Vipin M. Vashishtha Profile picture
Apr 8, 2023 16 tweets 8 min read Read on X
The indian saga of XBB.1.16 #Arcturus

It has been a month when @siamosolocani 1st flagged this variant. Later, I started tracking it. We are still amid an ongoing surge, it’s time to take a stock of the situation: what we do know, what we don’t 1/

What do we know for sure!

1-XBB.1.16 has succeeded in creating a new, significant surge in India after a gap of >6 months. A feat that even BA.5, BQ.1 & XBB.1.5 failed to achieve!
2/ ImageImage
2-XBB.1.16 definitely has got a growth advantage & more fitter than other circulating XBBs & has even replaced some other similar sublineages like XBB.1.5 & XBB.1.9 3/
@vinodscaria Image
3-XBB.1.16 is definitely not a more pathogenic variant than other Omicron’s progenies

4-This variant is still evolving, adding few more mutations. But not all new mutations are beneficial to the virus (i.e. E180V). 4/ Image
5-The chances of XBB.1.16 leading a new, significant wave (i.e. the 4th wave) akin to Jan’ 22 BA.2 wave are remote 5/
@JPWeiland Image
6-The new surge in cases is yet to peak in India. According to @JPWeiland India is more than 2 weeks from peak cases. 6/ Image
And, now let’s see what we still don’t know:
1-How big this new surge would be?
2-What are the key factors responsible for making XBB.1.16 a more fitter variant than its contemporaries? Higher immune evasion?
Higher infectiousness, i.e. higher ACE2 binding? 7/
A new study by @SystemsVirology suggests:

-a higher infectiousness (~1.2-fold greater than that of XBB.1.5) 8/

Image
However, XBB.1.16 doesn’t have significantly greater immune evasion than XBB.1.5. 9/

@SystemsVirology Image
We know XBB.1.5 & XBB.1.16 have almost similar Spike barring a few Spike mutations. However, above study suggests that mutations in the non-Spike region may be responsible for increased viral growth of XBB.1.16 10/ Image
The above mentioned study & some early work done by @StuartTruvile in NSW, Australia points that XBB.1.16 is not more immune evasive than XBB.1.5. @StuartTurville calls it “super similar to XBB.1.5 in neut evasion”. 11/ Image
Now, If it's not immune evasion, is the growth advantage is because of stronger ACE2 binding then?

No, in fact, the entry into cells is similar as with Omicrons including XBB.1.5. @StuartTurville has shown this 👇 12/ Image
Most evolutionary biologists now agree to believe that the increased fitness is mainly due to changes at non-Spike region of this variant.
Acc to @LongDesertTrain ORF1a:L3829F is probably the key mute responsible for its advantage over XBB.1.9 13/ Image
As per @SolidEvidence mutation in NSP6 of ORF1ab may be behind this higher fitness 14/ Image
Now, most experts believe the extra mutations at ORF9b & ORF1a are responsible to give “teeth” to this variant.
ORF9b is thought to be involved with suppressing interferon response, so they might make the virus slightly fitter by counteracting the innate immune system. 15/ Image
We still don’t know whether XBB.1.16 will become a global thing replacing the existing dominant variant XBB.1.5. However, all the indications point it will. This is the current projection by @JPWeiland for the US (an update on the CDC graph) 16/ Image

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More from @vipintukur

Aug 28
A pioneering study has demonstrated for the first time that myocardial infarction may be an infectious disease. This discovery challenges the conventional understanding of the pathogenesis of myocardial infarction and opens new avenues for treatment, diagnostics, and even vaccine development. 1/Image
According to the study, an infection may trigger myocardial infarction. Using a range of advanced methodologies, the research found that, in coronary artery disease, atherosclerotic plaques containing cholesterol may harbor a gelatinous, asymptomatic biofilm formed by bacteria over years or even decades. Dormant bacteria within the biofilm remain shielded from both the patient's immune system and antibiotics because they cannot penetrate the biofilm matrix. 2/Image
Of the bacteria detected, oral viridans group streptococcal DNA was the most common, being found in 42.1% of coronary plaques and 42.9% of endarterectomies. Immunopositivity for viridans streptococci correlated with severe atherosclerosis (P<0.0001) in both series and death from coronary heart disease (P=0.021) or myocardial infarction (P=0.042). 3/Image
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Aug 22
According to a new study, SARS-CoV-2 virus hijacks the machinery of testicular cells that produce the hormone testosterone in order to replicate.

It also appropriates the metabolic pathways of these cells and cholesterol, a precursor of testosterone, thereby altering lipid metabolism for its formation. 1/Image
The study revealed the presence of SARS-CoV-2 particles in lipid inclusions and organelles responsible for testosterone production in Leydig cells for the first time.

In addition, the researchers described the mechanism by which the virus interferes with the functioning of these testicular cells.

The discovery helps explain why male patients with severe COVID-19 have lower levels of testosterone, and possibly cholesterol. 2/Image
After infecting the Leydig cells in the testicles, the virus uses lipid metabolism pathways and the cell structure to replicate, which impairs testosterone production.

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Aug 18
A COVID infection, particularly in women, may lead to blood vessels aging around five years!

➡️ Blood vessels gradually become stiffer with age, but the new study suggests that COVID could accelerate this process. Researchers say this is important since people with stiffer blood vessels face a higher risk of cardiovascular disease, including stroke and heart attack. 1/Image
Since the pandemic, we have learned that many people who have had COVID are left with symptoms that can last for months or even years. However, we are still learning what's happening in the body to create these symptoms. 2/ Image
It is known that COVID can directly affect blood vessels. This may result in what we call early vascular aging, meaning that your blood vessels are older than your chronological age and you are more susceptible to heart disease.

If that is happening, we need to identify who is at risk at an early stage to prevent heart attacks and strokes. 3/Image
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Aug 14
A ‘universal’ antiviral for everyone!

🔥 A fascinating tale that reinforces the power of research driven by curiosity without preconceived notions.

➡️ For a few dozen people in the world, the downside of living with a rare immune condition comes with a surprising superpower—the ability to fight off all viruses.

➡️ An immunologist from Columbia discovered the individuals' antiviral powers about 15 years ago, soon after he identified the genetic mutation that causes the condition. 1/Image
At first, the condition only seemed to increase vulnerability to some bacterial infections. But as more patients were identified, its unexpected antiviral benefits became apparent.

The researcher soon learned that everyone with the mutation, which causes a deficiency in an immune regulator called IFN-I–stimulated gene 15 (ISG15), has mild but persistent systemic inflammation. 2/Image
The type I interferon (IFN-I) response is a conserved cascade of signaling and gene expression that, among other functions, confers protection of cells from viral infection.

After resolution of infection, the response is tamped down by regulators such as IFN-I–stimulated gene 15 (ISG15).

Cells from individuals lacking ISG15 are able to control viral infections in vitro as a consequence of maintaining a low-grade IFN-I response. 3/Image
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Jul 31
In a small trial, researchers have found that a drug designed to treat celiac disease supported a more rapid return to normal activities for patients following COVID. The researchers found the oral drug #larazotide—an experimental drug originally designed to treat celiac disease—was both safe and effective in treating children with MIS-C. 1/Image
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Jul 25
Researchers have discovered that gut bacteria produce a molecule that not only induces but also causes atherosclerosis, the accumulation of fat and cholesterol in the arteries that can lead to heart attacks and strokes.

This unexpected link between microbes and cardiovascular disease — the leading cause of death in humanity — is a paradigm shift. 1/Image
The new results show that some gut bacteria, in certain states, produce imidazole propionate, a simple molecule with six carbon atoms, eight hydrogen atoms, two nitrogen atoms, and two oxygen atoms (C₆H₈N₂O₂). This compound enters the blood, interacts with immature white blood cells, and triggers an inflammatory reaction in the arteries, which promotes the buildup of fatty plaques. Imidazole propionate induces atherosclerosis on its own. There’s a causal relationship. 2/Image
Furthermore, scientists observed elevated levels of imidazole propionate in one out of every five volunteers with active atherosclerosis, the type in which fatty plaques are more likely to rupture and form the blood clots that cause heart attacks and strokes. The new results demonstrate that atherosclerosis is not only a disease caused by fat, but that it also has an inflammatory and autoimmune component. 3/Image
Read 4 tweets

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