A reader asked me whether the scientific name is coronavirus, COVID-19, or something else. Without getting into the dispute over the common names, let me address that question specifically.
In a nutshell, coronaviruses are one major family of viruses. What they all have in common is their structure: They consist of a single strand of RNA which encodes the genetic “payload” , a shell of envelope proteins self-assembling around the strand, and a bunch of spikes on the shell whose job it is to stimulate receptors in the cell wall and effect an opening for entry. The spikes look like a kind-of ‘crown of thorns’ under an electron microscope, hence the name ‘coronavirus’.
The most common subgroup humans get exposed to are one type of common cold viruses (although most common colds are caused by rhinoviruses, a different family). There are other coronaviruses that are endemic in poultry and cause upper respiratory tract infections there. Others are endemic in bats, etc.
Alas, some coronaviruses are quite deadly to humans: SARS-nCoV (severe acute respiratory syndrome, novel coronavirus), also known as SARS-CoV, is the one that causes the disease simply named SARS. Originating in horseshoe bats, it somehow crossed the species border and caused a nasty epidemic in mainland China and Hong Kong, with another outbreak hitting Toronto hospitals. CFR (case fatality rate) of the disease is very high, at 9.6%, but no overt cases have reportedly been seen since 2004.
Another is MERS-CoV, causes MERS (Middle East Respiratory Syndrome, one colloquial name being “camel flu”). It apparently crossed the species barrier from bats to camels and thence (possibly via camel-based food products) to humans. MERS has a very high CFR (case fatality rate) of about 1/3 of diagnosed cases, but has a very low reproductive number (in part because it is so deadly?): since it was first described in 2013, we’ve had only about 2000 cases ever worldwide. An outbreak in South Korea in 2015 when a businessman returned from the Arab peninsula appears to have been when the South Koreans got their ‘dress rehearsal’ for how to deal with the present emergency.
The present virus is known as SARS-nCoV-2 because its RNA sequence is so similar (82 % sequence identity) to SARS-nCoV. The mutations that make up the difference (single-strand RNA viruses mutate very rapidly — for reason I’ll explain elsewhere) appear to have had two primary effects: (1) the virus is less deadly; (2) the spikes are more efficient at stimulating ACE2 receptors (angiotensin-converting enzyme 2), which it exploits to enter cells. (Remember, a virus that cannot enter a cell and take over its replication machinery can’t do much of anything. Like a computer virus without a computer ;))
What happens once the virus is inside, by the way? The RNA goes to a ribosome, which are the cell organelles that acts as protein ‘assembly plant’ of our cells. Gene expression in our cells involves chunks of DNA getting copied onto “messenger RNA”, which then makes its way to the ribosome and gets translated into a protein (by assembling amino acids according to what the “tape” says, until it hits what biologists call a “stop codon”: an “end of message” marker, so to speak). When the viral RNA enters the ribosome instead, that merrily carries out the work order written on the “imposter”, such as the enzyme needed to clone the viral RNA (RdRA, or RNA-dependent RNA polymerase), the envelope proteins, and the spike proteins. There is considerable speculation that the spike proteins in SARS-nCoV-2 are more effective than those in SARS-nCoV.
COVID-19 (coronavirus disease, [first outbreak in] 2019) is what WHO settled on as the name for the disease, not the agent.
UPDATE: statistician and software developer Charlie Martin weighs in more on the Italy data.
And a Japanese financial website reports that the campaign to get the residents of Wuhan to “thank” their dictator backfired badly.
Also, some signs that maybe the anomalously good statistics from Japan may be the product of selection bias: see here (especially the comments) and here. One of the articles, however, made a collateral point I’ve brought up here before:
Cases of seasonal flu have been declining for seven straight weeks, just as the coronavirus was spreading, indicating Japanese may have taken to heart the need to adopt some basic steps to stem infectious diseases. Tokyo Metropolitan Infectious Disease Surveillance Center data shows that influenza cases this year are well below normal levels, with nationwide cases hitting a low according to data going back to 2004.
Also, after Sen. Rand Paul (R-KY), German Chancellor Angela Merkel is the latest politician to go into 14-day quarantine after the doctor or nurse who gave her a standard flu vaccine tested positive for COVID-19.
UPDATE 2: leaked documents appear to indicate that the claim that “there are no new cases in Wuhan” needs to be taken with LOTS of sodium chloride.
UPDATE 3: on the other hand, there is some good news hidden in all the bad (via Instapundit):
And this one gets the Möbius Dick Award: NYT claims travel restrictions didn’t work in China — for the period they weren’t implemented