Covid, flu, and the fight against airborne viruses

Covid research has given us some unexpected insight into the flu: Contrary to what most of us have believed since forever, we’re not likely to catch the flu by touching contaminated surfaces. Yes, the viruses for flu and Covid can both survive on surfaces for some time, but the experiments demonstrating that used industrial strength amounts of virus–more than you’d find in real life–and that skewed the results. What’s more, a lot of the viral particles the experiments found were no longer infectious. It was viral RNA, which is “more like the corpse of the virus” than like the virus itself according to Emmanuel Goldman, of Rutgers University. 

Goldman was the first person to challenge the hygiene theater that had people sanitizing their groceries, washing their hands, and singing “Happy Birthday” to make sure they’d washed long enough. 

Or maybe it was only in Britain that people sang “Happy Birthday.” It was recommended by our then-prime minister–what was his name?–as a way to know you’d scrubbed for twenty seconds.

To be fair, that was relying on the medical advice available at the time. If he’d been marginally competent in other ways, I might forgive him.

Of course, I might not, but that’s a different post, and one I don’t plan to write. We could’ve skipped both the hand washing and the singing. Like Covid, the flu is airborne, and that’s how we’re most likely to catch it. During the first year of the pandemic, when people were still taking masks seriously (in spite of the people who hadn’t figured out that their noses were part of their breathing apparatus and that their chins weren’t), flu transmission went down to almost nothing.

Irrelevant photo: An azalea, now blooming indoors.

All that Covid-inspired hand washing did do one thing for us: It improved food safety.

Having called time on hygiene theater, Goldman is now pointing us toward a way out of the pandemic: 

Respiratory viruses like COVID-19 and the flu spread primarily indoors, so we need a safe virus-killing reagent that can be pre-deployed in occupied spaces. As it happens, we already have one.

“Triethylene glycol (TEG) is an air sanitizer that has been shown to be safe for humans to breathe at low concentrations. It’s also been found to kill viruses on surfaces and in the air at those same low concentrations. Given the science, regulatory agencies should fast-track approval of TEG-based air treatments.”

Will they? No idea.

A UK government study evaluates its safety this way: “There is some evidence that repeated exposures to a glycol-based aerosol may result in respiratory tract irritation, with cough, shortness of breath and tightness of the chest. However, it is not possible to extrapolate the findings to other workplaces/settings or to longer-term exposure impacts, without further research.” 

It’s generally used to make theatrical fog. That’s what the bit about “other workplaces” means.

 

A Report from the Department of Covid-Fighting Gizmos

This is going to sound like I’m wearing the proverbial tinfoil hat, but a gizmo that uses no batteries and no wires can detect the presence of Covid in air. It uses a “magnetostrictive clad plate composed of iron, cobalt and nickel, generating power via alternative magnetization caused by vibration.” I have no idea what that means, although I could define every last one of the words–or I could if I looked up magnetostrictive. Why bother when I still wouldn’t follow it? That’s why I’m quoting. 

I can’t give you a link on this, because it came as a download. The article’s title is the poetic “Batteryless and wireless device detects coronavirus with magnetostrictive composite plates.” If you ask Lord Google nicely, he may lead you to something at least vaguely related. 

Exactly what you do with the contraption once you have it is up to you. I imagine sending it into a roomful of people on the back of a small, dog-shaped robot and waiting for it to report back before I go in. If it’s not safe, I’ll just go home, thanks.

Why’s the robot dog shaped? To add a bit of charm to my tinfoil-hat look.

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Another invention allows you–or if not you, at least someone–to watch viruses die as they try to make their way through masks. 

I know. I prefer a book myself. Or TV. Or, hell, social media if I get desperate. But still, the thing’s out there and someone wants to use it.

What does it do? It gets viruses to light up when they die, and by doing that they tell us that very few viruses get all the way through multilayered FP2 masks. That’s reassuring, but the process can also identify what materials are most effective at killing viruses. In other words, we don’t need the dog-shaped robot for this one. People who design masks will find it useful. The rest of us can give it a miss.

 

Coordinating information on long Covid

Worldwide, some 100 million people are believed to be living with long Covid, and a new questionnaire is trying to get a better picture of its impact, giving researchers better information. 

Existing questionnaires don’t cover the full spectrum of its symptoms. It’s not just fatigue; it can also be vomiting, incontinence, erectile dysfunction, hair loss, and so much other other fun stuff. The new questionnaire breaks the symptoms into 16 categories and uses a single scale to measure their severity, nad it can be “e-migrated, translated, and cross-culturally validated,” which I think means it’s set up to be translated into hundreds of languages. Accurately. Taking into account the cultural context in which it’ll be used. 

So far, it’s been approved for use in 50 countries.

 

New drugs in the works

A couple of Covid drugs look promising. Others are in the works, but let’s not spread ourselves too thin. We’ll look at two.

One of them is already used to treat a liver disease (primary biliary cholangitis, in case anyone asks), so its safety has already been tested and its patent has expired, which means it doesn’t cost a fortune. What’s more, it’s easy to store, it’s easy to ship, and it can carry a tune even when a symphony orchestra’s playing an entirely different one. It never loses its temper. What’s not to like?

Dr. Fotios Sampaziotis, of Cambridge University, explained it this way: “Vaccines protect us by boosting our immune system so that it can recognize the virus and clear it, or at least weaken it. But vaccines don’t work for everyone—for example patients with a weak immune system—and not everyone have access to them. Also, the virus can mutate to new vaccine-resistant variants.

“We’re interested in finding alternative ways to protect us from SARS-CoV-2 infection that are not dependent on the immune system and could complement vaccination. We’ve discovered a way to close the door to the virus, preventing it from getting into our cells in the first place and protecting us from infection.”

The timing’s good on this one, because the virus has out-evolved the antivirals we’ve relied on. And because it works on the human cell rather than aiming at Covid’s spike protein, it should be variant-proof.

It’s done well in small clinical trials and will be going into larger ones.

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Another drug, in an earlier stage of development, also promises to be variant-proof. It’s called an ACE2 decoy, and it works by luring the virus to itself, so it ignores the cells’ ACE2 receptors, which is the normal route for infection. Once it’s done that, it takes off the top of Covid’s spike, which inactivates it.  

It sounds ugly, but there’s a microscopic war going on in there all the time. 

The drug could potentially be used against other coronaviruses, which enter human cells the same way. It hasn’t been tested in humans yet but they’re moving it in that direction.

Long Covid and the vaccines: do they give us any protection?

I come bearing a shred of good news about long Covid. Or at least it’ll look good to you if, like me, you worry about the prospect of long Covid. This comes from two doctors, Sarah Ryan and Lawrence Purpura, who’ve worked extensively with it. I’ll skip the details on their experience–just follow the link if you’re interested. It’s shortcut week here at Notes. In fact, the shortcuts are so short that I’m going to quote them interchangeably. They’ll never know–and if they do I’ll take no shortcuts in apologizing.

They say the long Covid cases they’re seeing have been less severe than the ones they used to see. They attribute that first to the omicron variants attacking the upper respiratory system, where they don’t cause as many of the heavy duty symptoms–lung complications, increased heart rate, lightheadedness, and chronic fatigue–and second to the vaccines being somewhat protective against long Covid. 

No, the vaccines don’t protect us completely, but “studies show that even one dose of a COVID vaccine reduces the odds of developing long COVID by seven to 10 times.”

Break out the ice cream so we can celebrate, will you? Or at least an M&M.

Irrelevant photo: Fields after a December frost.

Who’s most at risk? An article in Cell “identified four factors that correlate with greater risk of long Covid—type 2 diabetes, prior infection with Epstein-Barr virus, level of Sars-CoV-2 RNA detected in the blood, and the presence of autoantibodies.”

A different study sees being female as an increased risk. That same study saw people’s risk decrease by 30% if they’d have two doses of vaccine.

How likely are people with Covid to get long Covid? No one has a good answer to that. There’s no one definition of long Covid, which makes it next to impossible–or maybe that’s completely impossible–to compile statistics. 

Still, they estimate that something like 1% to 5% of Covid patients will go on to get moderate to severe long Covid. At twelve weeks, around 25% of them report fatigue, 25% report insomnia, 20% report increased heart rate or dizziness, and 15% report neurocognitive deficits–things like short-term memory problems. Some of those symptoms will be very mild to some disabling.

A different study came up with 1% of people who had Covid but weren’t hospitalized coming down with long Covid, 6% of people who were hospitalized, and 32% of people who ended up in intensive care units.

Many people will have what Ryan and Purpura call “profound recovery” in three to six months; 10% will have symptoms that go on for more than a year. An even smaller percentage will still have symptoms after a year and a half. 

So the news is far from an all-clear, but in a bad-news situation, this is good news.

 

Other long Covid news 

I’ve been stacking up articles on long Covid but never seem to get back to them. But here we are in shortcut week, so let’s do a few quick summaries and then run:

  • Covid’s associated with increased liver stiffness–a possible sign of liver injury–months after infection. Note the hesitancy in there: associated with; a possible sign. Nothing definite, just something worth looking into more.
  • Covid can affect the brain profoundly even months after infection.
  • A different study, from the early stages of the pandemic (I hope that’s significant), linked Covid to impaired reasoning, speed of thinking, and verbal abilities, comparing what they saw to the effects of sleep deprivation. The severity of the symptoms matched the severity of the infection.
  • A small study found Covid can damage the DNA in cardiac tissue. Compared to the 2009 flu, “Covid has led to more severe and long-term cardiovascular disease.”
  • Covid’s associated with increased chances of long-term brain problems, including strokes, cognitive and memory problems, depression, anxiety, and migraines. And if that doesn’t make you anxious, tremors, involuntary muscle contractions, epileptic seizures, brain fog, hearing and vision abnormalities, and balance and coordination problems–basically symptoms like the ones that come with Parkinson’s. Vaccines reduce the chances of having any of this joy land in your life by about 20%. Keep in mind, though, that a group of people who’ve had Covid are more likely to face these problems than a group that hasn’t, but that doesn’t mean all of them will.
  • Covid was associated with an increased chance of stroke and heart attack. If the study’s correct, over the course of a year, for every 1,000 people who had Covid, you’d expect to find five extra strokes, three extra heart attacks, and twelve extra cases of heart failure 

Those last two studies show a pattern but don’t show cause and effect so let’s not go off the deep end with them. 

 

Is Covid no worse than the flu?

The claim that Covid’s just like the flu translates to “Don’t get hysterical.” So an article from Australia has given us a comparison of the two. 

Between the beginning of 2022 and August 28, Australia had 44 times as many Covid cases as flu cases and 42 times as many Covid deaths. 

That makes the death rate from Covid lower, right? It looks that way to this number-phobe, but it also misses the point. The absolute numbers are higher. If you find yourself in the group of people who died, you’re not going to be consoled by the percentages. 

Okay, strictly speaking, if you find yourself in that group you’ll be dead and unlikely to care anymore, but still, you see my point: Some 1,700 people were hospitalized with the flu between the start of the year and some date in September–pick a number, any number, because here at Notes we don’t really care. Compare that to a single day in July 2022 when 5,429 people were hospitalized with Covid.

 

Life expectancy

I kind of ditched our good news theme there, didn’t I? Sorry. I had some, I spent it all in one place, and now it’s gone. To hell with it, let’s do more bad news. It’s cheaper.

The Covid pandemic lowered life expectancy worldwide. Or at least in the 29 countries included in one study. That leaves out a bunch, but close enough for our purposes.

Predictably, the losses aren’t evenly distributed. Countries with the most effective responses bounced back to pre-pandemic levels relatively quickly. Countries where the response was less effective may have what the study calls “a protracted health crisis.”

It’s another piece in the argument that Covid’s not just the flu in fancy clothes. Flu in the second half of the twentieth century caused smaller, less widespread drops in life expectancy. 

 

The new variant on the block

The new variant that’s emerged in China is BF.7, which is short for something more complicated, which we don’t need to bother with. It’s more infectious than earlier variants, has a shorter incubation time, and is better at infecting people who’ve already had Covid. The symptoms aren’t that different than we’re used to: fever, cough, sore throat, runny nose, and fatigue, but some people end up with vomiting and diarrhoea.

It’s been found in several countries other than China but doesn’t seem to be spreading as quickly in them, although (as I write this, in mid-December) it’s not clear why.

The future of mRNA vaccines

Covid may end up giving us an unexpected gift–a real one, not some snarky, I’m-saying-the-opposite-of-what-I-mean gift. All the work that went into developing the mRNA vaccines for Covid may soon translate into a flu vaccine that works against all 20 known subtypes of flu. It’s still in the testing stage, but it’s looking promising, and since flu can turn from annoying to lethal without having to file paperwork, this is no small thing.

In animal tests, it reduced symptoms as well as protected the little beasties against death. 

To be clear: protection against death is good. It’s not as good as 600% protection against illness, as we know from the Covid vaccines, which miss that 600% bullseye, but it’s a hell of a lot better than having zero protection against death.

The flu vaccines that are around now are seasonal: they protect against the recent versions but if some new strain that jumps unexpectedly from a bird or animal, adapts to humans, refuses to file paperwork, and turns out to be as potent as the 1918 flu–well, they’re not up to the job.

The 1918 flu? That’s the one those of us over a certain age learned to call the Spanish flu because it didn’t originate in Spain and because it’s important to have someone to blame, however inaccurately.

Thoroughly irrelevant photo: a neighbor’s dahlia

The developers of the new vaccine are currently designing human trials, and with luck the vaccine will be available by 2024.

Yeah, so what else can the technology do?

Since you asked, mRNA technology makes the creation of multivalent (be impressed with that word, please) vaccines relatively easy. 

Multivalent vaccines? They’re the ones like that flu vaccine that fore-arm us against bugs with pandemic potential, even when we’re not forewarned. 

The vaccine we really need these days is a pan-coronavirus vaccine, and one is moving into the human-trial stage. Or it’s fixin’ to get ready to think about moving into the human-trial stage. It’s close. In animal trials, three doses not only protected against severe disease, it also protected against infection and decreased the amount of virus the vaccinated animals shed, so they were less likely to pass it on.

Now we come to the hazy part: The article I read introduced it as a vaccine against coronaviruses in general, but the rest of the article focused on it as a Covid vaccine. I’ll leave you to figure out what that means. I’m short on time and can’t trace this one through the convolutions of the internet. 

The article did say, “The vaccine candidate is a combination of a nanoparticle antigen . . . along with an adjuvant—an ingredient that boosts a vaccine’s effects . . . . The adjuvant formulation, 3M-052-AF, significantly enhanced the immune responses in the animals when combined with the antigen.”

I’d translate that for you but I’m in so far over my head that not even the tips of my fingers reach the air. It does sound impressive, though.

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A Covid nasal vaccine is also in development, and it’s designed to piggyback on the immunity that previously vaccinated people carry. By coming in through the nose, it can work primarily on the mucus lining, which is where Covid likes to throw a housewarming party when it enters a body. If the vaccine works, it will be the emergency number you’ll want to call before the party starts, because you know what kind of neighbors Covid germs are. Loud music, fights, broken glass on the sidewalk. 

I could go on, but you get the picture.

In a trial, the spray protected previously vaccinated mice against both death and disease. It did zilch for unvaccinated mice. In hamster trials, it reduced transmission of the disease. It doesn’t use  live viruses, viral vectors, or adjuvants, and that may make the vaccine safer. 

Why? How much? No idea. Go do your own research.

So far, it hasn’t been tested in humans and the article I read was heavily spiced with the word may, so it’s not time to get too excited about this one. Although that hasn’t stopped me.

What about vitamin D and Covid?

Do vitamin D supplements protect against Covid? According to two studies, no. It makes sense that they would–vitamin D supports the immune system–but in a trial of 6,000 people vitamin D supplements made no difference in the number of either Covid or other respiratory tract infections. A second trial involved 35,000 people and tested vitamin D plus cod liver oil. Again, no noticeable difference emerged.

Both trials have their limits. In one, some people in the control group popped the occasional vitamin D supplement. In the other, most of the participants weren’t low on vitamin D at the start of the trial, so the real trial was with a much small group. And vaccines were rolled out during both trials, throwing the balance off. So don’t count them as conclusive, just suggestive.

The endless, depressing news about long Covid and (new word here) post-Covid

Having had Covid can–emphasis on can; it doesn’t always–leave people with nervous system  damage that messes with anything from their sense of smell to their ability to concentrate. It can increase their chances of having a stroke–not right away but eventually. 

It’s called neuro-Covid. Yes, folks, it’s another new word. Don’t say Covid hasn’t been generous with us.

A study that looked at the cerebrospinal fluid and blood plasma of people with neuro-Covid found an overblown immune response in the group with the most serious symptoms: impairments in the blood barrier that could have been caused by a cytokine storm; antibodies that had turned on the body’s own cells; and an overactivation of the microglia, which are immune cells responsible specifically for the brain. People with serious symptoms also had a smaller brain mass than healthy people, especially in the area responsible for the sense of smell.

“The virus triggers such a strong inflammatory response in the body that it spills over to the central nervous system,” Professor Gregor Hutter of the University Hospital of Basel said. “This can disrupt the cellular integrity of the brain.” 

The researchers are hoping to find a test that could predict long Covid and neuro-Covid before they strike, and to identify targets for drugs to attack–in other words, to identify the excessive immune response at an early stage so they can put the brakes on it. 

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A different study shows that having multiple Covid infections increases the risk of long Covid and of other post-Covid health risks. This was a massive study–5.8 million people in the US Veterans’ Affairs database. Its limitation is that this is a population primarily of older white males, so diverse it ain’t. 

The study showed that, compared to people who hadn’t been reinfected, people with repeat infections are twice as likely to die prematurely and three times more likely to be hospitalized. Heart and lung problems were more than three times more common, and reinfection also contributes to brain conditions, kidney disease, and diabetes.

The risk could increase with each infection.

Are you depressed yet? Sorry. It’s not pretty out there and I would have to open the damn curtains. But since I have . . . 

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Another study came at post-Covid brain problems from a different direction. 

To back up for a minute and state the obvious: The problem with studying brains is that as long as their owners are using them you have to accept some limits on the ways you study them. You only have access to certain information once their owners to die, which most people are reluctant to do, even in the interest of science. So this set of researchers created brain organoids–little clusters of brain cells the size of a pinhead. If the organoids object to being messed with, they have no way of letting us know, so it’s open season and the researchers infected them with Covid.

Sorry, guys. For the greater good and all that.

The researchers found that an unusual number of synapses were eliminated.

So what? Well, synapses are the social media of the brain. They allow the neurons to communicate with each other. In the normal wear and tear that goes on inside a brain, a number of synapses will be eliminated, which may explain why I can’t remember what I did five days ago, not to mention the fingering for an F chord on the guitar: The downsizing committee up there decided I no longer need to know those things and got rid of the relevant synapses in the name of efficiency. I might still want to know that stuff, but it’s austerity up there in my skull and something had to go. I should be grateful my brain didn’t ditch everything I know about commas, because, hey, that’s important.

I’m aware that that last paragraph implies that who- or whatever I am exists separately from my brain, but let’s stay out of that rabbithole while I remind you that austerity is what Britain’s government–or what passes for a government when it’s not tied up with more important business–calls cutting public services. Calling it austerity, though, makes it sound like it’s good for us. Think of it as the kale of the political world.

So what the researchers saw happening in the infected organoids was something like what’ll happen in austerity Britain 2.0, which is Sunakian austerity as opposed to Cameronian austerity. When the promised spending cuts kick in, it won’t just be the F chord that goes, it’ll be the smell of lilacs and where I put my car keys and the oomph I need to get from one end of the official looking letter that just came in the mail to the other so I can figure out if I’m being evicted or asked to serve as the next prime minister.

Did I lose you in that last paragraph? Sorry. I was having such fun–

I’ll summarize in a marginally sane way: In infected organoids, an excessive number of connections were downsized–or as serious people would put it, eliminated. That’s frighteningly like what happens in Alzheimers, Parkinsons, and schizophrenia. 

It’s true that our brains are bigger than organoids, and with luck, more complex. But post-mortems on Covid patients (post-mortems, I remind you, are carried out on people who are no longer using their brains), as well as brain imaging on live patients, show that the gray matter isn’t as thick in people who’ve been infected, which hints at a loss of synapses. 

Keep in mind that we’re still in the land of hints, though, not definitive conclusions, and also that I’m not clear on whether the post-mortems and scans were carried out on people who’d had serious cases of Covid or simply from people who’d been infected.

For the researchers, the next step is to look at whether various drugs will inhibit all that downsizing. 

Some of us living in Britain want to know if some drug can stop the government from downsizing services that have already been downsized so radically that they’re held together by nothing more than thread and newspaper headlines.

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Will you forgive me if I toss in a bit of good news? Paxlovid looks like it decreases the odds of developing long Covid.

Pax-what? It’s an antiviral pill that reduces the chances of hospitalization and death in people who’ve been infected–and reduces the chances of long Covid by 25%.

That’s from a preliminary study–it hasn’t been peer reviewed yet, and its study subjects were (again) mostly older white males in high-risk groups, but the US National Institutes of Health plan to study the drug’s effectiveness on people who already have long Covid to see if it works after the fact.

Covid news: Should we be losing sleep over the new variants?

If you’re even vaguely awake (or as our former and once again active home secretary would say, if you’re a Guardian-reading, tofu-eating wokeanista), then you’ll know that Covid has some new variants, and that they have good publicity agents. So how much sleep exactly should you lose?

Not as much as some of the nightmare-on-Covid-Street headlines would have you think.

Let’s sort the variants into separate piles and talk about them.

 

Irrelevant photo: A California poppy. Or since it’s growing in Cornwall and is at least four generations in, maybe by now it’s a Cornish poppy. (That’s a bit of an in joke and I’ll explain it if anyone’s interested.)

The BA variants

BA.2.75 begat BA.2.75.2, because viruses are good at begatting, even if they’re useless at naming their begotten, and since they work under pressure from both our immune systems and the vaccines that are loose in the world, the descendants that survive tend to be the ones that spread most easily or have some sort of hyped up immunity–and .2 does indeed have some of that.

According to Ben Murrell of the Karolinksa Institutet (that’s not a typo; it’s Swedish), “While antibody immunity is not completely gone, BA.2.75.2 exhibited far more dramatic resistance than variants we’ve previously studied. “

In layperson’s terms, that means, “Well, damn.” It also means some of the antiviral treatments given to people who’ve been hit the hardest won’t work against this one, but all is not lost because one still does. 

That was what passes for good news. (Don’t go away–there’s more good news later on.) On the other side of the balance, the antibodies running around in the blood of anyone with antibodies (that’d be people who’ve been vaccinated or who’ve had Covid) are only about a sixth as effective.

Still, a sixth means they’re not completely ineffective. This is good, but it’s not the good news I was waving signs about. For that, you have to wait. Or skip ahead.

What’s not known yet is how quickly the variant will spread. It’s in several countries but can claim only a minority of cases, so it may not become dominant. It’s also not known whether it’ll drive up hospitalization rates or how protective the vaccines will be against it

Balancing all that out, I’d say it’s not time to panic yet. If you’ll wait a bit, you can always panic later. 

 

The BQ variants

BQ.1 and BQ.1.1 are not to be mistaken for either meat cooked with a sticky sauce–that’s BBQ–or B&Q, which is a chain of British stores that claims to have everything you need for your home and garden. What my home needs is a good coat of paint, and they do have paint supplies, but the problem is getting the paint and the walls in the right relationship to each other. The last time I tried, the dog and the rug somehow got into the relationship and–

Anyway, no, they don’t really have everything I need.

The BQ variants are making headlines and US influencers are running around saying they’re worse than the CDC is admitting. 

The CDC is the Centers for Disease Control, which technically speaking should get a plural, but never mind. What matters is that if the CDC had said they were world-ending, somebody would jump up and say the CDC was trying to panic us all for dastardly reasons of their own. You can’t win this game.

The BQs were begat by BA.5 and last I looked (that was Octover 23) made up 11% of Covid cases in the US. Like BA.2.75.2, they’re pretty good at dodging the neutralizing antibodies we’ve spent so much time and effort developing.

By the beginning of 2023, the BQs are expected to make of 80% of Covid cases. I think that means the world’s Covid cases, but they could be talking about Europe’s. Let’s not split hairs. They spread, probably because of the way they dodge our antibodies. There’s no evidence so far that they’re more severe than the earlier versions or that they’ve completely sidelined the vaccines.

 

The XBB variants

Finally, we have the XBB variant, which instead of being begotten combines two earlier variants. I’m not going to try to explain that–let’s just say viruses have many ways to mutate–and you don’t really care which variants they were, do you?

XBB is already creating subvariants. You know, XBB.1 and all that mess. By October 20, it had popped up in 26 countries and was collecting headlines calling it a nightmare variant. It seems to spread rapidly and it too knows how to slip past our neutralizing antibodies–even more so than the new BQ and BA variants. The last of the monoclonal antibodies–the one that works on the B and BQ variants–doesn’t work here. 

It’s not clear yet whether it causes a more severe form of Covid, but in Singapore, where it’s spread widely and which has a 79% vaccination-and-booster rate and  strict control measures in place, it’s been milder. “The number of people dying or in the ICU is really low,” according to Eric Topol of Scripps Research. “Their protection level is really solid.”

What kind of strict measures

“Facemasks remain compulsory on public transport and in most healthcare facilities. Contact tracing requirements remain in effect for events with more than 500 people. Authorities continue to bar unvaccinated people from dine-in services.” People who test positive are quarantined at home.

There’s no evidence XBB and its kiddies make anybody sicker than the earlier variants, and it’s too early to tell how well the new booster shots will work against it, but educated guesses say they’re still be well worth having.

“We’re going to have another wave,” Topol said. “The question is, how bad is it going to be?”

Can’t remember who Topol is? He’s up a few paragraphs.

 

On the other hand

Should we all just go out and slit our wrists?

No. It’s messy, it causes pain, and it’s not necessary. The new variants are a problem, but–and it’s a big but (with one T, thank you very much)–neutralizing antibodies aren’t the only insult in our immune systems’ vocabulary. We focus on them because they’re easy to measure, but our immune systems know other ways to get under Covid’s skin–or maybe that’s its spike protein. Or–

You know what? Never mind. Failed metaphor. Move on. Nothing to see here.

Our immune systems have T cells. And B cells. And if they’re English speakers, they’ve still got 24 letters in the alphabet once they use those up. What’s more, people who’ve had Covid have some letterless (as far as I know) immune cells throwing parties in their lungs.

We’re not completely unprotected.

The phrase Immune escape (which I’ve avoided using but which serious people will) has been misinterpreted. It sounds like it means time to panic. It doesn’t. 

Especially since multiple articles are telling us about research groups edging closer to a universal (or near-universal–I’ll settle for that) coronavirus vaccine which would, at long last, put an end to this damn pandemic. So put the knife back in the drawer. We can do without the drama, thanks.

Bits of good news about Covid

We’re talking about Covid again, so let’s grab some shreds of good news and pile them up like hamster bedding–only (if I remember my brother’s hamster correctly) not as stale smelling.

 

Shred number one

A study involving older, high-risk adults showed that nasal irrigation reduced the risk of hospitalization and death from Covid and helped people recover faster. 

What does “older” mean if we don’t have a comparison group? C’mon, we all know that in our culture it’s not nice to say someone’s old. They’re trying to be polite. My best guess is, older than the researchers.

Next question: What’s nasal irrigation? An inexpensive and low-tech way of clearing out your sinuses. You squirt a mild sterile saline solution up one nostril, tipping your head so it dribbles helplessly out the other, having found its way via satellite navigation. As the solution falls into the sink, you’ll hear a small voice saying, “You have reached your destination.” 

Irrelevant photo: It must be time for another cat photo. This is Fast Eddie, who doesn’t look like he was assembled correctly but was. Really.

Okay, I asked Lord Google what it involves, and I even tried doing it. It’s mildly off-putting but I’ve done worse things in the name of health. It’s entirely survivable.

But let’s go back to the study: Only 1.3% of the subjects were hospitalized, and none died. Compare that to the control group, where 9.47% were hospitalized and 1.5% died. Group one also got better faster and had fewer symptoms hanging on at the end of two weeks. 

The inspiration behind the study was 1) that saline decreases Covid’s ability to attach to cells–to the ACE2 receptor, in case you’re taking notes and 2) that the larger a person’s viral load is, the sicker they’re likely to be, so if within 24 hours of testing positive (the study’s designers reasonsed) some of the virus was rinsed out, that might reduce Covid’s damage. 

Nasal irrigation is a common practice in Southeast Asia, and interestingly enough death rates from Covid were lower there. That’s not definitive proof, but it’s intriguing enough to make a person design a study around it–if the aforesaid person happens to be in the right line of work, of course. 

Irrigation also helps with colds, postnasal drip,  sinus headaches, and all sorts of fun stuff. It’s said to improve people’s sense of taste and smell and the quality of their sleep. 

I’m starting to sound like a true believer, aren’t I? Sorry. I’ll recover in a minute or two, as soon as I stop this saline solution dribbling out of my left nostril. In the meantime, I can balance things out by admitting that it won’t make you taller or reverse aging.

 

Shred number two

A small study hints that vaccination may be decreasing the number of people who come down with long Covid. The study comes from the long Covid clinic at the Cambridge University Teaching Hospital, which treats people on the severe end of the spectrum. Between August 2021 and June 2022, it saw a 79% drop in referrals compared to August 2020 and July 2021.

That’s not proof that vaccination’s the cause–it’s only correlation–but it does suggest it.

Other studies also show a decrease, although the numbers have been all over the map. One showed a 15% reduction and another 50%. A third showed “eight of the ten most-commonly reported symptoms were reported between 50 and 80% less often.” I’d translate that into a format that parallels the other studies but somebody glued the pieces in place and I can’t. 

The reason the numbers vary so much is that the studies weren’t defining long Covid the same way or following people for the same length of time. 

So does catching Covid multiple times increase your odds of getting long Covid? The assumption has been that with each infection, you roll the dice again, taking the same risk each time. But one author of the study expects that previous infections will have more or less the same impact as vaccination and the risk will turn out to diminish after the first infection.

Probably.

 

Shred number three

The omicron variant may be 20% to 50% less likely to turn into long Covid than the delta variant, depending on a person’s age and how much time has passed since they were last vaccinated. 

But–and isn’t there always a but?–because more people caught the omicron variant than the delta, the absolute number of people in the UK who came down with long Covid as a result was higher. 

Sorry. That second paragraph was as welcome as a thorny old blackberry cane sneaking into the hamster bedding.

 

Shred number four

Allergies might offer some protection against Covid. Do you have hay fever, allergic rhinitis, eczema, dermatitis? Be grateful for your bad luck, because you may be 23% less likely to get infected . Got one of those plus asthma? Be grateful twice: It may have down by 38%. 

That’s not proof, but it’s an interesting possibility.

 

Shred number five

A study estimates that in the first year Covid vaccines were available, they prevented 19.8 million deaths worldwide. Unfortunately, though, because of how unevenly they were distributed, the advantage was heavily skewed toward the richest countries.

You knew it wouldn’t all be good news here, didn’t you? 

During the first Covid wave, before vaccines were available, shutting schools cut daily deaths by 1.23 per million over 24 days and shutting workplaces cut daily deaths by 0.26 per million over 24 days. (Kids were less likely to get sick but they’re generous little creatures and they do like to share their germs.) For a population of 67 million (which just happens to be Britain’s population), that translates to roughly 82 deaths avoided every 24 days by shutting schools and 17 by shutting workplaces.

Lockdowns and restrictions on public transportation didn’t have as significant an impact. The difference is at least partially attributable to vulnerable people not being able to avoid workplaces and schools.  

 

Shred number six

India and China have approved inhalable vaccines, and many medical manufacturers are chasing their own inhalable versions. Injected vaccines concentrate antibodies in our muscles, which is useful, but we catch Covid by inhaling it, so the theory goes that loading the nose and mouth with antibodies could potentially keep us from spreading it. In other words, it really could end the pandemic.

Potentially. I don’t think the data on either of the new vaccines have been made public yet, so keep watching.

 

And now your weekly quota of bad-to-ambiguous news

Tedros Adhanom Ghebreyesus, head of the World Health Organization, said, “Last week, one person died with Covid-19 every 44 seconds. Most of those deaths are avoidable.”

That quote’s from early September .

“You might be tired of hearing me say the pandemic is not over. But I will keep saying it until it is.”

A week later, he said “We have never been in a better position to end the pandemic. We are not there yet, but the end is in sight.”

However, “If we don’t take this opportunity now, we run the risk of more variants, more deaths, more disruption, and more uncertainty.”

WHO is urging countries to continue testing for the virus, to continue sequencing it, and to vaccinate 100% of the most at-risk groups, including health workers and the elderly.

Covid: It ain’t over till it’s over…

…as the endlessly quotable Yogi Berra may or may not have said.

But forget Berra. The World Health Organization, a.k.a. WHO, isn’t as much fun to quote but it knows how to do footnotes, and that makes it more impressive. In its opinion, the pandemic isn’t over. Between the beginning of 2022 and late August, at least a million people around the world died of Covid. 

Or if you want to start counting at the beginning of the pandemic, that’s 6.45 million. Both numbers undercount the damage, but never mind that. Let’s work with what we’ve got.

”We have the tools that can actually prevent these deaths,” said Maria Van Kerkhove, WHO’s technical lead on Covid. “A lot of people are talking about living with COVID. But we need to live with this responsibly. A million deaths this year is not living with COVID. Having 15,000 deaths per week is not living with COVID-19 responsibly.”

In one recent week, more than 5.3 million new cases were reported worldwide, a number that doesn’t include people who registered positive only on a home test. Or who never tested.

“These are huge numbers, and that’s an underestimate,” said Van Kerkhove. “We do see this virus circulating really intensely around the world.”

Irrelevant photo: an orchid

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That brings me to the question of why I keep banging on about Covid. Apologies if I’ve gotten boring–Notes isn’t supposed to be mindless, but it is supposed to be a fun read. The problem is that scientists keep coming up with new information. What I’m saying here is, Blame the scientists. If they weren’t so damn good at this, it wouldn’t end up in your inbox.

And if that isn’t a good enough reason, it’s because it still matters. Living with Covid doesn’t have to mean pretending it’s no danger.

 

Long Covid 

Let’s talk about long Covid. Again. Sorry to keep coming back to it, but not long ago someone challenged me on the extent of the problem (my thanks; it was an interesting discussion) and since long Covid’s hard to define and at least as hard to measure, I didn’t have great statistics to offer. But I have started to see some lately, so let’s play with numbers. They all involve money, since it can be counted, and when you’re dealing with something as hazy as long Covid that’s useful. Besides, as we all know, money matters more than life itself.

So let’s talk money: A report from the US estimates that 4 million people are out of work with long Covid, which could mean $170 billion in lost wages. In a year. The report’s author,  Katie Bach, said, “If this looks like other post-viral illnesses, some people will recover, but there will be this big stock of people who don’t, and it will just continue to grow over time.”

She called it “a shocking number.” 

In mid-2021, the Federal Reserve Bank of Minneapolis estimated that 26% of people with long Covid were out of work or had cut their working hoursAn international survey found that 22% of people with long Covid weren’t working and 45% had cut their hours, and a U.K. survey found 16% had reduced their hours and 20% were on paid sick leave. That was between April and May 2021.

Australia’s treasury reports that the country’s lost 3 million working days to long Covid. Or to put that another way, 31,000 people have missed work every day because of it. 

 

So how many people have long Covid? I’m not sure anybody has a reliable count, but the U.S. Centers for Disease Control estimate that 19% of people who’ve had Covid get long Covid symptoms. Unfortunately, the number’s less helpful number than it sounds like, because long Covid’s symptoms range from relatively mild to completely hair-raising and the duration ranges from weeks to the possibility of a life sentence.  

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Are we having fun yet?

Evidence is growing that people who’ve had Covid face an increased risk of neurological and psychiatric problems as much as two years after their infection. That’s not the final word on the subject, but it comes from a study that followed 1.28 million cases over two years. It does seem to be a strong hint. 

The good news? Depression and anxiety are generally gone after two months and are no more common after Covid than after other respiratory infections. And kids are at the lowest risk for kids for later complications. 

End of good news.

Adults 64 and under showed an increased risk of brain fog–640 cases per 10,000 people vs 550 cases per. Over 65s? The number went up to 1,540 per compared to 1,230. For dementia (we’re still talking about the over 65s here) it was 450 instead of 330. Psychiatric disorders? That’s 85 instead of 60. 

Is there anything can we do about it? Hell yes. I’m going to petition the courts to lower my age.

Does the risk end after two years? We haven’t had enough time for anyone to find that out. 

*

A theory that’s loose on social media holds microclots responsible for long Covid, and some evidence does back that up, but (as one article says) hematologists worry that enthusiasm for the theory has gotten ahead of the data.

Danny Altmann, an immunologist at Imperial College London, said, “We’ve now got little scattered of bits of evidence. We’re all scuttling to try and put it together in some kind of consensus. We’re so far away from that. It’s very unsatisfying.”

But that’s not stopping a few medical groups from offering treatment to remove the clots, and some people with long Covid are desperate enough to try anything, which I can understand. But at least some treatments to get rid of clots risk messing with the blood’s ability to clot, and that (she said, indulging in a mild understatement) would not be a good thing.

 

How Covid’s changing

Its incubation period—the time between when a person gets infected and when they’re shedding enough of the virus to infect other people—is getting shorter, and the shorter that time that period is, the harder it is for vaccines to keep the virus from spreading.  

Yeah, that was news to me too. Measles and rubella have a two-week incubation period, which allows time for a vaccinated person’s immune memory cells to crank out antibodies and keep the person from passing the bug to other people. So vaccines for those diseases stop the spread. In contrast, a Covid vaccine, although it protects the wearer, doesn’t protect the wearer’s friends. Or enemies. 

On the bright  side, the shorter incubation time means people who test positive might not have to isolate themselves for as long.

Every cloud has a silver lining, but the problem with that is that silver linings are too heavy to float. Watch out for falling silver linings.

 

Expired tests

You may (or may not) remember that a while back I wrote about the expiration dates on Covid tests. After they pass those dates, I led you to believe (if and only if you read it, of course), they start to call in sick and miss work. Well, I need to update that. The U.S. Food and Drug Administration set the expiration dates in the early days of the pandemic, on the basis of the limited information that was available at the time, but manufacturers are testing aging tests them and some turn out to be good beyond their expiration dates.

How do you know if yours still good?

“To check whether your test kit is still good beyond the printed expiration date, you can search on the FDA’s “At-Home OTC COVID-19 Diagnostic Tests” website.

“Type in the brand name on the FDA site, and a link will appear showing a list of updated expiration dates.

“You may have to check the lot number on your package. For instance, say you’re trying to look up an iHealth COVID-19 test kit with lot number 222CO20208. Scroll down the document to find your lot number, and you’ll find that the original expiration date of Aug. 7 has been extended to Feb. 7, 2023.”

Apologies.

 

An update on Hafiza Qasimi

In early August, I wrote about Hafiza Qasimi, a woman artist fleeing Afghanistan after the Taliban destroyed her paintings and left her unable to work. The campaign to raise the 10,000 euros she needed to apply for a German visa has reached its goal. This allows her to demonstrate that she can support herself for her first year in the country. (The amount will be raised to 11,208 in January.)

In the meantime, Qasimi has reached Tehran. I have no idea how she did that. In Afghanistan, women aren’t allowed to either travel or leave the country unless they’re with their husband or a male a relative. But she managed it, she’s safe, and she’s been offered a three-month residency at a German art gallery is she can get that visa.

The group supporting her is trying to raise more than the 10,000 euro minimum so that she can afford health insurance and other basics. They’re also working with her on a grant application that would allow her to study at art school.

“This,” they say, “will provide her with the space she needs, as a free woman, to renew and develop her artistic work. We are full of confidence and look forward with Hafiza to the future.”

Her brother, who lives in Germany, will be flying to Tehran to see her for the first time in eight years.

If you want to contribute to the fundraising campaign, any amount will be welcome. And if you don’t (or would love to but can’t), that’s okay. Do what you can where you can and wish her joy in her freedom.

It’s variant day at the Covid Cafe

Welcome to the Covid Cafe, my friends. We have two variants on the menu today.

 

BA.5

Our first variant, BA.5, has gotten better than previous versions at evading both the vaccines and the immunity people acquired from earlier infections. But where previous omicron variants tended to stay in the upper respiratory tract, making it somewhat milder, BA.5 has picked up some mutations from the delta variant–that’s the most damaging variant to date–and it’s very pleased with them, thanks, and with itself for being so clever. 

They may be the reason it’s better at infecting cells than those respiratory-type omicron variants, and why it may be more serious. 

Seeing it circle back in this way doesn’t make me want to go out and celebrate. On the positive side, though, the current vaccines do still protect against its worst effects. But sensible people are recommending masks, ventilation, and distance–all those things governments and a lot of our fellow citizens have gotten bored with. 

 

Irrelevant photo: thistle with bee

BA.2.75

Are we having fun yet? 

Our second variant is BA.2.75. It seems to spread quickly and to evade immunity. How hard it hits people is yet to be determined. It’s also called Centaurus. I have no idea why and my brain isn’t willing to expend any bandwidth on it, but since it’s also possible that the thing has peaked, it has a second name: scariant. 

Come fall, updated vaccines are expected to target the omicron mutations. I’m in line already, and rolling my sleeve up.

 

However

Efforts to create a pan-coronavirus vaccine have slowed down for lack of funding, lack of any sense of pressure, and lack of even marginal good sense. The current vaccines are still keeping death and destruction to a minimum, and hey, that’s good enough. Let’s just stagger on.  I could toss in a quote or two here, but hell, you get the point. Follow the link if you like. It’s find-your-own-quote day here at the cafe.

In addition, testing candidate vaccines won’t be as easy it was at the beginning of the pandemic because Covid isn’t raging through populations the way it was. Pre-existing immunities make their effectiveness harder to measure.

 

Other mutations

A team that’s been analyzing millions of omicron samples in order to study its mutations reports that omicron alone has 130 sublineages. A member of the team, Kamlendra Singh, thinks vaccines might become less effective over time.  

“The ultimate solution,” he said, “will likely be the development of small molecule, antiviral drugs that target parts of the virus that do not mutate. While there is no vaccine for HIV, there are very effective antiviral drugs that help those infected live a healthy life, so hopefully the same can be true with COVID-19.” 

Singh helped develop CoroQuil-Zn, a supplement that infected people can take to help reduce their viral load. It’s currently being used in India, southeast Asia, and Great Britain and is waiting for FDA approval in the United States.

A virologist writing in the Conversation agrees, at least in part, saying that vaccines targeting recent variants will inevitably fall behind as the virus mutates. “Vaccines that generate antibodies against a broad range of SARS-CoV-2 variants and a cocktail of broad-ranging treatments, including monoclonal antibodies and antiviral drugs, will be critical in the fight against COVID-19.”

 

Long Covid news

Long Covid’s too stale for the cafe, but it’s not growing mold yet, so let’s have a nibble out here in the alley. 

The BMJ (formerly known as the British Medical Journal) has summarized 15 studies showing that the vaccinated are less likely than the unvaxxed to end up with long Covid. That’s most true of people over 60 and least true of people between 19 and 35. 

Long covid can range from annoying to life changing (in a bad way, in case that’s not already clear; it won’t make you grow wings or develop superpowers). It also ranges from transient to no-end-in-sight. In the UK, 2% of the population has reported having it and in the US, that’s 7.5%. 

Or by another count, 2 million people in the UK have it. That may or may not work out 2%. Don’t worry about it.  

Why is the percentage in the UK so different from the one in the US and why don’t I care if the UK numbers match? Because no one’s tracking long Covid systematically. It can get pretty weird out there.  

With that out of the way, let’s talk about the important stuff: “hy did the British Medical Journal change its name? I don’t know, but since my father did the same thing, I shouldn’t roll my eyes about it.

Which is unlikely to stop me. Especially since my father didn’t change his name to an abbreviation,but to the last name I use although I have no deep-rooted claim to it.

On the positive side, that bit of history means I know for a fact the Josh Hawley isn’t a relative–even a distant one.

*

In the absence of systematic tracking, a UK study compared a big whackin’ number of people’s medical records to see what they could learn about long Covid. 

Among other things, they were able to add 42 symptoms to the existing list. (Yeah, progress comes in some annoying colors.) The new ones include hair loss, reduced sex drive, erectile problems, swelling limbs, and bowel incontinence.

I did tell you it could be serious, didn’t I? You should listen to me. 

They also organized the symptoms into three categories: 80% of the people with long Covid symptoms had a broad spectrum of problems, from fatigue to pain; 15% had mental health and cognitive problems, from depression to brain fog; and 5% had respiratory problems.

*

A small study treated long Covid patients with cognitive symptoms by using hyperbaric oxygen therapy, and the results were enough to give a person hope. The group that got the real treatment had “significant improvement in their global cognitive function and more cognitive improvement related to their specific damaged brain regions responsible for attention and executive function,” along with improvement in their energy, sleep, and psychiatric symptoms.

The patients who got the placebo treatment didn’t, although they did get a simpler sentence with no fancy language or quotation marks.

The treatment, unfortunately, isn’t something you can set up in your garage. It involves five treatments a week for two months in a machine that looks like a mid-size submarine. 

 

Protective actions you never thought of

Covid is less likely to kill or hospitalize people who fast at least one day a month than it is to do either of those things to those of us who think eating should be a daily practice. This may be because fasting reduces inflammation or it may be attributable to a couple of other reasons that you can look up yourself by following the link.

The bad news? The study involved people who’d been fasting intermittently for decades. It offers no information on people who took it up twenty minutes before becoming infected.

 

A bit more about vaccines

I’ve found enough shreds of good news that I can spare you one more piece: Vaccination, although it doesn’t prevent Covid, does seem to reduce the odds of infection. Not by as much as we’d all like, but I don’t know about you, I’ll take any percentage I can get.

You want details, though, right? Fine: In the second wave of the pandemic, vaccinated National Health Service employees who worked face to face with patients were 10% less likely to get infected than unvaccinated ones. And I’ll remind the assorted anti-vaxxers who pop up here periodically that the primary value of the vaccines lies in preventing death and serious illness, which (do you really need to be reminded?) is not a bad thing. They haven’t turned out to create sterilizing immunity, and that’s a damn shame but doesn’t mean the people who recommend them should be burned at the stake. 

No one’s offered to do exactly that to me yet, but the conversations do have a way of turning hostile. Or starting out that way. A recent comment opened with, “Stop lying, Ellen.”

And I appreciated the suggestion, since hadn’t thought of that myself. I also appreciated the generous and high-minded approach to discussion. Let it be a model for us all.

*

But forget about me. Ben Neuman, a professor in the Department of Biology and chief virologist at the Texas A&M Global Health Research Complex, has another reason to get vaccinated: “to avoid the brain damage that often comes with COVID. During a natural infection, the immune response around your brain will starve cells of oxygen, and the effect is that you will lose a lot of gray matter—something like a stroke. Unlike a stroke, where usually only one part of the brain is affected, COVID seems to affect the entire brain, so you don’t necessarily lose one thing, like the ability to control nerves on one side of the face, you lose a bit from everywhere. COVID-associated brain damage only happens with infection, not with the vaccine, and having a strong set of white blood cells trained by the vaccine is likely to be helpful in preventing brain damage.” 

 

Okay, but what about monkeypox?

Let’s forget about whether monkeypox is a pandemic or an epidemic or just a damned nuisance. Those–especially damned nuisance–have technical definitions that, for a bunch of free-range blog readers, aren’t the most useful standards. The more pressing question is, How much of a problem is this likely to be?

After what sounds like a lot of internal argument, the World Health Organization declared it a global health emergency. The disagreement, as far as I understand it, comes from this: Diseases that spread on the air (think Covid or flu) are bigger worries. They’re easy to catch. Monkeypox is spreading through touch. That doesn’t make it fun and I don’t recommend rubbing up against anyone with a rash right now, but it does mean transmission’s slower and more difficult.

It’s also less deadly than Covid. 

If that’s not reassuring enough, existing vaccines can slow the spread–or they can once production catches up with the need.

On the other hand, it’s popping up in a wide range of countries and seems to have surprised the experts.

Monkeypox could (I’ve read) go in two directions: It could establish itself in many countries as a sexually (an also not-sexually) transmitted disease that people will have to deal with or it could be gotten under control. The first prospect isn’t fun, but it’s still not Covid all over again.

What causes long Covid?

A lot of clever people are chasing the cause of long Covid, but so far the virus is outrunning them–and we’re talking about a virus, remember, that doesn’t have a degree in either science or medicine and that’s rumored to be illiterate.

Not that I’m making fun of those clever people. Long covid scares the bejeezus out of me and I’m grateful for the work they’re doing, but I’m also painfully aware that they haven’t even found all the puzzle pieces yet, never mind gotten them in the right place. 

Puzzle pieces? What happened to the chase metaphor? 

I couldn’t keep up with it and had to grab something else off the shelf where I store my cliches.

Irrelevant photos: Morning glories–or as the British call them, bindweed.

But back to our actual subject: The clever folk are at the stage where they have theories, but that’s not all bad. Theories open up possibilities and they’re a good place to start. Let’s check in with a few of them:

Pediatrician Danilo Buonsenso noticed that some of his patients–these are kids, remember, with their habit of showing up at pediatricians’ offices and licking their fingers before touching the toys–

Where were we? Some of his patients who’d had mild Covid cases were left short of breath, exhausted and sporting a variety of other symptoms. That’s not common in post-Covid kids, but what with him being a doctor and all, and one who specializes in infectious diseases (I know, I didn’t get around to mentioning that earlier)–well, the kids he’s most likely to see are the ones who are sick, which skews the sample.

As the article I stole this from explains it, “He now suspects that, in some of them, the cells and tissues that control blood flow are damaged and the blood’s tendency to clot is amplified. Minute blood clots, leftover from the viral assault or fueled by its aftermath, might be gumming up the body’s circulation, to disastrous effect from the brain to joints. ‘In some patients we have specific areas where no blood flow comes in’ or the flow is reduced, Buonsenso says. 

Another theory comes from  microbiologist Amy Proal: that the virus hangs on in the body after the acute stage of the infection is over. Studies show that “the virus is capable of persistence in a wide range of body sites,” she said. 

A third theory comes from Chansavath Phetsouphanh, who’s observed that the immune cells of long Covid patients are still on high alert as much as eight months after they first tested positive. 

A fourth theory comes from Nick Reynolds, who found amyloid clumps in the brains of people with the neurological symptoms of  long Covid. They’re similar to the clumps that cause Alzheimer’s disease and dementia. That doesn’t necessarily mean the patients will have lasting damage or that the drugs used to treat those diseases help in these different circumstances. On the other hand–well, who knows at this stage? It might.

Are any of the theories right? Are all of them showing us a small piece of a large picture? Tune in sometime later–possibly a lot later–for the next exciting episode of What’re We Going to Do to Get Out of This Mess? And keep in mind that once the clever people figure out what’s driving long Covid, they or some colleagues still need to figure out a treatment.

Don’t you just feel better after you hang around here? 

In the meantime, an assortment of studies are following up on the possibilities these theories raise. Wish them well, please. It won’t make any material difference, but it might make you feel like you contributed to the effort.

 

Numbers

How many people actually have long Covid? Answering that depends on how we define long Covid, but let’s set that aside. We’re not scientists–or most of us aren’t and anyone who is must be slumming. We can get away with being hazy when it suits us. 

In May, the U.S. Centers for Disease Control and Prevention rampaged through the medical records of some 2 million people and reported that at least 1 in 5 people who’d had Covid came away with long Covid symptoms. For some of them, that meant struggling but hanging onto their normal lives. For others, it meant struggling, only with nobut at the end of the sentence.  

In the UK, some 2 million people have long Covid according to the Office for National Statistics, which does have a definition of the thing but never mind what it is. We’re not scientists, remember? Or else we’re slumming and will have to put up with the way other people’s minds work. 

Proal (remember her?) said, “I consider Long Covid to be a massive emergency.”

 

Who’s most at risk of long Covid?

A small study from Japan found that being over 40 increased the odds. So did being over 60. Since I’m over both (it took a while, but I got there), this is not good news where I live. 

In contrast to other studies, it didn’t find sex to be a big factor, although long Covid seemed to have a harder psychological impact on women than on men. 

In contrast, a UK study found that being female, being in poor pre-pandemic mental and physical health, being obese, and having asthma all increased the odds of long Covid. 

Do the two studies contradict each other? Partially. The data they’re working from is sketchy, but the issue’s important enough to use it anyway. Take them for what they’re worth.

The UK study finds that between 7.8% and 17%of the people who reported having Covid also reported symptoms that lasted longer than longer than 12 weeks, and between 1.2% to 4.8% reported  that the symptoms were debilitating. 

Why the range? I haven’t a clue. I find numbers debilitating.

The numbers were lower when they worked from doctors’ records as opposed to self-reports, but that could be because doctors weren’t reporting long Covid before November 2020.

 

A shred of good news

The omicron variant may be less likely than delta to cause long Covid–20 to 50% lower. To put that another way, with omicron, 4.4% of cases turned into long Covid. With delta, that was 10.8%. But that’s still a shitload of people.

 

More numbers: What have vaccinations ever done for us?

Well, in the first year they were available, they prevented an estimated 19.8 million Covid deaths. That’s based on excess deaths in 185 countries and territories. 

Excess deaths? It’s the figure you use when you don’t have any other consistent or reliable way to count the pandemic’s impact. In rough terms, it compares deaths during the pandemic to deaths in some pre-pandemic year. It’s imperfect, but the other systems are even more so. If you don’t use it, you end up counting the number of people who (if they weren’t dead) could brag about having Covid listed on their death certificates. You miss a lot of people that way. You can also count the number who are known to have had Covid and who then went on to die, leaving you counting people who died because a brick fell on their head and missing some who died undiagnosed. Or you can count people who die within 28 days of a diagnosis and miss the ones who took too long to die as well as include a few who had unfortunate encounters with bricks.

The UK switched methods midway through the pandemic, probably because the government wanted it to look like fewer people had died and the new way yielded a lower number. 

Yeah, I have absolute faith in the people leading the country. They’ll do whatever works best for them and to hell with everything and everyone else.

Not only is none of the systems accurate, different countries rely on different definitions of a Covid death, raising hell with international studies. 

But let’s put death on the shelf for a minute and go back to vaccines and lives saved, which is what we’re pretending to talk about. The study estimates that 599,300 more lives would’ve been saved if the world, lower case, had met the World (upper case) Health Organization’s target of getting  two or more vaccine doses to 40% of the population of every country by the end of 2021

By now, 66% of the world’s population has received at least one dose of vaccine.

 

More numbers

In 2020 and 2021, Covid was the third leading cause of death in the United States, crossing the finish line after cancer and heart disease. So it gets a bronze medal and modest bragging rights, but not as much glory as it was hoping for. 

Are the expiration dates on Covid tests for real?

I raise this question because I’m an expiration date-denier, at least in most situations. I’ll bake with flour that’s older than I am. I don’t toss food out until it reeks or evolves new life forms. I don’t take orders from the small print on food packaging. 

To my lasting disappointment, though, test kits do get to boss us around. When they pass their use-by date, they start returning false negatives. And the worst of it is, they expect us to be at least a little sympathetic about it. Wouldn’t we get tired of sitting on a shelf and waiting for someone to decide they might have a use for us? And don’t we also turn a little negative with all that passivity and waiting? 

So apologies, but we really do need to pay attention. 

When do the ones on my shelf expire? Haven’t a clue. I should go look but I think I’ll wait and go into a panic about it when I need one.

Irrelevant photo: a poppy

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Remember everything hopeful I’ve written about the possibility of universal Covid vaccines? 

Of course you do. You memorize every word I write. Which is good, because I don’t.

I ask because we’ve got some new Omicron subvariants working their way into the pandemic pipeline, and although they don’t seem to be any more vicious than the old versions, they do seem to be better at immunities. 

The one spreading in the US is called BA.2.12.1, which as far as I can tell means it’s a variant on Omicron 2.0. The others were spotted in South Africa and are called BA.4 and BA.5, which are, at least, easier to remember.

Is it time to panic? Nah. There’s always time for that later. 

The new subvariants are able to infect people who had the first version of Omicron–the one that came out before Elon Musk bought the entire genome. They can also infect people who’ve been vaccinated. But the picture isn’t simple. A lot of vaccines are out there and the study couldn’t cover them all. They may provide greater protection. And in case that doesn’t introduce enough unknown quantities, the variants’ ability to slither past people’s immunities could be, in part, because people’s immunity was starting to wane. It could also be because so many people spell Musk’s first name wrong. So don’t jump to conclusions.

What does it all mean for the fight against Covid? A lot of experts are asking that, including the vaccine makers, who could tweak their vaccines to target Omicron and find themselves, yet again, three steps behind a virus that knows the Greek alphabet better than they do. Translation: We don’t know what the next variants will look like (never mind what letter it will be named after), but we do know that a new variant will appear. And experience tells us that Covid’s good at finding ways to dodge our immune systems.

The obvious solution is a vaccine that targets all forms of Covid, and possibly its coronavirus friends and relations as well, and any number of scientists are chasing after that. But they haven’t caught it yet. It’s fast, it’s clever, and it’s small enough to hide in the undergrowth.

Another possibility is to use a mix of monoclonal antibodies that target various strains of Covid. 

A mix of what? A brew made from antibodies created in response to assorted forms of Covid. Pour the mix into an infected person’s system and it can get to work on whatever it finds.

The problem is cost. One dose currently costs $1,000 per patient, so at best it would have to be limited to the most vulnerable people, and only in countries that can afford it. Or if you’re in the US, it would be limited to individuals who can afford it.But if the brew could be gotten down to $50 or $100 per dose, it would be cheaper than constantly updating vaccines.

What does seem to be certain–at least to observers who haven’t drunk the KoolAid labeled “What the Hell, Let’s Say It’s Endemic and Move On”–is that letting the virus spread and mutate while we shrug our shoulders and tell ourselves to live with it is a recipe for trouble.

Sorry–make that more trouble than we already have, since we’re hardly trouble-free just now.

 

Studies, updates, and patent pools on the spread of Covid

According to one study, you’re a thousand times less likely to catch Covid from touching stuff than you are from breathing in its presence. That’s true not only of you, but also of your friends, your relatives, and your enemies (if you have any, and if you don’t please substitute a few people you never managed to like. And also of me. So if you’re still trying to find that pack of disinfectant wipes you lost at the back of your cupboard (or your neighbors’ cupboard–who knows how these things happen?), relax. You may not need them.

Emphasis, as usual, on may.

Details? Oh, you fussy people. The study was done when lots of antibacterial cleaning was going on and crowds were nonexistent, so let’s not go off the deep end and decide it translates completely to the world we’re living in now. Still, it’s information and it’s worth reading:

The riskiest places, in terms of both air and surface samples, were gyms, with gym drinking fountains rating high on the list of things to avoid. The exercise equipment itself didn’t turn up any positive samples. 

In offices, the study found few positive samples on keyboards, light switches, tables, microwaves, or refrigerator handles. In schools, the same was true of desks.

The survey estimates that the chances of getting Covid after airborne exposure are one in a hundred. From a contaminated surface, it’s one in a hundred thousand–factoring in, of course, that a lot of cleaning was going on at the time, so you might want to move a zero or a decimal point in some random direction to make up for that.

The study didn’t look at the surfaces in people’s homes, dorms, or other places where people live together. I’m not sure how useful any of it is, but I thought I’d mention it.

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A different study looked at the effect of what it called layered controls–basically, masks, distance, and ventilation–and found that the three used together would reduce Covid transmission by 98% in 95% of the scenarios it studied. The study involved the gloriously named atmospheric scientist Laura Fierce. She gets a mention solely on the basis of her last name. 

Ventilation alone doesn’t do much to reduce transmission, although if you add in a distance of six feet it does, and masks reduce the safe distance from six feet to three. 

This is all wonderfully sensible, but are we going to do it? Hell no. The pandemic’s over, hadn’t you heard? If you get sick, it’s your own silly fault.

It’s infuriating. Allow me to refer you to the scientist mentioned above. We need to clone her. 

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A research team in Japan is developing a decoy virus receptor that promises to keep the virus so entranced that it never finds the human cells it set out to infect.This is in the early stages yet, so we don’t know if it’ll keep its promises, but if it does it should stand up to Covid’s shape-shifting ways, at least for a decent interval. 

It doesn’t sound like the decoy would completely neutralize the virus. They’re still talking about less severe infection and increased chances of survival. But staying a step ahead of the virus’s evolution would be good.

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And finally, a bit of good news: The US has put the licenses for eleven Covid-related technologies into a patent pool so that low- and middle-income countries can access them. 

I gather that we don’t have poor countries anymore. We have low-income ones. 

Never mind. The patents include vaccines, drugs, research tools, and diagnostic whatsits. 

The bad news? In some cases, this only gets rid of one roadblock. Countries that want to work with these technologies would still need to negotiate with other patent holders, since nothing about this disease is simple, including who owns what. Nonetheless, it could help pressure companies to do the decent thing, and it could also increase the odds of the World Health Organization making medicines and vaccines available more quickly in the future.

Or so I read. It’s not as if I actually know this stuff.

“It’s a pretty big deal,” according to James Love, director of Knowledge Ecology International, which pushes (reckless radicals that they are) for intellectual property to be shared so it benefits the public. 

Shreds of hope in the pandemic

A Covid vaccine that’s in development could, potentially, create sterilizing immunity.

Sterilizing immunity? That’s the kind that prevents infection, which means a disease not only can’t get you sick, it also can’t use you to pass itself along to anyone else. If we could get enough people vaccinated with a sterilizing vaccine, we could stop this sumbitch in its tracks.

The snag, of course, is hidden in that word potentially. The thing’s still in development. But if all goes well, it could work on both the existing variants and any new ones and could create immunity even in people whose immune systems sleep through the current vaccines, through bouts of Covid itself, and through math class.

How does it work

The SARS-CoV-2 subunit vaccine (PreS-RBD) developed at MedUni Vienna is based on a structurally folded fusion protein consisting of two receptor binding domains (RBD) of the SARS-CoV-2 virus and the PreS antigen from hepatitis B, which serve as immunological carriers for each other, thereby strengthening the immune response.”

Allow me to translate that for you: It’s magic. Don’t worry about it. Although you might want to know that it involves a series of shots to build up to full immunity, and the first trials could start this year. But that depends on funding. 

Irrelevant photo: an ornamental cherry tree. Or I think it’s a cherry.

What doesn’t depend on funding?

Hmm. Dunno. As society’s organized, not much.

Why do I ask so many questions? They’re a cheap and easy way to organize a piece of writing. 

See? Even that depends on funding.

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A second shred of hope is that researchers have found a monoclonal antibody that could potentially be a treatment for all Covid variants as well as for SARS and MERS (if they reappear), and for some versions of the common cold. But there’s that word potentially again. So far, it’s gone through animal studies. Next they have to capture some humans and test it on them.

It’s being combined with another monoclonal antibody, and the two together are going by the name AR-701 cocktail right now, but before they’re released into the wild someone will have to give them a less pronounceable name to make them sound more scientific. 

The plan is for people to inhale it, and it could–again, that word–potentially last for a year. 

Covid and male fertility

A very (very) small study raises the possibility that catching Covid could have long-term effects on male fertility. 

Long-term effects? When someone says that,they’re never talking about  good long-term effects. In this case, it means that men who had recovered from Covid had lower sperm counts, more misshapen sperm, and sperm with lower motility than the comparison group. 

Again, it was a small study, so don’t go off the deep end with it. But I can’t help thinking that if you want to discombobulate someone who’s pounding the table about vaccines messing with women’s fertility–

Nah. I’m not going to suggest that. I’ll leave it to you to sink that low.  

News about Covid tests

Two rapid, accurate Covid tests are in development. I’ve written that sentence so many times before, changing only the number at the beginning, that I’m not even going to give you the details. But testing’s another area where–out of sight of the general public–work’s going on that could have an impact on the way this mess plays out.

 

Covid and the sense of smell 

Omicron’s less likely than the Delta variant to mess up the senses of smell and taste, but a failed attempt to lower people’s viral load–that’s how much Covid they carry around–turned out to protect patients’ sense of smell and taste. It also left them less tired than the patients who got a placebo.

They were using a drug called camostat mesylate, and it’s not clear yet whether it would help restore smell and taste to people who’ve lost them. You can live without both of them, but taste and smell are not minor losses.

The drug will need more testing–which in turn means more time, not to mention more money–before it can be used this way. 

An update on Covid in Africa

One of the mysteries of an already pretty weird disease has been its impact on Africa. According to a World Health Organization’s estimate, 65% of people in Africa have been infected by Covid. That’s something like 100 times more cases than have been reported. Covid cases are undercounted everywhere, and more so in Africa, because so many people have no symptoms. 

When they say “estimated,” they’re not talking about an educated hunch. They’re basing it on blood samples from around the continent. It’s not as accurate as counting every head, but it’s not pulling numbers out of thin air either. 

Earlier in the pandemic, the fear was that Covid would devastate Africa, but it’s turned out to be one of the least affected parts of the world. Multiple explanations are on offer. It has a low percentage of people with risk factors like diabetes, high blood pressure, and heart disease. It has a relatively young population. And some studies suggest that having been infected with other diseases, including malaria, may be protective, but that hasn’t been confirmed and rushing out to buy yourself a case of malaria is not recommended.

But being one of the least affected parts of the world doesn’t mean Africa’s unaffected. It’s had 250,000 Covid deaths. Or known Covid deaths–they also tend to be underreported worldwide. Only 15% of Africa’s population has been vaccinated, and that may mean only one vaccination, since the article doesn’t say “fully vaccinated,” which is the phrase that usually pops up.