Are the antiVaxers already relatively immune?

As delta, omicron and god knows what other Greek letter variant of the pandemic virus marches through our population, it is time to find out how many of the unvaccinated have actually been infected asymptomatically.  It could well be most of them.  Studies done July 2020, a year and a half ago in New York State (before we even had vaccines) showed high levels of antibodies to the virus.

Do distinguish what an antibody to the virus means from a positive PCR or antigen test.  A positive antibody test means you’ve been infected with the virus at some point — almost certainly it’s long gone (the footprint of the bear is not the actual bear — sounds like Zen).  A positive antigen or PCR test means that the virus is within you now.

https://www.nytimes.com/2020/07/09/nyregion/nyc-coronavirus-antibodies.html

At a clinic in Corona, a working-class neighborhood in Queens, more than 68 percent of people tested positive for antibodies to the new coronavirus. At another clinic in Jackson Heights, Queens, that number was 56 percent. But at a clinic in Cobble Hill, a mostly white and wealthy neighborhood in Brooklyn, only 13 percent of people tested positive for antibodies.

Note the date — July of 2020.   Clearly most of these people did not require hospitalization.

So it’s time to look for antibodies in the never vaccinateds (there is no point in looking at the already vaccinated as they should have them).  If the never vaccinated antibody rate is as high as I think it is (>80%), it’s time to stop the lockdowns, the maskings, and the school closures.  Why — because they’ve already been infected and fought off the virus.

It is clear that vaccination will not keep you out of the hospital.

At the end of 25 January the state of Massachusetts had 2,617 people in the hospital with COVID19, 405 in the ICU and 248 intubated.  Half of them are described by the department of Health are described as ‘fully vaccinated’  (which just means 2 shots as of their definition of September 2021 — clearly this should be updated).   Probably almost all of these are with omicron.

Although this is bad, it represents a drop from 3,192, 466 and 290 just a week ago.

I doubt that such a study will be done, but it would be useful.

Addendum  Science 28 January 2022  p. 387.  Well how wrong could I be . “A serosurvey he led in Gauteng province, home to one-quarter of South Africa’s population, showed close to 70% of unvaccinated people carried SARS-CoV-2 antibodies at the start of the Omicron wave. In the next survey, he expects that number to have gone up to at least 85%, a level that should prepare South Africa for a post-Omicron future.”

Second Addendum 28 January 2022 — Here’s a link to (and a bit more about)  the paper on which the proceeding paragraph was based — It’s not peer-reviewed yet, but it’s from the S. African Medical Research Council, so it is likely to be valid. https://www.medrxiv.org/content/10.1101/2021.12.20.21268096v1.full.pdf

The serosurvey was recent (22 October – 9 December 2021) and just before omicron hit the country.   Only 1,319 of the 7,010 people in the study were vaccinated.  An amazing 70% of the unvaccinated were seropositive (had antibodies to the pandemic virus).  As (not quite expected) the vaccinated had a higher seropositive rate (93%) but I thought it would be higher.

This is exactly the sort of study carried out in New York, where the testers went out and grabbed people to get a sample of what was actually going on in the population at large which makes it highly likely to be valid.  We should do a similar study in the USA.

What would really be terrific (but I don’t think it exists yet) would be a test for antibodies to omicron which distinguishes them from antibodies to older SARS-CoV-2 variants.

There is some evidence that vaccination protects against severe infections with omicron, so leave that to the unvaccinated, and leave the rest of us alone.

Kinetic traps and life

“It is well known that the thermodynamically stable state of proteins in a crowded environment is insoluble fibrils” [ Proc. Natl. Acad. Sci. vol. 119 pp. e2122078119 ’22 ].  However even under ideal conditions the time scale for their formation is hours to days [ Nat. Rev. Mol. Cell Biol. 15, 384–396 (2014) ].  Hopefully it’s even longer (decades) for senile plaques (abeta) neurofibrils (tau) and Lewy bodies (alpha-synuclein) to form.  The fact that equilibrium takes such a long time to reach, allows rapid synthesis and degradation of proteins to avoid their aggregation.  So we live because our proteins are trapped in a less the equilibrium (metastable) state by kinetics — e.g. a kinetic trap.

So hush, little baby, don’t you cry/transcribe

“So hush, little baby, don’t you cry” is from the lyrics of Summertime in Porgy and Bess, the first true American opera.  Although first performed in 1935, scandalously it didn’t get its Met performance until 1985.

But HUSH in this context means Human Silencing Hub which keeps invaders into our genome quiet.  One class of invader is the l1 retrotransposon, which comprises 17% of our genome (there are others).  It is not transcribed into mRNA, clearly a good thing.  Unfortunately HUSH will block some attempts at gene therapy (those putting a new gene into our genome, rather than just correcting a mutated one).

HUSH is made from 3 proteins TASOR, MPP8 and periphilin. A great paper (Nature vol. 601 pp. 440 – 445 ’22) shows how it works.  HUSH recruits an ATP dependent chromatin remodeler producing chromosome compaction (so the transcription machinery can’t get to the gene) and SETDB1, which methylates the lysine at position #9 of histone H3.  This modification binds other proteins which further compact DNA.

Why doesn’t HUSH shut everything down?  It appears to recognize transcripts longer than 1.5 kiloBases — typical of L1 which is > 5 kiloBases long.   How HUSH does this isn’t known at present.

Our genes are broken into pieces called exons (average length 237 bases) separated by introns.  L1 and all retrotransposons, don’t have them as they are reverse transcribed from cytoplasmic RNA which has had the introns removed.

So HUSH’s incredible cleverness silences a DNA sequence it (and you) have never heard of, just by its absence of introns.

 

We now understand what amyloid actually is

Lately we have received an embarrassment of riches about amyloid and the diseases it causes.  I’ll start with the latest — the structure of TDP amyloid.

I must say it is a pleasure to get back to chemistry and away from the pandemic, however briefly.  So relax and prepare to enjoy some great chemistry and protein structure.

TDP43 (you don’t to know what the acronym stands for) is a protein which binds to RNA (among other things).  It also forms aggregates, and some 50 mutations are known producing FrontoTemporal  Dementia (FTD) and/or Amyotrophic Lateral Dementia (ALS).  I saw a case as a resident (before things were worked out) and knew something was screwy because while ALS is a horrible disease, patients are clear to the end (witness Stephen Hawking) and my patient was clearly dementing.

Mutations in TDP43 occur in 5% of familial ALS.  More to the point cytoplasmic aggregates of TDP43 occur in 95% of sporadic cases of ALS (no mutations), so neurologists have been fascinated with TDP43 for years.

Back before we knew much about the structure of amyloid, it was characterized by the dyes that would bind to it (Congo Red, thioflavin etc.) and birefringence (see below).  None of this is true for the aggregates of TDP43.

Well we now know what the structure of amyloid is.  You simply can’t do better than  Cell vol. 184 pp. 4857 – 4873 ’21 — but it might be behind a paywall.

So here’s the skinny about what amyloid actually is —

 

It is a significantly long polypeptide chain  flattening  out into a 4.8 Angstrom thick sheet, essentially living in 2 dimensions.  Thousands of sheets then pile on top of each other forming amyloid.  So amyloid is not a particular protein, but a type of conformation a protein can assume (like the alpha helices, beta pleated sheets etc. etc. ).

The structure also explained why planar molecules like Congo Red bind to amyloid (it slips between the sheets).   Or at least that’s what I thought.

 

Enter Nature vol. 601 pp. 29 – 30, 139 – 143 ’22 showing that some 79 amino acids of the 414 amino acids of TDP43 flatten out into single sheet in the aggregates, with the sheets piling on top of each other.  If that isn’t amyloid, what is?

 

Where are the beta strands producing birefringence if this is amyloid.  In fact where is the birefringence? (see below). The paper says that there are 10 beta strands in the 79 amino acids, but they are short with only two of them containing more than 3 amino acids (I guess they can see beta strands by measuring backbone angles a la Ramachandran plots).  The high number of glycine mediated turns prevents beta sheets from stacking next to each other precluding the crossBeta  structure (and birefringence).

 

Why doesn’t Congo Red bind?  My idea about how it binds to other amyloids (slipping between the sheets) clearly is incorrect.

 

There are all sorts of fascinating points about the amyloid of TDP43.  The filaments derived from patients are stable to heating to 65 C.   The structure of the TDP43 fibrils derived from patients with FTD/ALS are quite different in structure from synthetic filaments made from parts of TDP43, so possibly a lot of work will have to be done again.

 

Here is some more detail on amyloid structure:

 

So start with NH – CO – CHR.  NH  CO and C in the structure all lie in the same plane (the H and the side chain of the amino acid < R >  project out of the plane).

Here’s a bit of elaboration for those of you whose organic chemistry is a distant memory.  The carbon in the carbonyl bond (CO) has 3 bonding orbitals in one plane 120 degrees apart, with the 4th orbital perpendicular to the plane — this is called sp2 hybridization.  The nitrogen can also be hybridized to sp2.  This lets the pair of electrons above the plane roam around moving toward the carbon.  Why is this good?  Because any time you let electrons roam around you increase their entropy (S) and anything increasing entropy lowers their free energy (F)which is given by the formula F = H – TS where H is enthalpy (a measure of bond strength, and T is the absolute temperature in Kelvin.

 

So N and CO are in one plane, and so are the bonds from  N and C to the adacent atoms (C in both cases).

 

You can fit the plane atoms into a  rectangle 4.8 Angstroms high.  Well that’s one 2 dimensional rectangle, but the peptide bond between NH and CO in adjacent rectangles allows you to tack NH – CO – C s together while keeping them in a 3 dimensional parallelopiped 4.8 Angstroms high

 

Notice that in the rectangle the NH and CO bonds are projecting toward the top and bottom of the rectangle, which means that in each plane  NH – CO – CHR s, the NH and CO are pointing out of the 2 dimensional plane (and in opposite directions to boot). This is unlike protein structure in which the backbone NHs and COs hydrogen bond to each other.  There is nothing in this structure for them to bond to

 

What they do is hydrogen bond to another 3 dimensional parallelopiped (call it a sheet, but keep in mind that this is NOT the beta sheet you know about from the 3 dimensional structures of proteins we’ve had for years).

So thousands of sheets stacked together form the amyloid fibril.

 

Where does the 9 Angstrom reflection of cross beta (and birefringence) come from?  Consider the  [ NH – CHR – CO ]  backbone as it lies in the 4.8  thick plane (Having studied proteins structure since entering med school in ’62, I never thought such a thing would even be possible ! ).  It curves around like a snake lying flat.  Where are the side chains?  They are in the 4.8 thick plane, separating parts of the meandering backbone from each other — by an average of 9 Angstroms.

Here is an excellent picture of the Alzheimer culprit — the aBeta42 peptide as it forms the amyloid of the senile plaque

https://pubmed.ncbi.nlm.nih.gov/27355699/#&gid=article-figures&pid=figure-7-uid-6.

You can see the meandering backbone and the side chains keeping the backbone apart.

Then Nature [ vol. 598,  pp. 359 – 363 ’21] blows the field wide open, finding 19 different conformations of tau in clinically distinct diseases. Each clinical disease appears to be associated with a distinct polymorphism.  This is also true for the polymorphisms of alpha-synuclein, with distinct conformations being seen in each of Parkinsonism, multiple system atrophy and Lewy body dementia.

In none of the above diseases is there a mutation (change in amino acid sequence) in the protein.

Henry J. Heinz claimed to have 57 varieties of pickles in 1896, but Cell [ vol. 184 pp. 4857 – 4873 ’21  ] Page 4862 claims that 24 amyloid polymorphs of alpha-synuclein have been found and structurally characterized.  Recall that alpha-synuclein amyloid is the principal component of the Lewy body of Parkinsonism  and Lewy Body disese

How did they get the 24 different conformations?  They incubated the protein under different conditions (e.g. different salt concentrations, different alpha-synuclein concentrations, different salts).

Why is this incredibly good news? 

Because it moves us past amyloid itself, to the conditions which cause amyloid to form.  Certainly, removing amyloid or attacking it hasn’t resulted in any clinical benefit for the Alzheimer patient despite billions being spent by Big Pharma to do so.

We will start to study the ‘root causes’ of amyloid formation.   The amino acid sequence of each protein is identical despite the different conformations of the chain in the amyloid. Clearly the causes must be different for each of the different polymorphs of the protein.  This just has to be true.

I hope to Hell I was wrong about China

From the South China Morning Post — 9:52pm, 15 Jan, 2022

“The Chinese capital reported its first community case of the Omicron coronavirus variant on Saturday, with local and imported infections of the strain now detected in about half of the country’s provinces and municipalities.”

https://www.scmp.com/news/china/politics/article/3163525/china-braces-omicron-variant-extends-its-reach-and-lunar-new-

If true, containment, quarantine, lockdowns and isolation are hopeless.  The quote implies that they’ve already failed.

I find this very worrisome for reasons listed in a post 12 December 2021, a copy of which is below.

The short answer is that the mainland Chinese are immunologic virgins to exposure to the variants of the pandemic virus.  Hopefully their vaccines will work better against omicron than those of the west, but there is no reason to think they will.

Is China following a Smokey the Bear policy on the pandemic?

China is following a prevent pandemic virus infection policy, just as Smokey the Bear followed a prevent forrest fires policy.  The latter didn’t work out well, as although fires were prevented for a while. However, when fires did occur, they were much much worse than the smaller ones Smokey prevented.  There was much more tinder and stuff to burn.

Actually Smokey has changed his tune slightly.

https://en.wikipedia.org/wiki/Smokey_Bear  SmokeyBear.com’s current site has a section on “Benefits of Fire” that includes this information: “Fire managers can reintroduce fire into fire-dependent ecosystems with prescribed fire. Under specific, controlled conditions, the beneficial effects of natural fire can be recreated, fuel buildup can be reduced, and we can prevent the catastrophic losses of uncontrolled, unwanted wildfire.”

Revision 14 December 2021 — China’s policy of prevention has resulted in a Chinese population which has been vaccinated using two killed virus vaccines (Sinopharm, Coronavac).  They have not had any natural infections with the virus (aside from the original cases) as far as we know given what China has allowed out.

Infection with the virus itself exposes you to all its proteins, with your immune system responding to all of them.   Western vaccines are just to the spike protein.

It tends to be forgotten that moist cases of pandemic viral infection are asymptomatic.

Given 800K deaths  from COVID19  in the USA, how can I possibly say this is good. Here’s how :>

If you had an infection with the virus, you develop antibodies.  Nowadays, everyone who is vaccinated has antibodies so there is no point in testing for them, but what were things like in the days before vaccines?

The following is from a post July/2020.

https://www.nytimes.com/2020/07/09/nyregion/nyc-coronavirus-antibodies.html–https://www.cnbc.com/2020/04/23/new-york-antibody-study-estimates-13point9percent-of-residents-have-had-the-coronavirus-cuomo-says.html.

New York State  randomly tested 3,000 people at grocery stores and shopping locations across 19 counties in 40 localities to see if they had the antibodies to fight the coronavirus, indicating they have had the virus and recovered from it. With more than 19.4 million people residents, according to U.S. Census data, the preliminary results imply that at least 2.7 million New Yorkers have been infected with Covid-19.They weren’t all hospitalized.

Here’s some work the same month from Queens — https://www.nytimes.com/2020/07/09/nyregion/nyc-coronavirus-antibodies.html

At a clinic in Corona, a working-class neighborhood in Queens, more than 68 percent of people tested positive for antibodies to the new coronavirus. At another clinic in Jackson Heights, Queens, that number was 56 percent. But at a clinic in Cobble Hill, a mostly white and wealthy neighborhood in Brooklyn, only 13 percent of people tested positive for antibodies.

So the disease has already to spread to half the population in some neighborhoods in Queens. If even 10% of them were sick that would have been 140,000 hospitalizations.  They didn’t happen.

OK, so a lot more people were infected than got sick.  Why is this good?

Enter the omicron variant of the pandemic virus.  It can evade the antibodies produced by all the current vaccines (in the West — protection against the Chinese killed viral vaccines CoronaVac and Sinopharm isn’t known yet).   Yet omicron doesn’t appear to produce severe disease. Thus far…

 

The CDC in the past week said of the 40+ omicron cases it knows about (there certainly are more out there, and more to come), there was one hospitalization (for two days) and no deaths.

Here is Dr. Fauci 12 December 2021 — “We’re getting anecdotal information … not necessarily confirmed yet, that the level of severity appears to be maybe a bit less than in the Delta. But there are a lot of confounding issues that it may be due to the underlying protection in the community due to prior infections,”

Source — https://nypost.com/2021/12/12/omicron-appears-to-evade-some-protection-from-covid-vaccines/

So the Chinese population may be sitting ducks for omicron having been given vaccines (Sinopharm, Coronavac) of unknown potency against omicron.  If their statistics are true there has been little or no natural infection with the pandemic virus in the Chinese population (which Fauci has just implicated is protective),.  Given that I have a son, daughter in law and two grandkids living in Hong Kong, I find this extremely disconcerting.

The pandemic of the ‘fully vaccinated’

At the end of 12 January ’22 the state of Massachusetts had 3,180 COVID19 patients in hospital.  484 were in the ICU and 278 were on respirators.  Of those 3,180, some 1,005 were ‘fully vaccinated’.  — https://www.mass.gov/info-details/covid-19-response-reporting#covid-19-interactive-data-dashboard-

Addendum 15 Jan: Thanks to MStriker for picking up the error.  1,005 above should be 1505, giving 49%.

That’s nearly 50% of the hospitalized.  This,  in Massachusetts where we believe in Science.  We’re not talking about the toothless peasantry of West Virginia.  The fully vaccinated are serious and important people; news anchors, members of congress, white house staff, not the unvaccinated riffraff we’ve heard about.  What are the faithful believers in Science of Massachusetts to do? ,

If this sounds like Schadenfreude it is.  I’ve listened and read plenty of it in the press in the past two years, with much gloating over the deaths of the unvaccinated.   .  These people died and snarkery (such as the above) is inappropriate and cruel. So let those who formerly thought they were safe worry a little (including me) and realize that science is never settled.

What can be done to restore the faith?  It would certainly be of interest to know the percentage of the fully vaccinated in the ICU or on respirators.  This might actually be evidence of some protective effect of the vaccines.

This data is certainly known to the department of health.

Also, the definition of fully vaccinated can be found (with some difficulty) on their website.  It is clearly outdated e.g. two shorts of Pfizer or the other vaccine longer than 14 days ago.  There is nothing in the definition about boosters.  The definition goes back to September 2021.

I’m sure that in the charts of all 3,180 hospitalized COVID19 patients, the presence and time of  booster administration is noted.  So the State Department has in hand evidence for the efficacy/nonefficacy of boosters, to prevent hospitalization, and when in hospital to prevent serious complications of COVID19.  This should be released immediately.

Sometimes your licked before you’ve even started

The first issue of Neuron for 2022 got off to a rather depressing start, with two papers stating that the die was cast before you leave the uterus.

The first concerned Huntington’s chorea a hereditary movement disorder which doesn’t begin for decades after birth (like many hereditary disorders).  Or does it?

Well over 10,000 papers have been written to figure out why mutations in the huntingtin protein produces neurodegeneration, primarily in a small set of neurons deep in the brain.

Now that we know the genetic cause, it is possible to study people with the mutation long before they get sick.  One finding is a thin tract of axons connecting the two hemispheres (the corpus callosum).

So a transgenic mouse was created with a typical huntingtin mutation (111 glutamines in a row instead of the normal 7 for the mouse).  Even in utero axons forming the corpus callosum were shorter and fewer.  This was due to defects in bundling of microtubules in the axon growth cone.  It was due to a deficiency not of huntingtin but of a microtubule binding protein called NUMA1 (Nuclear Mitotic Apparatus 1) whose function we thought we knew in the mitotic spindle.  Giving NUMA1 reversed the axonal defect (in tissue culture).   So the problems with Huntington’s chorea go back to fetal life.

Even worse, 4 human fetuses of 13 weeks gestation (presumably aborted because the parents didn’t want a child with the gene, showed also sorts of abnormalities in the developing brain Science vol. 369 pp. 771 – 772, 787 -792 ’20 ].  Read it if you wish, I found it rather creepy.

The second paper is on congenital hydrocephalus [ Neuron vol. 110- pp. 12 – 15 ’22 ].  Several parent child trios were sequenced, and damaging mutations were found in 25% of the probands.  All of them were regulators of neural stem cell fate.  So the ventricles got big (that’s hydrocephalus after all), because there weren’t enough neurons to keep them small.

Even worse, the most consistent macroscopic (e.g. visible) finding in schizophrenia is large ventricles.  Were they doomed from birth?

If that isn’t depressing enough here’s a Supreme Court Justice holding forth on COVID19 in children. “We have over 100,000 children, which we’ve never had before, in serious condition, and many on ventilators” due to the coronavirus.  Presumably the Justice believes in science as many of her party claim.

Who is Gabriel Leung and why you should very much care what he says

From today’s (5 Jan) South China Morning Post (SCMP)

“Fellow government adviser Professor Gabriel Leung, dean of the University of Hong Kong’s faculty of medicine, told a radio programme there were “probably five to 10 invisible transmission chains in the community. It’s a very alarming situation”.

Here is what Dr. Leung had to say almost two years ago to the day in the SCMP of 27 Jan 2020.

“As of a few days ago the virus had been found in 29/31 Chinese provinces. ” and “research shows self-sustaining human-to-human transmission is already happening in all major mainland cities.”

Clearly he was right 2 years ago, and widely ignored in the west.   I thought the US government had people watching China.

There were 38 cases of COVID19 in Hong Kong today.  Some of them have the omicron variant (if not all).

This is very scary as despite immunization with Sinopharm and Coronavac, the Chinese are basically immunologic virgins as they have had little exposure to the pandemic virus (Wuhan excepted).  Hopefully it will work better than the Western vaccines.  As of 4 January 2022 Massachusetts had 2,426 hospitalized cases of COVID19 of which 973 were ‘fully vaccinated’ e.g. 40% of cases– not sure if this means 2 shots or 2 shots plus a booster.  On 21 December we had 1621 cases in hospital and the fully vaccinated accounted for only 29%.  So it’s getting worse here.

For an elaboration of why I think the Chinese are particularly vulnerable to omicron see yesterdays post — https://luysii.wordpress.com/2022/01/04/were-about-to-find-out-just-how-good-the-chinese-vaccines-are-against-omicron/

Addendum 7 January 2022

As of 6 Jan Massachusetts had 2,637 COVID19 cases of which 42% are described as ‘fully vaccinated’.

It looks like Dr. Leung was right (again).  From today’s SCMP

“At least 18 locally transmitted cases have been reported in Hong Kong in recent days and the city is reimposing some of its toughest Covid-19 social-distancing measures.”

https://www.scmp.com/news/china/science/article/3162526/shenzhen-covid-19-cases-lower-hopes-hong-kong-border-reopening?module=perpetual_scroll_1&pgtype=article&campaign=3162526

We’re about to find out just how good the Chinese Vaccines are against omicron

A very disturbing article in the South China Morning Post (SCMP) today — https://www.scmp.com/news/hong-kong/health-environment/article/3162088/coronavirus-hong-kong-reports-first-untraceable?module=storypackage&pgtype=homepage.

First: some background. There has been an outbreak of COVID19 traced to the Moon Palace restaurant  in Kowloon recently.   It began with an aircrew member from Cathay Pacific Airways Ltd., who was subsequently found to be infected with omicron.  He ate lunch there 27 December with his family. . Five other customers later tested positive. Yesterday’s paper said that transmission occurred between the first known case and others not sitting close to each other.  I can’t find that particular article, so this is from memory.

Today’s news is particularly bad, because the current case was acquired within the community (with no obvious contact to an infected person, or time at the restaurant), His virus has two of the mutations typical of omicron (further testing is in progress).

Given how infectious omicron is and the population density of Hong Kong (mask or no mask) omicron is likely to spread widely in Hong Kong (and likely China itself).

You won’t find any schadenfreude here.  I have a son, daughter-in-law and two grandkids living there.  This is why I was able to see that a pandemic was in store 2 years ago –https://luysii.wordpress.com/2020/01/27/what-to-do-about-the-wuhan-flu/

It seems quaint now, but I the reason I was reading the SCMP regularly in 2019 – 2020 was the Hong Kong riots in the summer of 2019 their possible effects on my family.

So why am I concerned presently?  Due to the Chinese attempts at tight control, the majority of the Chinese population  have had no infectious experience with the pandemic virus (aside from Wuhan of course). This is unlike Western populations which have been exposed and symptomatically/asymptomatically infected with various strains of the pandemic virus for nearly two years.  So the Chinese are immunologic virgins as far as omicron is concerned.  We are about to see how protective the vaccines they’ve received (Sinopharm, Coronavac) are against omicron.

 

Hopefully, the Chinese are better protected than we have been by the Pfizer, Moderna, etc. etc vaccines.  As of yesterday,  37% of the 2000 or so COVID19 patients in Massachusetts hospitals are said to be ‘fully vaccinated’ (I’m not sure if this means 3 shots or the original 2).

Addendum 5 Jan ’22 — If you want to see how tenaciously the Chinese are tracing cases in the outbreak in Hong Kong — look at today’s SCMP — https://www.scmp.com/news/hong-kong/health-environment/article/3162190/coronavirus-hong-kongs-fifth-wave-has-already?module=lead_hero_story&pgtype=homepage.

Particularly fascinating is a diagram of the diners and seating arrangements in  the Moon Palace restaurant in Kowloon, the source of one outbreak — they have each confirmed case — the table they were sitting at, the times they were there.  Particularly scary is the 20 meter distance between the index case (an airline stewardess) and one of the infected.

Even scarier is the pronouncement of Gabriel Leung — he’s the MD who said the pandemic was in 31 Chinese cities  in 27 Jan ’21, so anything he says must be taken seriously.  See the link to my post  — https://luysii.wordpress.com/2020/01/27/what-to-do-about-the-wuhan-flu/

“Fellow government adviser Professor Gabriel Leung, dean of the University of Hong Kong’s faculty of medicine, told a radio programme there were “probably five to 10 invisible transmission chains in the community. It’s a very alarming situation”.

Stay tuned.   The article said that there 38 COVID19 cases in Hong Kong — it isn’t clear how many are the omicron variant.

So here’s a repeat of a post written 12 December ’21

Is China following a Smokey the Bear policy on the pandemic?

China is following a prevent pandemic virus infection policy, just as Smokey the Bear followed a prevent forrest fires policy.  The latter didn’t work out well, as although fires were prevented for a while. However, when fires did occur, they were much much worse than the smaller ones Smokey prevented.  There was much more tinder and stuff to burn.

Actually Smokey has changed his tune slightly.

https://en.wikipedia.org/wiki/Smokey_Bear  SmokeyBear.com’s current site has a section on “Benefits of Fire” that includes this information: “Fire managers can reintroduce fire into fire-dependent ecosystems with prescribed fire. Under specific, controlled conditions, the beneficial effects of natural fire can be recreated, fuel buildup can be reduced, and we can prevent the catastrophic losses of uncontrolled, unwanted wildfire.”

Revision 14 December 2021 — China’s policy of prevention has resulted in a Chinese population which has been vaccinated using two killed virus vaccines (Sinopharm, Coronavac).  They have not had any natural infections with the virus (aside from the original cases) as far as we know given what China has allowed out.

Infection with the virus itself exposes you to all its proteins, with your immune system responding to all of them.   Western vaccines are just to the spike protein.

It tends to be forgotten that moist cases of pandemic viral infection are asymptomatic.

Given 800K deaths  from COVID19  in the USA, how can I possibly say this is good. Here’s how :>

If you had an infection with the virus, you develop antibodies.  Nowadays, everyone who is vaccinated has antibodies so there is no point in testing for them, but what were things like in the days before vaccines?

The following is from a post July/2020.

https://www.nytimes.com/2020/07/09/nyregion/nyc-coronavirus-antibodies.html–https://www.cnbc.com/2020/04/23/new-york-antibody-study-estimates-13point9percent-of-residents-have-had-the-coronavirus-cuomo-says.html.

New York State  randomly tested 3,000 people at grocery stores and shopping locations across 19 counties in 40 localities to see if they had the antibodies to fight the coronavirus, indicating they have had the virus and recovered from it. With more than 19.4 million people residents, according to U.S. Census data, the preliminary results imply that at least 2.7 million New Yorkers have been infected with Covid-19.They weren’t all hospitalized.

Here’s some work the same month from Queens — https://www.nytimes.com/2020/07/09/nyregion/nyc-coronavirus-antibodies.html

At a clinic in Corona, a working-class neighborhood in Queens, more than 68 percent of people tested positive for antibodies to the new coronavirus. At another clinic in Jackson Heights, Queens, that number was 56 percent. But at a clinic in Cobble Hill, a mostly white and wealthy neighborhood in Brooklyn, only 13 percent of people tested positive for antibodies.

So the disease has already to spread to half the population in some neighborhoods in Queens. If even 10% of them were sick that would have been 140,000 hospitalizations.  They didn’t happen.

OK, so a lot more people were infected than got sick.  Why is this good?

Enter the omicron variant of the pandemic virus.  It can evade the antibodies produced by all the current vaccines (in the West — protection against the Chinese killed viral vaccines CoronaVac and Sinopharm isn’t known yet).   Yet omicron doesn’t appear to produce severe disease. Thus far…

The CDC in the past week said of the 40+ omicron cases it knows about (there certainly are more out there, and more to come), there was one hospitalization (for two days) and no deaths.

Here is Dr. Fauci 12 December 2021 — “We’re getting anecdotal information … not necessarily confirmed yet, that the level of severity appears to be maybe a bit less than in the Delta. But there are a lot of confounding issues that it may be due to the underlying protection in the community due to prior infections,”

Source — https://nypost.com/2021/12/12/omicron-appears-to-evade-some-protection-from-covid-vaccines/

So the Chinese population may be sitting ducks for omicron having been given vaccines (Sinopharm, Coronavac) of unknown potency against omicron.  If their statistics are true there has been little or no natural infection with the pandemic virus in the Chinese population (which Fauci has just implicated is protective),.  Given that I have a son, daughter in law and two grandkids living in Hong Kong, I find this extremely disconcerting.

Parts of your brain that move

Sick of COVID19 and omicron are you?  So am I.  It’s time for some hard core neuroscience.  Looking at slides or electron micrographs gives a very static picture of the brain.  There are parts of the brain that move.

Microglia are the macrophages of the brain.  They’re actually rather creepy, extending and retracting processes and feeling up neurons, removing synapses from processes.  They use receptors for ATP and ADP to detect when a neuron is in trouble.  A new cellular specialization is described — Somatic Purinergic Junctions — a combination of mitochondria, reticular membrane structures, vesicle-like membrane structures and clusters of a particular voltage gated potassium channel (Kv2.1).  You can actually watch this happening.   [ Science vol. 367 pp. 510 – 511, 528 – 537 ’20 ].

For about the past 20 years we’ve been able to observe dendritic spines for months in the living (rodent) brain.  In 1970, if you told me that, I’d have said you were smoking something.  The surprising finding is that dendritic spines are a work in progress, being newly formed and removed all the time.  The early literature (e.g. 10 years ago) is contentious about how long a given spine lasts, but most agree that spine plasticity is present every time it’s looked for.  Here are a few references [ Neuron vol. 69 pp. 1039 – 1041 ’11, ibid vol. 49 pp. 780 – 783, 877 – 887 ’06 ].

It is yet another reason why a wiring diagram of the brain wouldn’t help you understand it.   For much more on this please see — https://luysii.wordpress.com/2021/04/25/the-wiring-diagram-of-the-brain-takes-another-hit/

Now on to Long Term Potentiation — https://en.wikipedia.org/wiki/Long-term_potentiation.  This is basically a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons.One of the things that happens with long term potentiation is that the potentiated dendritic spines enlarge.  Now we know that there are all sorts of proteins crossing the synaptic cleft between presynaptic axon terminal and post-synaptic dendritic spine.  They hold the two together.

So the authors of Nature vol. 600 pp. 696 – 689 ’21 wondered if the enlargement of the spine changed neurotransmission.  They studied CA3 neurons in slice culture preparations of the rat hippocampus.  Synapses formed between axons and dendrites. The mimicked LTP (and produced dendritic spine enlargement) by two photon uncaging of glutamic acid.  Spine enlargement ensured which then pushed on the presynaptic bouton.  This caused increased release of glutamic acid by the presynaptic neuron.

This may actually be the mechanism behind long term potentiation.