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A coronavirus update: new variants

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Everyone wearing a mask in this Tokyo airport, but still there are lots of problems, and lots of travellers

So there’s much concern about new variants of the SARS-CoV2 virus, one from the UK, now known as the Kent variant, and one from South Africa. My main source of info on this will be the SGU podcast 809, from January 6.
The Kent strain is more infectious than the original, by 50-60%, though not more deadly. However its infectiousness is fast making it the more dominant strain. The South African variant, though, is causing most concern, as virologists are uncertain about its response to the vaccines now available. It has some of the same mutations that are in the Kent variant, making it also more infectious, but it also has mutations that allow it to evade antibodies targeting previous variants. This won’t make the variant immune to the vaccine, but it will make the vaccine less effective, though exactly how much less effective is the big question currently.
Another major concern is that this new variant can infect people who’ve already contracted and recovered from the virus. As Dr Steven Novella and others on the podcast argue (and this quote is ‘tidied up’ from direct speech):

This is the result of allowing a pandemic to simmer along over time. Mutations are inevitable, though different viruses mutate at different rates. SARS-CoV2 has error-correction mechanisms when it replicates, so that’s why it mutates more slowly. But if an infection in an individual, or an epidemic, lingers long enough, you’ll still get mutations. Part of the problem is that, with so many people infected, for so long, there are a great number of opportunities for new variants to arise. There are thousands of roughly equivalent variants, which are neutral or inconsequential in effect, but now we have two variants that are more mutated, and more consequential. They have a suite of mutations that seem to have developed much faster than the background mutation rate of the virus. It’s thought that this is because in individual patients who’d had the infection for months and were being treated during that time, the increased selective pressure on the virus may have caused this suite of mutations to be formed. This kind of mutation rate has been shown in the lab with respect to antibiotic resistance in bacteria. 

The point here for the future is to get to a level of herd immunity through vaccination. Considering that new strains arise regularly, as with the flu (and we don’t yet know how regularly this will happen with SARS-CoV-2), it may be that the vaccine will have to be tweaked regularly to cover these new strains. Time will tell, and of course we don’t yet know how effective the new vaccines will be against these current major variants. In fact we don’t know for sure how long the vaccines, or the antibodies they create, will be effective, regardless of these variants. But mRNA vaccines can apparently be produced, and tweaked, quite quickly, once the variant’s RNA is sequenced.

All of this tells us that the science is generally on top of this. The major problem is political, and social. Trying to get people to do the right thing, to wear a mask, physically distance, avoid large indoor gatherings and to get vaccinated when the vaccine becomes available. This is easier in some regions of the world than in others, and the problems ranges from distrust or ignorance of modern science, to conspiratorial thinking, to rights over responsibilities, to cultures of compliance and non-compliance. Humans are delightfully diverse, or just a mess, and the WHO warns us that this may not be ‘the big one’ in pandemic terms. The year 2021 will not see the end of all this – far from it. 

Stop press – a new variant has just been found in Japan in four travellers from Brazil, the Sydney Morning Herald reports. Twelve mutations have been identified, one of which is shared by the UK and South African strains, suggesting a higher infection rate. The travellers are in quarantine in Tokyo airport. Due to a steep rise in cases, a state of emergency has been declared for Tokyo and surrounding prefectures. And so it goes.


Written by stewart henderson

January 11, 2021 at 10:47 am

more on rapid antigen testing, and the vaccine race

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So to continue with this issue of rapid at-home testing, there are/were many tests of a more simple and potentially cheaper type being manufactured, but they were all diagnostic tests (i.e tests that require expert interpretation as part of a diagnosis), and even if they’d been scaled up fairly rapidly they wouldn’t meet the kind of demand Dr Mina was envisaging. That’s to say, not doubling the tests available but multiplying those tests by a hundred or more, for nationwide availability in the US. 

I want to get clear here, for myself, about the difference between an antigen test and a PCR test. An antigen test detects viral proteins. The paper strip test Dr Mina refers to contains antibodies that will bind to the antigens, or proteins, if those antigens are present in sufficient numbers. The presence of those antigens, or viral proteins, indicates that the virus is active – it is producing the antigens via the ribosomes of host cells. The PCR test detects viral RNA, whether or not the RNA is active. And so the antigen test reveals infectivity. The PCR test more often than not finds inactive viral fragments, since this RNA remains in the cell for some time after the period of infectivity, the upswing, which is relatively short. 

Dr Mina has this to say about the sensitivity of the two test types. The PCR test will pick up virus from a few days to six weeks (or more) after infection, but the subject may be infective, that is, able to spread the virus, for the first two weeks (or less) after acquiring it. So its sensitivity to detecting an infective subject is not so great as its sensitivity to the virus itself (living and reproducing, or dead, or disabled). An antigen will be testing negative, both in the very early phase of infection, when the virus isn’t yet producing enough viral protein to show up on the test, and in the long phase when the virus, or parts of it, are still present but no longer replicating and infecting. So it is actually more sensitive to infectivity, which is exactly what’s required. And this essentially has to do with the frequency with which the antigen test can be used, because the PCR test has this lag time built into it. 

It’s hard to believe that it’s this simple and straightforward, and that supposedly smart regulators aren’t jumping on this and getting these tests out there. Could I be missing something? I note that Dr Mina uses transmissible rather than infective, by the way.

So why aren’t such tests available? In the USA, it’s because it sounds a lot like a diagnostic, which requires approval or licensing from an organisation called CLIA – but that’s for them to work out. As to the situation here in Australia, which hasn’t had to deal with anything like the mess they’ve made for themselves in the USA, such a testing system would still help to detect spreaders, providing there was blanket use, and this would mean fewer lock-downs and less economic impact. As would be the case globally. An ABC article from late October features an interview with Prof. Deborah Williamson, director of clinical microbiology at Melbourne’s Doherty Institute, who recognises the value of rapid antigen testing, but feels that we need ‘to better understand their effectiveness as a screening tool in different epidemiological contexts’. This is understandably cautious, but then there isn’t the urgency in Australia that there so obviously is in the USA. But the USA has another major problem, which is almost incomprehensible considering the disaster that has unfolded there – and that is lack of compliance. Even if rapid antigen testing – cheap and in such supply that it could be utilised on a daily basis by the whole population – even if this was made available, there’s surely a major question as to whether most people would use the test any time they looked a bit peely-wally [under the weather], let alone when they were completely asymptomatic. So you could say that Americans are paying the price for their ‘rights without responsibility’ ideology – not shared by all Americans of course, but apparently shared by too many for them to escape from this, or any other pandemic, lightly. 

Anyway, if we imagine a world, or a country, of largely compliant, responsible individuals, and widely available, cheap or free antigen testing, there would be no need for the quite onerous contact tracing mechanisms that we now have – signing in by phone or by hand at restaurants, pubs and the like – because those testing positive at home wouldn’t be attending those places until they tested negative again. Businesses could run, schools, airlines, etc. Economies could function almost as normal. 

Of course now we have the vaccine, or almost. So far though it’s the Pfizer/BioNTech two-shot vaccine, which needs to be kept at way below zero (celsius) temperature, so, difficult to scale up and make available to those without proper facilities. No sign of that one coming to Australia for a while. I read an article yesterday, ‘The Amazing Vaccine Race’, in Cosmos mag. It outlines some of the contenders – the companies and the vaccine types. It points out that some companies are trying to play the long game, to try not for the first vaccine, or one of the first, but the best. The problem though, says, Nicolai Petrovsky, whose company Vaxine is based here in Adelaide, is that ‘the first runners end up getting all the resources’. And it may take quite a while to work out the best, and if the early runners turn out to be good enough, we may never find out which would’ve been the best. Vaxine is currently trialling a covid19 vaccine which combines the virus’s spike protein with an adjuvant (a treatment which enhances the immune response of the vaccine) based on a plant polysaccharide. And there are some 160 other contenders, according to the article. One in Sydney is combining the spike protein with bacillus Calmette-Guerin (BCG) which has been shown to reduce mortality from a range of viral respiratory infections. And there are others, just sticking with Australia, some with a degree of complexity that defeats me, for now. However, there are scant resources for local production here.

Although phase 3 trials of the current front-runners tested for safety among many thousands, it’s unlikely that scaling up to the millions will be without casualties, however minimal. And there’s the question of long-term immunity, which can’t really be tested for in this rushed situation. So it will be very interesting to see which of the current contenders wins out in the ultra-long run, or if something we’ve barely heard of yet finally proves the best option. 


Rapid Coronavirus Testing – At HOME (COVID-19 Antigen Tests) with Dr. Michael Mina (video)

Dyani Lewis, ‘The Amazing Vaccine Race’, in Cosmos: the science of everything, issue 88, September-December 2020.

Written by stewart henderson

December 9, 2020 at 5:44 pm

reading matters 7

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She has her mother’s laugh, by Carl Zimmer , science author and journalist, blogger, New York Times columnist, etc etc

content hints – inheritance and heredity, genetics and epigenetics, Darwin and Galton, the Hapsburg jaw, eugenics, Hugo de Vries, Theodor Boveri, Luther Burbank, Pearl and Carol Buck, Henry Goddard, The Kallikak Family, Hitler’s racial hygiene laws, morons, the five races etc, Frederick Douglass, Thomas Hunt Morgan, Emma Wolverton, PKU, chromosomal shuffling, meiosis, cultural inheritance, mitochondrial DNA, Mendel’s Law, August Weismann, germ and soma, twin studies, genetic predispositions, mongrels, Neanderthals, chimeras, exosomes, the Yandruwandha people, IVF, genomic engineering, Jennifer Doudna, CRISPR, ooplasm transfers, rogue experiments, gene drives, pluripotency, ethical battlegrounds.

Written by stewart henderson

July 28, 2020 at 12:22 pm

Covid-19 – conspiracies, remdesivir

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tricky micky plumpeo, vying with old frumpy to become US muckraker-in-chief

Canto: So, getting back to Covid-19, I want to look at two unrelated issues – the limited approval of remdesivir as a treatment, and the claim by the US government that the virus escaped from a lab in Wuhan. What do you think?

Jacinta: Well let me briefly address the second matter – I haven’t yet looked into the claim, but I will say that, IMHO, the current US federal government is possibly the largest misinformation machine on the globe at present, and I won’t be happy till I see every member of that non-administration in jail.

Canto: Okay, be prepared for a life of misery. I agree though, that Pompeo is a slimeball, and it’s very likely that this is largely designed as another blame-shifting distraction by the US maladministration. I don’t remember hearing about this from any news source before Pompeo announced it.

Jacinta: Well it’s interesting that, in investigating this, we have to contend with, and generally ignore, two of the most untrustworthy governmental sources of information on Earth, the USA and China. So thank dog for independent journalists, scientists and investigators. We need them so much at this time. The Washington Post has a 2000-word article on the issue, posted on May 1, undoubtedly in response to moves by Frumpy & co to get the US public to blame China for the pandemic. The article describes an assessment from the US intelligence community:

While asserting that the pathogen was not man-made or genetically altered, the statement pointedly declined to rule out the possibility that the virus had escaped from the complex of laboratories in Wuhan that has been at the forefront of global research into bat-borne viruses linked to multiple epidemics over the past decade.

Canto: ‘Pointedly declining to rule out’ means very little. They’re making a point of saying it’s possible? Isn’t it more likely to have come from the ‘wet markets’ – wet with blood that is – as a result of that traditional Chinese fondness for dining and medicating on exotica?

Jacinta: ‘Murky’ is how the WaPo describes the origins. Some scientists are saying it’s highly likely to have been ‘naturally transmitted’, others, not so sure. But the thing is, the scientists are the ones to trust on this, certainly not the Chinese or US governments. And even then you need to check those scientists’ allegiances.

Canto: I should also point out, as so many scientists are doing, that now is not the time for playing the blame game. Knowledge is power, and we need to be pooling our global resources, and our knowledge, to combat this and future pandemics. We need to try and build trust, not to sow distrust. And this isn’t to say that accidents can’t and don’t happen in virology and microbiology labs around the world, including in the USA.

Jacinta: The WaPo also has much to say about renowned virologist Shi Zhengli, team leader at the Wuhan Institute of Virology, which is being targeted by the Trump administration’s propaganda campaign. According to Shi, ‘the institute never possessed the SARS-CoV-2 virus’, while Wuhan’s health commission has found, or claimed, that the first person who died of the virus purchased goods at the Huanan Seafood Wholesale Market.

Canto: So it may have come from seafood?

Jacinta: Don’t know. Probably they sold more than seafood there, or it was part of a wider market. Anyway, many virologists, including US scientists who’ve worked with her, vouch for Shi’s extreme rigour and brilliance. But clearly that won’t stop the US government’s attempt at character assassination. I’ve heard they’re trying to say, or infer, that the virus was engineered at the Wuhan lab – and no doubt millions of Yanks will believe this brilliant theory, that the virus was engineered by mad scientists and then let loose to kill thousands of their own people before being unleashed upon the world – to be followed up by Chinese chem-trails, no doubt.

Canto: And not just Yanks. Anyway let’s move on to a happier topic. Remdesivir.

Jacinta: Well the news is that the FDA in the USA has issued an Emergency Use Authorisation for remdesivir, and the Gilead company which owns this pharmaceutical, has issued a company statement (on May 5), and here’s a quote:

Gilead’s overarching goal is to make remdesivir both accessible and affordable to governments and patients around the world, where authorized by regulatory authorities…. Gilead is in discussions with some of the world’s leading chemical and pharmaceutical manufacturing companies about their ability, under voluntary licenses, to produce remdesivir for Europe, Asia and the developing world through at least 2022. 

I’ve listened to an interview with Gilead’s CEO Daniel O’Day, and he was making all the right caring-and-sharing noises…

Canto: Can we revisit what remdesivir is and does?

Jacinta: Of course. For starters it’s not a cure, it’s essentially ‘an investigational antiviral drug’ (I’m quoting again from the company statement) which, O’Day is careful to point out, ‘has not been approved by the FDA for any use’ (meaning presumably besides this emergency use). He also admits that the drug is the subject of multiple ongoing clinical trials and ‘the safety and efficacy of remdesivir for the treatment of COVID-19 are not yet established’. It’s a nucleoside analogue, one of many that have been formulated over the years, and dozens have been approved for use in treating viruses, cancers, bacterial and other pathogens. Nucleoside (and nucleotide) analogues are designed to resemble naturally occurring molecules used to build the RNA and DNA so essential to our biology. Some of the best-known nucleosides are cytidine, thymidine, uridine, guanosine, adenosine and inosine. The difference between a nucleoside and a nucleotide is that nucleosides are nucleobases linked to a sugar molecule while nucleotides are linked to phosphate groups (oxygen and phosphorus).

Canto: And the key is that in creating an analogue which functions differently from the real thing, they’re trying to obstruct the replication of the pathogen that takes up this analogue, right?

Jacinta: Yes, you’re getting it. Remdesivir actually has several modifications to the nucleoside structure while still functioning as an analogue – that’s to say it still manages to trick the virus into utilising it, and so becoming dysfunctional in terms of replication. A professor of chemistry and biochemistry, Katherine Seley-Radtke, describes the process in relatively simple terms:

Remdesivir works when the enzyme replicating the genetic material for a new generation of viruses accidentally grabs this nucleoside analogue rather than the natural molecule and incorporates it into the growing RNA strand. Doing this essentially blocks the rest of the RNA from being replicated; this in turn prevents the virus from multiplying.

She writes that remdesivir is a three-times-modified version of the adenosine molecule. Firstly, it’s a ‘prodrug’, in that it has to be modified in the body before it becomes active. The active form has three phosphate groups and is then recognised by the RNA polymerase enzyme of the virus. The second modification is a carbon-nitrogen group attached to the sugar, which is the key to terminating the RNA strand’s production. The third modification is a little change to the molecule’s chemical bond, replacing one nitrogen with a carbon, which prevents one of the enzymes of the virus from recognising and excising ‘foreign’ nucleosides. Remdesivir’s modified adenoside remains in the RNA chain, ultimately terminating further production. Got all that?

Canto: I refuse to confirm or deny. But I can read too. There’s a proper clinical trial of the drug being conducted in the USA at present, and other trials elsewhere. Preliminary results show faster recovery in a statistically significant number of patients, but it isn’t a cure, and will likely be part of a cocktail of treatments as other and hopefully even better antivirals are formulated. This follows the approach to treating other dangerous viruses such as hepatitis C and HIV. It’s about getting the death rate, and the badly-affected rate, down. This is as important as a vaccine, at present.

Jacinta: And I’ve heard it’s quite a tricky drug to manufacture, so getting supplies up and sharing expertise globally will be key factors in saving lives.


Written by stewart henderson

May 7, 2020 at 4:17 pm

a DNA dialogue 6: Okazaki fragments, as promised

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Canto: Okay, so first off, why are Okazaki fragments so called?

Jacinta: Well as anyone would guess, they’re named after someone Japanese, in this case two, the husband and wife team Reiji and Tsuneko Okazaki, who discovered these short, discontinuously synthesised stretches of DNA nucleotides in the 1960s.

Canto: Yes their story is intriguing – tragic but also inspiring. Reiji, the husband, was born in Hiroshima and died in 1975 from leukaemia, related to the 1945 A-bomb. He was only 44. Tsuneko Okazaki continued their research and went on to make many other contributions to genetics and molecular biology, as a professor, teacher, mentor and director of scientific institutes. Her achievements would surely make her a Nobel candidate, and she’s still alive, so maybe…

Jacinta: Now the key to Okazaki fragments is this lagging strand. Its directionality means that the DNA primase, followed by the DNA polymerase, must work ‘backwards’, away from the replication fork, to add nucleotides. This means that that they have to have periodic breaks – but I’m not sure exactly why – in creating this lagging strand. So the entire replication process is described as semi-discontinuous because of this fundamental difference between the continuously created leading strand and the stop-start ‘fragmentary’ (at least briefly) lagging strand.

Canto: But we need to know why this ‘backward’ movement has to be stop-start, and I’d also like to know more about this primase and polymerase, thank you.  

Jacinta: Well the Okazakis and their team discovered this semi-discontinuous replication process in studying the replication of good old Escherichia coli, the go-to research bacterium, and it was a surprise at the time. Now, I’m looking at the explanation for this necessarily discontinuous process in Wikipedia, and I confess I don’t really understand it, but I’ll give it a go. Apparently the Okazakis ‘suggested that there is no found mechanism that showed continuous replication in the 3′ to 5′ direction, only 5′ to 3′ using DNA polymerase, a replication enzyme’, to quote from Wikipedia. So they were rather cleverly hypothesising that there must be another mechanism for the 3′ to 5′ lagging strand, which must be discontinuous. 

Canto: And another way of saying that, is that the process must be fragmentary. And they used experiments to test this hypothesis? 

Jacinta: Correct, and I won’t go into the process of testing, as if I could. It involved pulse-labelling. Don’t ask, but it has something to do with radioactivity. Anyway, the test was successful, and was supported by the discovery shortly afterwards of polynucleotide ligase, the enzyme that stitches these fragments together. Now, you want to know more about primase, polymerase, and now ligase no doubt. So here’s a bit of the low-down. DNA primase is, to confuse you, an RNA polymerase, which synthesises RNA from a DNA template. It’s a catalyst in the synthesis of a short RNA segment, known as a primer. It’s extremely important in DNA replication, because no polymerase (and you know how polymerase keeps getting associated with primase) can make anything happen without an RNA (or DNA) primer.

Canto: But why? This is getting so complicated.

Jacinta: I assure you, we’ve barely scratched the surface….

Canto: Well, Socrates was right – there’s an essential wisdom in being aware of how ignorant you are. We’ll battle on in our small way.    





Written by stewart henderson

February 27, 2020 at 5:48 pm

a DNA dialogue 5: a first look at DNA replication

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schematic of ‘replisome’ structures involved in DNA replication


Jacinta: So let’s scratch some more of the surface of the subject of DNA and genetics. A useful datum to remember, the human genome consists of more than 3 billion DNA bases. We were talking last time about pyrimidines and purines, and base pairs. Let’s talk now about how DNA unzips.

Canto: Well the base pairs are connected by hydrogen bonds, and the two DNA strands, the backbones of the molecule, run in opposite, or anti-parallel, directions, from the 5′ (five prime) end to the 3′ (three prime) end. So, while one strand runs from 5′ to 3′ (the sense strand), the other runs 3′ to 5′ (the antisense strand). 

Jacinta: Right, so what we’re talking about here is DNA replication, which involves breaking those hydrogen bonds, among other things. 

Canto: Yes, so that backbone, or double backbone whatever, where the strands run anti-parallel, is a phosphate-sugar construction, and the sugar is deoxyribose, a five-carbon sugar. This sugar is oriented in one strand from 5′ to 3′, that’s to say the 5′ carbon connects to a phosphate group at one end, while the 3′ carbon connects to a phosphate group at the other end, while in the other strand the sugar is oriented in the opposite direction. 

Jacinta: Yes, and this is essential for replication. The protein called DNA polymerase should be introduced here, with thanks to Khan Academy. It adds nucleotides to the 3′ end to grow a DNA strand…

Canto: Yes, but I think that’s part of the zipping process rather than the unzipping… it’s all very complicated but we need to keep working on it…

Jacinta: Yes, according to Khan Academy, the first step in this replication is to unwind the tightly wound double helix, which occurs through the action of an enzyme called topoisomerase. We could probably do a heap of posts on each of these enzymes, and then some. Anyway, to over-simplify, topoisomerase acts on the DNA such that the hydrogen bonds between the nitrogenous bases can be broken by another enzyme called helicase.

Canto: And that’s when we get to add nucleotides. So we have the two split strands, one of which is a 3′ strand, now called the leading strand, the other a 5′ strand, called the lagging strand. Don’t ask.

Jacinta: The leading strand is the one you add nucleotides to, creating another strand going in the 5′ to 3′ direction. This apparently requires an RNA primer. Don’t ask. DNA primase provides this RNA primer, and once this has occurred, DNA polymerase can start adding nucleotides to the 3′ end, following the open zipper, so to speak.

Canto: The lagging strand is a bit more complex though, as you apparently can’t add nucleotides in that other direction, the 5′ direction, not with any polymerase no how. So, according to Khan, ‘biology’ adds primers (don’t ask) made up of several RNA nucleotides.

Jacinta: Again, according to Khan, the DNA primase, which works along the single strand, is responsible for adding these primers to the lagging strand so that the polymerase can work ‘backwards’ along that strand, adding nucleotides in the right, 3′, direction. So it’s called the lagging strand because it has to work through this more long, drawn-out process.

Canto: Yes, and apparently, this means that you have all these fragments of DNA, called Okazaki fragments. I’m not sure how that works…

Jacinta: Let’s devote our next post on this subject entirely to Okazaki fragments. That could clarify a lot. Or not.

Canto: Okay, let’s. Goody goody gumdrops. In any case, these fragments can be kind of sewn together using DNA ligase, presumably another miraculous enzyme. And the RNA becomes DNA. Don’t ask. I’m sure all will be revealed with further research and investigation.


Leading and lagging strands in DNA replication (Khan Academy video)

Written by stewart henderson

February 26, 2020 at 10:59 pm

coronavirus – a journey begins

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this is an electron micrograph of 2019-nCoV – ref JOHN NICHOLLS, LEO POON AND MALIK PEIRIS/THE UNIVERSITY OF HONG KONG. The cell is infected with the virus (the little black dots), which migrates to the cell surface and is released

Lots of information and disinformation around the recent outbreak of coronavirus, and my own occasional workplace, a college that teaches academic English to overseas, predominantly Chinese students, is naturally affected by the precautionary procedures and the possibly OTT concern.

This is a new strain of coronavirus, first detected late in 2019. It hasn’t been given a specific name, as far as I’m aware (apart from 2019-nCoV,  which I doubt will catch on) so lay people tend to think this is the one and only coronavirus, since most have never heard the term before. These viruses are zoonotic, transmitted between animals, from bats to humans. My interest is most personal, because when I read that the signs are ‘respiratory symptoms, fever, cough, shortness of breath and breathing difficulties’, I recognise my life over the past several years. I wouldn’t go as far as to say I have a fever, but all the other signs are just features of my life I’ve become inured to over time. I’m reluctant to even talk to people lest my voice catch in my throat and I have to give myself up to hideous throat-clearing, which I do scores of times a day. I’m also afraid to get too close as I assume my breath smells like rotten meat. I should probably wear a face mask at all times (hard to get one for love or money at this point). My condition has been diagnosed as bronchiectasis, possibly contracted in childhood, but I’m fairly sure it was exacerbated by a very severe bout of gastro-enteritis in the late eighties, which left me bed-ridden for several days, too weak to even get to the toilet. When I eventually recovered enough to drag myself to the doctor, she arranged for me to go to the hospital next door for blood tests. It was unspoken but obvious to me she thought I might have AIDS, which I knew was impossible given my non-existent sex life and drug habits. It seems to me, but I might be wrong, that my life of coughing, sniffling and raucus throat-clearing took off from that time.

All this by way of explaining why these types of illness catch my attention. WHO advice is for people to, inter alia, wash hands regularly, cook meat and eggs thoroughly, and keep clear of coughy-wheezy-sneezy people like me. 

Coronaviruses are RNA viruses with a long genome, longer than any other RNA virus. According to Sciencealert they’re so called because of the crown-shaped set of sugar-proteins ‘that projects from the envelope surrounding the particle’. This one is causing perhaps a larger panic than is warranted, when you compare its fatalities (and the numbers should be treated with skepticism at this stage) with those associated with regular flu season. Of course, the difference is that this coronavirus is largely unknown, in comparison to seasonal flu, and fear and wariness of the unknown is something naturally ‘programmed’ into us by evolution.  

There’s an awful lot to be said about this topic, biochemically, so I’ll write a number of posts about it. It’s not only of great interest to me personally, but of course it fits with my recent writings on DNA and its relations, including RNA of course, and to a lesser extent epigenetics. I’m becoming increasingly fascinated by biochemistry so it should be an enjoyable, informative journey – for me at least.


Cases of the new coronavirus hint at the disease’s severity, symptoms and spread

Updated: Your most urgent questions about the new coronavirus

Written by stewart henderson

February 8, 2020 at 10:57 am

Posted in coronavirus, health, RNA, viruses

Tagged with , , ,