona virus. They find that there are four short insertions that distinguish it from the SARS virus:
We then translated the aligned genome and found that these inserts are present in all Wuhan 2019-nCoV viruses except the 2019-nCoV virus of Bat as a host [Fig.S4]. Intrigued by the 4 highly conserved inserts unique to 2019-nCoV we wanted to understand their origin. For this purpose, we used the 2019-nCoV local alignment with each insert as query against all virus genomes and considered hits with 100% sequence coverage. Surprisingly, each of the four inserts aligned with short segments of the Human immunodeficiency Virus-1 (HIV-1) proteins.
The inserts in the 1387 units long string which also occur in HIV-1 have a length of 6 to 8. They are in my estimate too few and too short to make a statistically viable case. But the researchers suggest, without providing a statistical model or calculations, that these are not only significant but probably artificial:
Although, the 4 inserts represent discontiguous short stretches of amino acids in spike glycoprotein of 2019-nCoV, the fact that all three of them share amino acid identity or similarity with HIV-1 gp120 and HIV-1 Gag (among all annotated virus proteins) suggests that this is not a random fortuitous finding. In other words, one may sporadically expect a fortuitous match for a stretch of 6-12 contiguous amino acid residues in an unrelated protein. However, it is unlikely that all 4 inserts in the 2019-nCoV spike glycoprotein fortuitously match with 2 key structural proteins of an unrelated virus (HIV-1).
The math that would support the assertion that it is unlikely that short sequences in parts of nConV19 and HIV-1 amino acid strings are identical is not in the paper. I doubt that the researchers made the necessary calculations.
The researchers then show that the insertions may help to form a part of the binding structure that allows the virus to attach to a host cell. They conclude:
This uncanny similarity of novel inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag is unlikely to be fortuitous.
and
Taken together, our findings suggest unconventional evolution of 2019-nCoV that warrants further investigation.
What those researchers found is interesting. It suggests that something modified the SARS virus RNA by adding four small elements from HIV-1 to create nCoV19. If this is proven correct it might help to find a vaccine against nCoV19.
But the conclusions are in my view too strong and not substantiated enough to make them fully acceptable. While the similarities may not be 'fortuitous' they may make evolutionary sense and may have evolved through some natural process which is not 'unconventional'. If a host (a bat or human) carries the HIV-1 virus and the SARS virus might the replications of those viruses mix?
The presented paper nowhere tests or discusses that hypothesis.
The authors may well deserve more research money for the 'warranted further investigations' but that should be decided only after other experts have discussed their proposition.
I haven’t found anything definitive on whether coronaviruses, specifically, are affected by season like the regular seasonal flu. As far as I can tell, it will be seasonal and transmission will drop just like transmission of the ‘regular’ flu viruses at the end of a region’s ‘flu season’. Don’t have a any kind of authoritative source for that, just speculation. If anyone has read anything different than this, please let us know.
Random things I was wondering about the flu answered by this an obviously non-authoritative but intersting AccuWeather article:
People in the tropics don’t get the flu too much, although it’s possible – why?
There is also no real flu season in the tropics. Flu viruses are more stable in cold air and the low humidity allows the virus particles to remain in the air, according to Peter Palese, who was the lead author on a key flu study in 2007.
I live in the U.S., and our flu season starts about October, peaks around January and sometimes lasts until March. Southern hemisphere? The article (from October 2019) references Australia’s last flu season:
Australia, which is finishing its flu season, had an unusually early and initially severe season, beginning in April, two months earlier than usual, and lasting into October. However, initial dire projections leveled off as the season continued. “The overall number of cases of influenza-linked illnesses (ILI) and hospitalizations weren’t unusual in their overall size, though the timing is certainly strange,” Dr. Lewis said.
So which hemisphere gets the flu ‘first’?
Why does Australia’s flu season matter? It doesn’t. Or it does. Or maybe it does just some of the time.
“It’s too early to tell for sure, because sometimes Australia is predictive and sometimes it’s not,” Dr. Daniel B. Jernigan, director of the influenza division of the CDC, told The New York Times.
“Anecdotally, we’ve seen bad seasons in Australia presage bad seasons in the U.S., but we’ve also seen the opposite,” Dr. Lewis said. “Given the back-to-back unusual seasons we’ve seen in the last two years, I’m having trouble thinking that this season in the U.S. can again be unusually long or intense.”
Slightly more than half of the flu confirmations in the US this season have been Influenza B, but those seem to have peaked while the number of Influenza A confirmations is still rising (slightly). Graph here
I couldn’t find anything specific on Wuhan’s ‘regular’ flu season or illness numbers. If anyone has a source, please post.
The CDC has a page about past pandemics. The last one was in the 2009-2010 season:
From April 12, 2009 to April 10, 2010, CDC estimated there were 60.8 million cases (range: 43.3-89.3 million), 274,304 hospitalizations (range: 195,086-402,719), and 12,469 deaths (range: 8868-18,306) in the United States due to the (H1N1)pdm09 virus.
…
Additionally, CDC estimated that 151,700-575,400 people worldwide died from (H1N1)pdm09 virus infection during the first year the virus circulated.
…
It is estimated that 0.001 percent to 0.007 percent of the world’s population died of respiratory complications associated with (H1N1)pdm09 virus infection during the first 12 months the virus circulated.
Incidentally, (H1N1)pdm09 is by far *87%) the dominant type of influenza A this year. It’s not the exact strain that caused the 2009 pandemic because… flu viruses mutate.
Posted by: PavewayIV | Feb 3 2020 22:13 utc | 217
LIke I said previously,
The comments on SARS2 ranges from..
ignorant, stupid, willfully obtuse, in denial, to typical murkkan M,O…..blaming the victim.
Too much B.S.. , too little time.
To recap…
pr[BSL4 LAB leak] = freak accident, meaning highly unlikely.
Pr [bsl4 leak/ given that it occurs at a time of mass
exodus , at Wuhan which is an economic powerhouse, a central hub of fast rail and international air link AND happens to be the site of a BSL4 LAB, when [[[they]]] have been mounting an intensive hybrid warfare on China since Trumps’ appointment….trade war blitzkrieg, Uighur and Tibet destabilisation, provocations in SCS,
TW strairts, swine flu, SARS2 and now H7N9….]
= practically zero.
Ian Fleming says
‘I’d be damned if this isnt an enemy action’
Who might that be ?
well,
who’ has been assaulting China by covert, covert wars since 1949, thats right, all of 70 years incessant attacks, including biowarfare during the Korean war, SARS1 ?
Who’ has the motive ?
This from the horse mouse….
During the peak of HK riots,
Pelsoi
‘What a beautiful sight to behold’
Former senior adviser in the Trump and Bush administrations Christian Whiton,
“causing this crisis for the Chinese government … is good in the national interests of the US.””
http://www.informationclearinghouse.info/52253.htm
Who benefits, cui bono ?
Again from the horse mouse,
Wilbur Ross
‘This is a godsend to bring back our factories and revamp the entire supply chain’
Then there’s the ultimate insult…
‘This is a Chinese FF’,some even hinted at a Jew/Chinese joint op.
Imagine there’s a certified arsonist in JOhn’s neighborhood, he was caught red handed setting fire to John’s house , the attacks has been intensifying lately.
John’s house caught fire last night.
Any sane person would suspect the serial arsonist who hates John’s gut, only those with a sick mind would suggest that John would do this to himself, may be to claim insurance !
USA is truly the land of idiots and sick mind.
Ian Fleming
Why else do you think they keep electing producing one psycho after another to run [[[their]]] country….???
From the horse mouth…
Pompeo
WE LIE, WE CHEAT AND WE ROBBED, Thats how we make a living folks,
Mind you, the sob is actually bragging it, like its a badge of honor.
sob is at it again…
China is our central threat
When I said,
‘dont blame others, its the people stupid’
Many people protest indignantly, yet they keep coming
back to vincdicate my assertion.
Too much B.S.
Too little time,.
Posted by: denk | Feb 4 2020 5:38 utc | 223
farm ecologist @ 177
john brewster @196
Thank you for the article critical of the Indian research paper. I was hoping it would put a serious hole in the analysis, particularly given it was written by a big pharma bioinformaticist – and as the writer’s credentials do appear to check out. Except he just graduated and holds an entry level position, Ph.D. notwithstanding. He told you part but not all, and his article is not much better. I wrote this up not to criticize him, deserved or not – I was not familiar with this field until last week, and I want to check and question my own analysis. So I did with this what I have done with the Indian paper. Here you go:
Author’s note: I have a Ph.D. in bioinformatics, and am a principal data scientist at a major pharmaceutical company. [Dude – you just graduated.] This paper isn’t directly in my wheelhouse, but it’s pretty close. [Not in comparison to the credentials of the people who wrote the paper.]
This has led many to credulously [Gratuitous adjective] assume that this is evidence, or even a strong indication, that 2019-nCoV was engineered from its bat ancestor by humans inserting HIV sequences…An analysis of the paper clearly [!?!] reveals that…
• There is nothing remarkable about the fact that 2019-nCoV’s sequence diverges from its nearest known relative, or that its unique sequences are conserved among cases of 2019-nCoV. [Nobody said there was.]
• The sequence matches with HIV are very short [Complete functionality was transferred in each of the four cases and each is as it appears in HIV-1.] and appear in hypervariable regions of both virus, and similar overlaps are seen between 2019-nCoV sequences and many other organisms. [Hypervariable regions are where one would presumably perform a splice as it would be easier there. Similar overlaps are seen anywhere there is genetic material.]
• The unique biological properties that HIV sequences could theoretically impart to another virus are completely missing from 2019-nCoV [Like infection and mortality?], and 2019-nCoV has no unique clinical properties that are outside what is known to be possible for a coronavirus. [Again, it doesn’t have to be an effective bioweapon to have been engineered and it could have been engineered during a research process, but more importantly we obviously do not know the unique clinical properties of 2019-nCoV just yet.] [Note – the big four bullet points are made after the proverbial foregone conclusion was stated, and the points in the original study are not addressed at all.]
The virus has a close 96% sequence overlap to a naturally occurring bat coronavirus, and coronaviruses have been known to jump from bats to humans by way of intermediates before, like the SARS coronavirus. The differences between the genome sequences, including the ones identified by the Indian study, are in variable regions of the genome that we’d expect to differ, and the 4% difference in the genomes is hard to call as “high” or “low,” given that we don’t know exactly which bats the 2019-nCoV strain came from or when it diverged from its closest known ancestor. [He actually made the argument that because 96% is a naturally occurring bat coronavirus and 4% changes in DNA are not unusual (fair assumption but we don’t know much about bat coronavirus) there’s no reason to suspect this is bioengineered. He ignored almost every aspect of the original article’s reasoning as to why the coronavirus is suspect, and his argument is based on the given fact that the base is a bat coronavirus which is equally true (or not) whether engineered or naturally occurring. He hasn’t made a relevant argument regarding the original article. There’s a tendency to argue the Indian researchers needed to prove the inserts are definitely coming from HIV-1 and definitely not coming from someplace else or at least perform the statistical analysis to show how likely or unlikely that is, while they are simply pointing to the stacking of the probabilities being unrealistically beyond coincidence.]
Very short sequences are not really what pBLAST was designed for, especially not when searching huge databases. Looking through three million viral genomes for a sequence that short means you’re bound to find something, and other scientists have pointed out in the hours since the Indian paper was posted that similar overlaps, just as strong, may be found in a wide variety of viruses, and also bacteria, protists, fungi, fruit flies, and plants. [This sounds great, but again, it doesn’t address the aspects that are low probability in nature, upon which the researcher’s reflections were based. It addresses other aspects of what is observed and notes these aspects are not low probability in nature.]
The overlap to HIV is not to a “characteristic” HIV region that is conserved among HIV, but to particular samples (in fact, three different ones from three different countries). They’re just the flotsam and jetsam of variable regions generating a lot of different sequences which get picked up in mass sequencing efforts, not a smoking gun. [This is the closest the second article comes to actually challenging the first article. Are the HIV-1 sections themselves really indicative of bioengineering? The argument is made that they’re three different HIV-1 segments from three different countries. This is stated with confidence although it is also stated with confidence that the segments are just “flotsam and jetsam,” a peculiar reference for such a young author to use (I wonder where on earth he might have picked that up.). These segments have functionality. If someone is trying to build something, they do not necessarily intend to put their name on it so you know who made it, and they do not need to use more material than is necessary to build it in the first place. That these are small goes to the question of whether they might not have come from someplace else – that they are small and could have come from someplace else does not negate the chance they were deliberately spliced in. We don’t know. But that they all are part of HIV-1 (regardless of whether they might be part of something else as well), all show up at the same time, in the same place, to do the same sort of thing…is the supermarket analogy. None of that is addressed in this article.
Parisian Guy @ 213
It doesn’t look like there’s any reliable information about what happened first. Even if everyone had contact with the seafood market, it could have been engineered and gotten to the seafood market after that. The thesis of the Indian paper is that it is engineered, not by whom, or when or where or for what purpose. I think they did a good job of explaining it, and the politeness and softness of the message were likely intentional given the obvious controversy it would generate, which it did. I contacted one member and I have not yet heard back. I keep waiting for the elements of their argument to be addressed and picked apart but the counter arguments are all tangential or unrelated, or just not clear enough for someone of my limited background. Meanwhile the news is getting slowly, incrementally worse.
Posted by: Bruce | Feb 4 2020 6:47 utc | 224
Bruce@227, Jackrabbit, Dave –
I understand the criticism of the 2020 Pradhan paper, but it finally clicked (in my simian brain) how unusual (unfortuitous) that the four S-protein segment insertions really are. Maybe I got this wrong:
1) They’re all in different places on the S-protein, rather than in a continuous segment.
2) The chances are pretty remote that ANY random set of two or three, much less four small inserts somewhere along the S-protein would leave it functional AT ALL. It would be expected that such a set of inserts would deactivate it or otherwise alter its function for the worse.
3) These new four inserts incredulously leave the S-protein’s existing function perfectly intact, specifically it’s critical ACE2 binding affinity (same as SARS). What are the chances that a random 4-segment insert doesn’t change the binding surface, but only adds previously unseen functionality to a coronavirus S-protein?
4) Those new segments 1) ADD binding affinity for human white blood cells (T-cells) at the CD4 site, ADD the capability to invade and corrupt T-cell functionality to make it produce yet more coronavirus, and CREATES a high affinity binding site for a chemokine co-receptor like CXCR4 and/or CCR5.
The paper’s authors describe the four inserts relation to HIV, but (from what I read) its nearly impossible for those four particular segments to have been produced naturally by some mutation with HIV or anything else and miraculously produce such an enhanced S-protein.
To your point, Bruce:
“The unique biological properties that HIV sequences could theoretically impart to another virus are completely missing from 2019-nCoV [Like infection and mortality?], and 2019-nCoV has no unique clinical properties that are outside what is known to be possible for a coronavirus.”
Those sequences’ theoretically imparted unique biological properties ARE there, according to The Lancet in this article:
Are Pradhan et. al.’s findings right or wrong? If correct, the virus should be able to invade human CD4 T cells and result in corresponding clinical features. A paper published in The Lancet on Jan. 24, 2020 by Professor Chaolin Huang from Jin Yin-tan Hospital, Wuhan, China, et. al., reviewing “Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China” supports Pradhan et. al’s conclusions.
…
Although low white blood cell counts are common in viral infections, it is surprising that 63 percent of all infected patients and 85 percent of those admitted to the ICU had lymphopenia with lymphocyte counts <1·0 × 109/L. In a study on SARS published March 2004 by C.M. Chu et. al. in the journal Thorax, the mean lymphocyte count was often reported as normal.
On Jan. 22, 2020, two clinical guidelines for the diagnosis and treatment of Wuhan 2019-nCoV were posted on China websites. One is “Quick Guide for the Diagnosis and Treatment of New Coronavirus Pneumonia” authored by the expert group of Tongji Hospital, and the other is “Instructions for Handling 2019 New Coronavirus” from the Wuhan Union Hospital of Tongji Medical College of Huazhong University of Science and Technology. The first guideline clearly points out a “progressive lymphocyte reduction” while the second guideline highlights “the importance of monitoring the absolute value of lymphocytes.” (emphasis added)
Therefore, the observed lymphocyte reduction must be of clinical significance in a certain proportion of patients. CD4 positive T lymphocytes constitute a major fraction of all lymphocytes. Although not a routine test for patients with coronavirus infection, perhaps monitoring CD4 cell counts would be helpful in 2019-nCoV patients.
nCoV attacks lymphocytes reducing counts UNLIKE SARS or other coronaviruses. How about the CXCR4 and/or CCR5 and resulting cytokine storm and respiratory distress?
Another clinical feature of patients infected with 2019-nCoV is the high levels of serum cytokines and chemokines, which is defined as a cytokine storm (Huang et al 2020 Lancet). This is consistent with the observation from Pradhan et al. that the 2019-nCoV S-protein inducing structural rearrangements in GP120, creating a high affinity binding site for a chemokine co-receptor such as CXCR4 and/or CCR5. It is well known that activating T cell surface receptors can cause a cytokine storm. Cytokine storms have potential to create significant damage to organs and bodily tissues. If a cytokine storm occurs in the lungs, for example, immune cells such as macrophages and fluid may trigger tissue damage that results in acute respiratory distress and possible death.
Sounds like the result of those unique biological properties since doctors are distinguishing nCoV presentation with what they have seen in SARS.
Improbable for this mutation to have occurred naturally. And if I was and evil bioweapons engineer/scientist trying to ‘enhance’ SARS, I might just look for 1) someplace insert a few segments in the spike protein without screwing it up, and 2) something particularly nasty to insert in those segments, like gp120 and gag from HIV.
And it occurs to me that you all have probably already concluded as much in earlier posts – it all just flew over my head. Sorry!
Posted by: PavewayIV | Feb 4 2020 18:00 utc | 234
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