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About half of NZ reckon the red light settings have struck the right balance, according to a new poll.
About half of NZ reckon the red light settings have struck the right balance, according to a new poll.

ScienceFebruary 1, 2022

What will the next Covid variant look like?

About half of NZ reckon the red light settings have struck the right balance, according to a new poll.
About half of NZ reckon the red light settings have struck the right balance, according to a new poll.

Every time it seems the world is coming to grips with the virus, a new variant sneaks around immune systems and infects people like never before. So what form will the virus take next? Is there even any way to know? And does omicron mark the beginning of the end?

The latest variant of concern, the fifth since Covid original, is spreading around the world faster than glitter on the hands of kids at a birthday party.

With some countries once again putting travel restrictions in place, limits on gatherings in force and hospitals full, you can hear the cries of “when will it end?!”

The good news is the pandemic will end. As other pandemics have. But what that ‘end’ looks like is still somewhat mysterious.

Scientists have laid out six, main possible scenarios and one that’s looking particularly likely is that the virus becomes endemic.

Endemic means the virus is still around, circulating in communities, and that outbreaks crop up every now and again. The comparison that’s often made is to seasonal flu (read: still bad and still kills people but not world-stopping).

But how quickly we get there, and what the path there looks like, is difficult to predict. “The virus becoming endemic is likely, but the pattern that it will take is hard to predict,” Angela Rasmussen, a virologist from Georgetown University, told Nature.

Why is that pattern hard to predict? Because we’re dealing with a biological organism and, even though we’ve more or less understood the dynamics of evolution since Darwin’s time, it’s still hard to predict how that organism will change and mould itself to its surroundings.

“Predicting biological or evolutionary outcomes is really, really hard,” says Jemma Geoghegan, a senior lecturer in the department of microbiology and immunology at the University of Otago. “We don’t know how the selection pressures might play out and how that’s going to affect the evolution of the virus.”

Quick evolution recap: individual organisms look and act slightly differently. In some cases, those differences give an individual an advantage in their environment. Depending on the conditions, or selection pressures, of the environment, those traits grow in number over generations.

When it comes to the virus, it’s looking to spread to as many people as possible and it needs traits like changing the shape of its spike protein so antibodies don’t stick, to do that.

But, theoretically, if those changes mean that a person gets sicker and stays away from others or if the person dies before the virus can move on, that’s not very useful in an evolutionary sense. It’s a balance between transmissibility and virulence (how severe an infection the virus causes).

Which is why there’s been some talk about omicron being the beginning of the end of the pandemic because it’s more easily passed from person to person and doesn’t make them as sick.

But according to Geoghegan, because the SARS-Cov-2 virus is usually passed on before someone gets sick, there’s not a strong evolutionary pressure for the virus to become less virulent, or less severe.

“It’s not necessarily the case that the virus will always become avirulent. It really comes down to how it affects its transmission,” she says.

“It might also be true though that as more people get some protection from the virus, through vaccination or past infection, then infection might become milder for them since they have some immunity.”

Researchers do have some information to go on to predict what course the pandemic will take.

For one, they can look at other coronaviruses that circulate and pop up as outbreaks, such as the seasonal 229E virus. Recent research has shown that the likely reason the virus reinfects people periodically is because it’s evolving to escape our immune response (sound familiar?) rather than that our immunity is just waning.

Also, scientists can use what they know about all of the known previous SARS-Cov-2 variants to try to build predictive models of what might be around the corner. Researchers recently developed a computer model based on what mutations have helped a particular virus variant spread in the past.

When they ran it on old data, the model could predict which mutations spread up to four months in advance of it actually happening. It’s early days, but a model like this could be used to monitor how the virus is changing worldwide.

Despite having previous variants to go on, Omicron showed scientists that sometimes, mutations just seem to come out of left field. Some 13 of Omicron’s 30 spike protein mutations have very rarely been seen before in other human coronaviruses or even other animal coronaviruses. One theory is that these rare mutations formed because the virus spent a long time evolving in someone with a weak immune system, like someone with HIV.

Which is why it’s important to bolster people’s immune system and give the virus fewer opportunities to mutate, say experts.

“As long as the virus is spreading, the virus has a chance to mutate. So if you slow the spread, you’re slowing the chances of new mutations arising and therefore new variants,” says Geoghegan.

That means getting people vaccinated, and particularly getting vaccines to parts of the world with low vaccination rates, is crucial. “If 2021 was the year of vaccine production, 2022 must be the year of vaccine equity,” said WHO regional director for Europe Hans Henri Kluge in a statement.

The WHO also says that if we stick to monitoring for new variants, high vaccination rates and third doses, adding ventilation in enclosed spaces, affordable and equitable access to antivirals, targeted testing, and shielding high-risk groups, then we could be on our way to the end.

Keep going!
Image: Getty Images/Tina Tiller
Image: Getty Images/Tina Tiller

ScienceJanuary 29, 2022

Irritating, yes, dangerous, no: The truth about cracking your knuckles

Image: Getty Images/Tina Tiller
Image: Getty Images/Tina Tiller

The sound of it may drive others up the wall, but cracking your joints probably won’t do you any harm, says musculoskeletal expert Neil Tuttle.

Some people habitually crack their joints, others can’t, and many are irritated by those who do.

So what’s going on? Why do people do it, is it harmful, what makes the noises, and what would happen if our joints weren’t able to crack?

Before going on, it’s important to note we’re talking here about people cracking their own joints. This is also known as “self-manipulation”. But when a physiotherapist or chiropractor cracks (or manipulates) your spine, what makes the noises is the same, but the implications can be very different than what’s being discussed here.

Although it may irritate friends and family, self-manipulating our joints is probably neither useful nor harmful for the individual.

Why do we crack our joints?

People crack their joints because they feel better, looser, or less stiff afterwards.

The relief is temporary and they typically repeat it at some point after 20 minutes, when the effects wear off.

While joint cracking may seem incomprehensible to us non-crackers, we all do similar behaviours.

“Pandiculation” is the nearly universal type of stretching we do after being inactive – even dogs, cats, elephants, spiders and unborn sheep do it.

The drive to “pandiculate” and it’s transient effects are similar to joint cracking. However, pandiculation is thought to have positive effects on the body, by restoring and resetting the structural and functional equilibrium. The same is not the case for cracking joints.

Even spiders need to stretch now and then.

It doesn’t cause arthritis

Probably everyone who self-manipulates has been told – usually by someone irritated by the behaviour – not to do it because it will cause arthritis.

It’s now clear this isn’t the case.

American doctor Donald Unger famously cracked knuckles only on one hand for over 50 years, and found no sign of increased arthritis compared to the other hand. For this he received an IgNoble Prize in Medicine in 2009, an award for unusual achievements in research.

In another study, knuckle cracking was not found to increase the incidence of arthritis in an elderly population who had cracked their knuckles compared to those who didn’t. Also, the incidence of arthritis was not greater in the knuckles they did crack, compared to the other joints of the hand that weren’t cracked.

There are a few reports of injury from knuckle cracking, but these are probably too minor and infrequent to be of much concern.

Put simply, there don’t appear to be significant adverse effects to cracking your joints.

What makes the noise?

When people crack their knuckles they separate the joint surfaces and the pressure within the joint decreases. At a certain point the surfaces suddenly separate and a bubble forms by a process known as cavitation.

A similar effect can also occur with a simulated joint, as in the video above.

It’s not entirely clear however which part of the process causes the actual cracking noise in humans. One theory is the noise is produced by the formation of the bubble itself. Another theory suggests it’s the breaking of the fluid “adhesive seal” between the joint surfaces as occurs with pulling a suction cup off of a wall.

High speed MRI image of knuckle cracking. As the joint surfaces are separated the volume suddenly increases and a bubble (the dark area that appears in the middle of the joint) is formed.

Why have our joints evolved to crack?

Perhaps the most interesting question is why our joints developed in such a way that they’re able to crack.

I had a conversation recently with Jerome Fryer, a Canadian researcher who was involved in the above study with the simulated joint. He raised an interesting idea which hasn’t been published. Could the ability of our joints to crack actually serve a useful purpose?

When the simulated joints in his study were filled with normal water, the joint surfaces separated easily, which formed bubbles but didn’t produce the cracking sound.

But when the water was treated to remove all of the dissolved gasses and microscopic bubbles, the simulated joint performed more like a real joint. That is, much more force was needed to separate the surfaces, and only then did it produce a cracking sound.

Perhaps the fact it requires a large force to separate our joints, which happens to also produce a cracking sound, may be very useful by assisting in joint stability and thereby providing protection from our joints being damaged.

Neil Tuttle is a musculoskeletal physiotherapist and senior lecturer at the University of Tasmania

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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