When is the AIDs virus really dead?

When should we regard an AIDs virus lurking in the genome of a white blood cell as dead (or at least harmless).  Such proviruses are called defective, and commonly formed, because the process of reverse transcription (of RNA into DNA) is quite error prone.

Most would say an HIV1 provirus in the genome is dead  if can’t reproduce and get outside the cell carrying it.  Not so fast says Proc. Natl. Acad. Sci. vol. 117 pp. 3704 – 3710 ’20.  They show that such defective proviruses can be transcribed into RNA and these RNAs can produce proteins (when translated).

There is some evidence for this as the Nef protein of HIV1 can be detected in cells and plasma even when HAART (Highly Active Anti Retroviral Therapy) has knocked plasma viremia down to a level of under   50 copies/milliLiter.

How could this cause trouble ? Easy.  This would be chronically stimulating the immune system and in effect wearing it out.

This is very new stuff, and the fate of white cells containing replication incompetent proviruses which are still producing proteins isn’t known (but I’m sure this isn’t far off).

The ubiquitin wars

Ubiquitin used to be simple.  All it had to do was form an amide between its carboxy terminal glycine and the epsilon amino group of lysine of a target protein, and bingo — the protein was targeted for degradation by the proteasome.

Before proceeding, it’s worth thinking why this sort of thing doesn’t happen more often, by which I mean amide formation between carboxyl groups on aspartic and glutamic acid on one protein and lysines on the surface of another.  That’s where the 3 amino acids are likely to be found, because they are charged at physiological pH, meaning they cost energy (and probably entropy) to put into the relatively hydrophobic interior of a protein where there isn’t a lot of water around to hide their charges.   Also, every noncyclic protein (which is just about all of them) has a carboxy terminal amino acid — why don’t they link up spontaneously to the lysines on the surface of other proteins?

Well, ubiquitin does NOT link up spontaneously.  It has a suite of enzymes to do so.  Like a double play in baseball, 3 enzymes are involved, which move ubiquitin to E1 (the shortstop) to E2 (the second baseman) to E3 (the first baseman).  We have over 600 E3 enzymes, 40 E2s and 9 E1s.  650/20,000 protein coding genes is a significant number — and the 600 E3s are likely there to provide specificity to just what protein gets linked to.

Addendum 21 Feb — Silly me, I should have added in the nearly 100 genes coding for proteins that remove attached ubiquitins (e.g. the deubiquitinases).

A few more fun facts and then down to business.  First ubiquitin is so stable that boiling water doesn’t denature it [ Science vol. 365 pp. 502 – 505 ’19 ].  Second ubiquitin can link to itself, as it contains 7 lysines at amino acids 6, 11, 27, 28, 33, 48 and 63 of the 72 amino acids contained in the protein.

Polyubiquitin chains are often made up of multiple ubiquitin monomers with lengths up to 10 [ Nature. vol. 462 pp. 615 – 619 ’09  2009 ] meaning that there could be a lot of different ones ( 7^10 = 282,475,249.  However chains found in nature seem to use just one type of link, e.g. linking the carboxyl group of one ubiquitin to just one of the 7 lysines over and over, forming a rather monotonous polymer.

On to the interesting paper, namely the ubiquitin wars inside a macrophage invaded by TB [ Nature vol. 577 pp. 682 – 688 ’20 ]  Ubiquitin initially was thought to be a tag marking a protein for destruction.  It’s much more complicated than that.  A host E3 ubiquitin ligase (ANAPC2, a core subunit of the anaphase promoting complex/cyclosome) promotes the attachment of lysine #11 linked ubiquitin chains to lysine #76 of the TB protein Rv0222.  In some way this helps Rv022 to suppress the expression of proinflammatory cytokines.

We do know that the ubiquitination of Rv022 facilitates in some way the recruitment of the protein tyrosine phosphatase SHP1 to the adaptor protein TRAF6 (Tumor necrosis factor Receptor Associated Family member 6) preventing the its ubiquitination and activation.  Of interest is the fact that TRAF6 itself is an E3 ubiquitin ligase which acts on many proteins.

Now to continue and show the further complexity of what’s going on inside our cells.  Autophosphorylated IRAK leaves the TLR (Toll Like Receptor) signaling complex forming a complex with TRAF6 resulting in the oligomerization of TRAF6.  Somehow this activates TAK1, a member of the MAP3 kinase family and this leads to the activation of the family of IKappaB kinases which phosphorylate IKappaB leading to its proteolysis.  Once IKappaB is removed from NFKappaB, translation of NFKappaB to the nucleus occurs where it turns on transcription of cytokines and other proinflammatory genes.

It is really amazing when you think of all the checks and balances going on down there.  How crude our weapons against inflammation are now, compared to what we might have when we know all the mechanisms behind it.

4 quotes saying the same thing — who wrote them?

Here are 4 longish quotes (with no ellipses) from 4 different writers on politics.  They all say pretty much the same thing.  What is remarkable is the political spectrum of the writers.  Answers at the end

Quote #1: “Donald Trump was in many ways an unappealing figure. He never hid that. Voters knew it.  They just concluded that the options were worse — and not just Hillary Clinton and the Democratic Party, but the Bush family and their donors and the entire Republican leadership, along with the hedge fund managers and media luminaries and corporate executives and everyone else who created the world as it was in the fall of 2016: the people in charge.

Trump might be vulgar and ignorant, but he wasn’t responsible for the many disasters America’s leaders created.  Trump didn’t invade Iraq or bail out Wall Street.  He didn’t lower interest rates to zero, or open the borders, or sit silently by as the manufacturing sector collapsed and the middle class died.  You couldn’t really know what Trump might do as president, but he didn’t do any of that.

There was also the possibility that Trump might listen. At times he seemed interested in what voters thought.  The people in charge demonstrably weren’t.  Virtually none of their core beliefs had majority support from the population they governed.  It was a strange arrangement for a democracy.  In the end, it was unsustainable.”

Quote #2: “The American white-collar class just spent the year rallying around a super-competent professional (who, it turns out, really wasn’t all that competent) and either insulting or silencing everone who didn’t accept their assessment.  And then they lost.  Maybe it’s time to consider whether there’s something about ear-splitting self-righteousness, shouted from a position of high social status, that turns people away.

The even larger problem is that a chronic complacency has been rotting American liberalism for years, a hubris that tells Democrats they need do nothing different, they need deliver nothing really to anyone — except their friends on the Google jet and those nice people at Goldman.  The rest of us are treated as though we have nowhere else to go and no role to play except to vote enthusiastically on the grounds that these Democrats are the ‘last thing standing’ between us and the end of the world.  It is a liberalism of the rich, it has failed the middle class, and now it has failed on its own terms of electibility.  The time is up for these comfortable Democrats and their cozy Washington system.  Enough is enough.”

Quote #3: “In 2018, Hillary Clinton told Britain’s Channel Four News: “The real question is how did the Russians know how to target their messages so precisely to undecided voters in Wisconsin or Michigan or Pennsylvania —that is really the nub of the question.”

No, the real question is why so much of the US and European establishment accepted and promulgated Clinton’s alibi for her failure to follow her husband into the office of president of the United States.  A Clinton or Bush was president, vice president, or secretary of state in every year between 1981 and 2013, years in which working class incomes stagnated, offshoring devastated US and European manufacturing, the world suffered the worst economic collapse since the Great Depression of the 1930s, and the US lunged into multiple disastrous wars in the Middle East and Central Asia. Trump became president by running against a Bush in the Republican primaries and a Clinton in the general election.  The desire of many American voters to disrupt the quarter-century cycle of nearly identical versions of technocratic neoliberalism under alternating Bushes and Clintons is quite sufficient to explain the presidential election of 2016.”

Quote #4: “Iowa was the real “beginning of the end” to a story that began in the Eighties.

Following the wipeout 49-state, 512 electoral-vote loss of Walter Mondale in 1984, demoralized Democratic Party leaders felt marooned, between the awesome fundraising power of Ronald Reagan Republicans and the irritant liberalism of Jesse Jackson’s Rainbow Coalition.

To get out, they sold out. A vanguard of wonks like Al From and Sen. Sam Nunn at the Democratic Leadership Council devised a marketing plan: two middle fingers, one in each direction.

They would steal financial support for Republicans by out-whoring them on economic policy. The left would be kneecapped via “triangulation,” i.e., the public reveling in the lack of choices for poor, minority, and liberal voters.

Young pols like Bill Clinton learned they could screw constituents and still collect from them. What would they do, vote Republican? Better, the parental scolding of disobedient minorities like Sister Souljah combined with the occasional act of mindless sadism (like the execution of mentally ill Ricky Ray Rector) impressed white “swing” voters, making “triangulation” a huge win-win — more traction in red states, less whining from lefty malcontents.

Democrats went on to systematically rat-fuck every group in their tent: labor, the poor, minorities, soldiers, criminal defendants, students, homeowners, media consumers, environmentalists, civil libertarians, pensioners — everyone but donors.

They didn’t just fail to defend groups, but built monuments to their betrayal. They broke labor’s back with NAFTA, embraced mass incarceration with the 1994 Crime Bill, and ushered in the Clear Channel era with the Telecommunications Act of 1996. Welfare Reform in 1996 was a sellout of the Great Society (but hey, at least Clinton kept the White House that year!). The repeal of the Glass-Steagall Act gave us Too Big to Fail. Shock Therapy was the Peace Corps in reverse. They sold out on Iraq, expanded Dick Cheney’s secret regime of surveillance and assassination, gave Wall Street a walk after 2008, then lost an unlosable election, which they blamed on a conspiracy of leftist intellectuals and Russians.

Still, if you were black, female, gay, an immigrant, a union member, college-educated, had been to Europe, owned a Paul Klee print, or knew Miller’s Crossing was a good movie, you owed Democrats your vote. Why? Because they “got things done.”

Now they’re not getting much done, except a lost reputation. That feat at least, they earned. To paraphrase Joker: What do you get when you cross a political party that’s sold out for decades with an electorate that’s been abandoned and treated like trash?

Answer: What you fucking deserve!”

Quote #1: Tucker Carlson “Ship of Fools” p. 3 — a classic conservative

Quote #2: Thomas Frank: “Rendesvous with Oblivion” p. 185.  A classic liberal

Quote #3 Michael Lind:  “The New Class War” p. 98.  Although he’s been writing for 25 years, I was unfamiliar with his work

Quote #4 Michael Taibbi: — a reporter who writes incredibly well for Rolling Stone, probably very liberal. https://www.rollingstone.com/politics/politics-features/iowa-caucus-democrats-disaster-trump-sanders-949655/amp/

I find it remarkable that 4 writers, from nearly as wide a political spectrum as it is possible to get, are basically saying the same thing.

4 Interesting papers

Here are brief summaries of 4 recent very interesting papers, each of which may be the subject of a future post (now that I’m not as worried about the effects of the Wuhan flu on family members over in Hong Kong).  They are likely behind a pay wall unfortunately

l. Watching an endoplasmic reticulum extruded tubule cut a P-body in half. Very significant as we begin to appreciate the phase transitions going on in our cells — for an overview of this see — https://luysii.wordpress.com/2018/12/16/bye-bye-stoichiometry/.

The paper(s) itself [ Science vol. 367 pp. 507 – 508, 537, eaay7108 ’20 ]

2. Watching microglia caress the cell body (soma) of neurons [ Science vol. 367 pp. 510 – 511, 528 – 537 ’20 ].  They’re actually rather creepy, extending 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)

3. The ubiquitin wars inside a macrophage invaded by TB [ Nature vol. 577 pp. 682 – 688 ’20 ]  Ubiquitin initially was thought to be a tag marking a protein for destruction.  It’s much more complicated than that.  A host E3 ubiquitin ligase (ANAPC2, a core subunit of the anaphase promoting complex/cyclosome) promotes the attachment of lysine #11 linked ubiquitin chains to lysine #76 of the TB protein Rv0222.  In some way this helps Rv022 to suppress the expression of proinflammatory cytokines.

4. FACT (FAcilitates Chromatin Transcription)  is a heterodimer of two proteins which form a heterodimer [ Nature vol. 577 pp. 426 – 431 ’20 ].  If you’ve ever wondered how the monstrously large holoenzyme of RNA polymerase II, manages to work its way around the nucleosome copying one strand, you need to know about FACT, which basically grabs the disclike nucleosome with DNA wrapped around it twice, grabs both H2A-H2B dimers and holds them outside while pol II passes.  You have to wonder which came first the nucleosome or FACT. Neither would be of much use by themselves.  Probably they both grew up together, but it’s hard to envision the intermediate stages.

The Wuhan flu epidemic in China has likely peaked

Could the Wuhan flu epidemic in China be peaking, or am I indulging in wishful thinking because of a son, daughter-in-law and two grandkids living in Hong Kong?  Possibly but here’s why.

The South China Morning post (https://www.scmp.com) keeps a total of the cases of the flu in China and worldwide.  The figures change throughout the day, but they don’t vary too much during the US day (Chinese night).

Looking at the totals in the US evening

From 2 Feb to 3 Feb there were just under 3,000 new cases

From 3 Feb to 4 Feb there were just over 3,000 new cases

From 4 Feb to 5 Feb there just under 4,000 new cases (3891)

From 5 Feb to 6 Feb there were slightly fewer newer case (3789)

From 6 Feb to 7 Feb there were definitely fewer new cases (3143)

 

Even though the totals are horrible — 31,161 cases in China (worldwide 31,482) with 636 worldwide deaths as of 5AM Eastern Standard time  7 Feb (USA), this is the second time in the China epidemic that there have been fewer new cases (and more importantly with a significant reduction from yesterday’s increase). This means we are likely at or over the peak of spreading of the epidemic (although the number of cases will continue to increase).

The number of new cases probably doesn’t contain any false positives, because of the thoroughness of the way they’ve been checked.

Caveat — only those lucky enough to make it into a hospital get checked, and stories I’ve read about how crowded they are and the long waits for care and admission, means that the number of cases are likely much higher.

Note that I include both the Chinese totals, and those worldwide as when the disease spreads worldwide (as it has) the total number of new cases will continue to increase (even if the Chinese new cases drops).

Having flown back and forth to Hong Kong several times, you couldn’t ask for a better way to spread the flu than cooping up 100+ people packed cheek by jowl in the steerage section of a large airplane for 16 – 18 hours.   This is particularly true since we now know asymptomatic people can spread the disease.

A very smart friend asked me ‘Why the excitement since influenza in the USA causes many more deaths each year’.  Well from the Center for Disease Control (CDC) we have the following — https://www.cdc.gov/flu/about/burden/index.htmlhttps://www.cdc.gov/flu/about/burden/index.html

“CDC estimates that influenza has resulted in between 9 million – 45 million illnesses, between 140,000 – 810,000 hospitalizations and between 12,000 – 61,000 deaths annually since 2010.”

That’s quite a range (5 fold) for number of illnesses and number of deaths, but the ratio is the same.  So what is the mortality of the flu we have in the USA?  Well 12,000/9,000,000 = .0013 or .13% which is 20 – 30 times less than the current known mortality rate of 2 – 3% for Wuhan flu.

Remember the figures are for symptomatic diagnosed cases.  There may well be many more cases with minimal or no symptoms.  Remember for every case of paralytic poliomyelitis, there were 99 infections where that didn’t happen.  Hopefully soon, we’ll have a way to test for human antibodies to Wuhan flu with specific antibodies (not all antibodies are specific) and we’ll find out the true prevalence of Wuhan flu infection.

Could the Wuhan flu epidemic in China be peaking?

Could the Wuhan flu epidemic in China be peaking, or am I indulging in wishful thinking because of a son, daughter-in-law and two grandkids living in Hong Kong?  Possibly but here’s why.

The South China Morning post (https://www.scmp.com) keeps a total of the cases of the flu in China and worldwide.  The figures change throughout the day, but they don’t vary too much during the US day (Chinese night).

Looking at the totals in the US evening

From 2 Feb to 3 Feb there were just under 3,000 new cases

From 3 Feb to 4 Feb there were just over 3,000 new cases

From 4 Feb to 5 Feb there just under 4,000 new cases (3891)

From 5 Feb to 6 Feb there were slightly fewer newer case (3789)

Addendum 6 Feb (USA) 9:20 PM 7 Feb China  (10:20 AM) — the news is good — the total number of new cases from 6 Feb to 7 Feb in China dropped significantly (967).  Hopefully this is accurate, and not due to some reporting glitch, or suppression of the numbers by directive from above.  If so, the epidemic has peaked, and all people have to do is stay indoors and not infect others.   Let’s hope this holds up.  Tomorrow’s count will be very important.   End Addendum 6 Feb 

Even though the totals are horrible — 28,396 cases worldwide with 566 deaths the morning of 6 Feb (USA), this is the first time in the China epidemic that there have been fewer new cases. This means we may be at the peak of epidemic spreading (although the number of cases will continue to increase).

The number of new cases probably doesn’t contain any false positives, because of the thoroughness of the way they’ve been checked.

Caveat — only those lucky enough to make it into a hospital get checked, and stories I’ve read about how crowded they are and the long waits for care and admission, means that the number of cases are likely much higher.

Note that I include only the Chinese totals, as when the disease spreads worldwide (as it has) the total number of new cases will continue to increase (even if the Chinese new cases drops).

Having flown back and forth to Hong Kong several times, you couldn’t ask for a better way to spread the flu than cooping up 100+ people packed cheek by jowl in the steerage section of a large airplane for 16 – 18 hours.   This is particularly true since we now know asymptomatic people can spread the disease.

A very smart friend asked me ‘Why the excitement since influenza in the USA causes many more deaths each year’.  Well from the Center for Disease Control (CDC) we have the following — https://www.cdc.gov/flu/about/burden/index.htmlhttps://www.cdc.gov/flu/about/burden/index.html

“CDC estimates that influenza has resulted in between 9 million – 45 million illnesses, between 140,000 – 810,000 hospitalizations and between 12,000 – 61,000 deaths annually since 2010.”

That’s quite a range (5 fold) for number of illnesses and number of deaths, but the ratio is the same.  So what is the mortality of the flu we have in the USA?  Well 12,000/9,000,000 = .0013 or .13% which is 20 – 30 times less than the current known mortality rate of 2 – 3% for Wuhan flu.

Remember the figures are for symptomatic diagnosed cases.  There may well be many more cases with minimal or no symptoms.  Remember for every case of paralytic poliomyelitis, there were 99 infections where that didn’t happen.  Hopefully soon, we’ll have a way to test for human antibodies to Wuhan flu with specific antibodies (not all antibodies are specific) and we’ll find out the true prevalence of Wuhan flu infection.

The Reimann curvature tensor

I have harpooned the great white whale of mathematics (for me at least) the Reimann curvature tensor.  Even better, I understand what curvature is, and how the Reimann curvature tensor expresses it.  Below you’ll see the nightmare of notation by which it is expressed.

Start with curvature.  We all know that a sphere (e.g. the earth) is curved.  But that’s when you look at it from space.  Gauss showed that you could prove a surface was curved just be performing measurements entirely within the surface itself, not looking at it from the outside (theorem egregium).

Start with the earth, assuming that it is a perfect sphere (it isn’t because its rotation fattens its middle).  We’ve got longitude running from pole to pole and the equator around the middle.  Perfect sphere means that all points are the same distance from the center — e.g. the radius.  Call the radius 1.

Now think of a line from the north pole to the plane formed by the equator (radius 1).  Take the midpoint of that line and inscribe a circle on the sphere, parallel to the plane of the equator.  Its radius is the half the square root of 3 (or 1.73). This comes from the right angle triangle just built with hypotenuse is 1 and  one side 1/2.   The circumference of the equator is 2*pi (remember the sphere’s radius is 1).  The circumference of the newly inscribed circle is 1.73 * pi.

Now pick a point on the smaller circle and follow a longitude down to the equator.  Call this point down1.  Move in one direction by 1/4 of the circumference of the sphere (pi/2).  Call that point on the equator down then across

Now go back to the smaller circle at the first point you picked and move in the same direction as you did on the equator by absolute distance pi/2 (not by pi/2 radians).  Then follow the longitude down to the equator.  Call that point across then down.  The two will not be the same.  Across then down is farther from down 1 than down then across.

The difference occurs because the surface of the sphere is curved, and the difference in endpoints of the two paths is exactly what the Reimann curvature tensor measures.

Here is the way the Riemann curvature tensor is notated.  Hideous isn’t it?

If you’re going to have any hope of understanding general relativity (not special relativity) you need to understand curvature.

I used paths in the example, Riemann uses the slope of the paths (e.g derivatives) which makes things much more complicated.  Which is where triangles (dels), and the capital gammas (Γ) come in.

To really understand the actual notation, you need to understand what a covariant derivative actually is, which is much more complicated, but knowing what you know now, you’ll see where you are going when enmeshed in thickets of notation.

What the Riemann curvature tensor is actually saying is that the order of taking covariant derivatives (which is the same thing as the order of taking paths)  is NOT commutative.

The simplest functions we grow up with are commutative.  2 + 3 is the same as 3 + 2, and 5*3 = 3*5.  The order of the terms doesn’t matter.

Although we weren’t taught to think of it that way, subtraction is not.  5 – 3 is not the same as 3 – 5.  There is all sorts of nonCommutativity in math.  The Lie bracket is one such, the Poisson bracket  another, and most groups are nonCommutative.  But that’s enough.  I wish I’d known this when I started studying general relativity.

Riemann curvature tensor

Hideous isn’t it ? — this will be fleshed out tomorrow night, with a comprehensible explanation of what the Riemann curvature tensor is all about.  Just wanted to see if I could get these formulas to print out in my blog

What would Woodward do — take II

“It’s no wonder that truth is stranger than fiction. Fiction has to make sense.”  Mark Twain.

The Harvard Chemistry Department chair arrested?  And for what?  For lying and hiding research work he was doing for China.

“The arrangement between Lieber and the Chinese institution spanned “significant” periods of time between at least 2012 and 2017, according to the affidavit. It says the deal called for Lieber to be paid up to $50,000 a month, in addition to $150,000 per year “for living and personal expenses.”

Who knew betraying your country could be so lucrative?  Of course these are allegations, and have to be proved in court.

What would the great Robert Burns Woodward (https://en.wikipedia.org/wiki/Robert_Burns_Woodward) say to this?  He’s already spinning in his grave over the slings and arrows heaped on pure synthetic organic chemistry.  For details see part of an old post at the end.

Interesting how the department has changed.  No Chinese there at all ’60 – ’62 (even postdocs).  There were several Japanese and Sikh postdocs along with a fair number of happy go lucky Australians.

Chemistry applications can be lucrative.  The new Princeton Chemistry Building was built thanks to professor Ted Taylor, whose royalties on Alimta (Pemetrexed), an interesting molecule with what looks like guanine, glutamic acid, benzoic acid and ethane all nicely stitched together to form an antifolate, to the tune of over 1/4 of a billion dollars built it.

It’s interesting to note that the Princeton undergraduate catalog for ’57 – ’58 has Dr. Taylor basically in academic slobbovia — he’s only teaching Chem 304a, a one semester course “Elementary Organic Chemistry for Basic Engineers” (not even advanced engineers)

For details please see  — https://luysii.wordpress.com/2011/05/16/princeton-chemistry-department-the-new-oberlin/

What would Woodward do ?

Sleeper is one of the great Woody Allen movies from the 70s.  Woody plays Miles Monroe, the owner of (what else?) a health food store who through some medical mishap is frozen in nitrogen and is awakened 200 years later.  He finds that scientific research has shown that cigarettes and fats are good for you.  A McDonald’s restaurant is shown with a sign “Over 795 000 000 000 000 000 000 000 000 000 000 000 000 000 000 000 000 000 Served”

I returned from my father’s 100 year birthday blowout and band camp and began attacking a giant pile of accumulated unread journals.  In the 9 August Nature (p. 630 – 631)  2007 he was amazed to read criticism of a 64 step 22 year synthesis of an exquisitely complex molecule (azadirachtin) — a molecule in which it is easier to count the number of optically INactive carbons than the optically active ones.  Back in the 60s we were all impressed with how Woodward got the 5 asymmetric centers in a 6 membered ring of reserpine (which was in use as an antihypertensive at the time, and whose fairly common side effect of depression was one of the clues leading to the amine theory of affect).  Rip was surprised to find that the criticism was not that the synthesis was incorrect, but that the project shouldn’t have been done at all.  Apparently a significant body of organic chemists think this way.

Political correctness has left few groups which it is safe to disparage.  With apologies to one of them (Christians) I’ve got to ask “What would Woodward do?”

What to do about the Wuhan flu

What to do about the Wuhan flu?  The short answer is to lay in a month or two of dried food and drink, and have plenty of bottled water around.

The long answer depends on whether the new corona virus (called 2019-nCOV) becomes a pandemic and if the (symptomatic) case fatality rate continues at 3.5% (based on 80 deaths in 2,800 cases as of yesterday).

With a son, Chinese daughter in law and two grandchildren living in Hong Kong, I’ve followed the outbreak ever since hearing of it 1 January.

The best and most current source of info about the outbreak is the South China Morning Post — https://www.scmp.com.  It is in English and is not a government mouth piece.

Here’s the bad news

(1) As of a few days ago the virus had been found in 29/31 Chinese provinces.  This means that confining the virus to China is nearly impossible — how do you cut off a billion or so people from the rest of the world?

(2) Here’s more from today

• Hong Kong University  faculty of medicine dean Gabriel Leung says research shows self-sustaining human-to-human transmission is already happening in all major mainland cities.   Here’s a link
• https://www.scmp.com/news/hong-kong/health-environment/article/3047813/china-coronavirus-hong-kong-medical-experts-call
•  Why is this significant?  You have to know how docs operate.  When I wanted information about some issue or disease, I’d call a doc whose opinion and background I respected.  It is likely that Leung made this statement after calling med school deans he personally knew in major mainland cities.

(3) There is no treatment, in the sense of stopping the virus in its tracks.  All we have is supportive care, oxygen rest, medication for fever, bronchodilators.  This is true for the vast majority of viruses.  Remember the joke that modern medical science can cure a cold in 14 days, but otherwise it takes two weeks.

(4) We know that you don’t have to be clinically ill to transmit the disease.  Screening new arrivals for fever is well and good but that won’t totally prevent spread.

(5) Some individuals are what is called ‘superspreaders’ — one individual infected 15 hospital personnel.

(6) I wouldn’t hope for a specific treatment any time soon — look how long it took to get any treatment for AIDS, despite the huge amount of resources devoted to it.

Here is some good news. It is quite possible that there are many more cases out there with people who were either asymptomatic or  just mildly ill.  The classic example is polio, in which for every case with paralysis there were 99 cases with mild GI illness or nothing at all.

This will need to wait until we can test people for antibodies to 2019-nCOV to find out how many people have had it.  This is probably at least a month away

Vaccines (if they can be made) are even more months away.  We’ll just have to hunker down and hope for the best.

Why lay in dried food ?– in a pandemic people will panic and clear out all food they can get their hands on.  There were pictures of empty bins in a Wuhan food market last week.

People are getting serious about it.  From Reuters -“U.S. President Donald Trump offered China whatever help it needed on Monday”.  It would be nice to have some of our people from the Center for Disease Control over there. Hopefully the Chinese won’t be too proud to accept the offer.

Addendum 28 Jan — apparently the US (in the form of the CDC) is begging China to let them help out — sad — why should they have to beg?  Apparently the first overture was 3 weeks ago ! ! ! ! — https://www.scmp.com/news/china/article/3047967/china-coronavirus-washington-asks-beijing-permission-send-health-team