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WHO declares JN.1 COVID-19 variant a “variant of interest; The latest health stories from around the world

For the first time since it declared an end to the global Public Health Emergency for COVID-19 on 05 May,  the World Health Organization (WHO) has called the COVID-19 variant JN.1 a standalone “variant of interest.” WHO has gone further to state that JN.1 will drive an increase in cases of the virus. 

JN.1 was previously grouped with its relative, BA.2.86, but has increased so much in the past 4 weeks that the WHO moved it to standalone status, according to a summary published by the agency. The prevalence of JN.1 worldwide jumped from 3% for the week ending November 5 to 27% for the week ending December 3. During that same period, JN.1 rose from 1% to 66% of cases in the Western Pacific, which stretches across 37 countries, from China and Mongolia to Australia and New Zealand. 

In the United States, JN.1 has also been increasing rapidly. The variant accounted for an estimated 21% of cases for the 2-week period ending December 9, up from 8% during the 2 weeks prior. 

The WHO and the US Centers for Disease Control and Prevention (CDC) have said the current COVID vaccine appears to protect people against severe symptoms due to JN.1, and the WHO called the rising variant’s public health risk “low.” 

In its weekly risk analysis, the WHO did acknowledge that it’s not certain whether JN.1 has a higher risk of evading immunity or causing more severe symptoms than other strains. The WHO advised countries to further study how much JN.1 can evade existing antibodies and whether the variant results in more severe disease. 

The latest CDC data shows that 11% of COVID tests reported to the agency are positive, and 23,432 people were hospitalized with severe symptoms within a 7-day period. Last week, the CDC urgently asked people to get vaccinated against respiratory illnesses like the flu and COVID-19 ahead of the holidays as cases rise nationwide. 

“Getting vaccinated now can help prevent hospitalizations and save lives,” the agency advised. 


The World Health Organization (WHO) last week added noma, a disease that disfigures the face and can be fatal if not treated, to its official list of neglected tropical diseases. The designation is intended to attract more research and funding for curbing the disease, also known as cancrum oris and gangrenous stomatitis.  

More than 30,000 cases are estimated to occur annually, predominantly in malnourished children in remote parts of Africa; specialists suspect more go unreported. WHO says the fatality rate is as high as 90%, although early treatment with antibiotics is effective. Researchers think bacteria and poor oral hygiene help cause the disease, which begins as an inflammation of the gums and evolves into a gangrene that damages the nose, mouth, and eyes. Survivors face stigma, and some need reconstructive surgery. WHO’s listing comes after years of advocacy to raise awareness about the disease, including a January request from Nigeria and 32 other countries with significant numbers of noma cases. 


People trying to lose weight embark on gruelling diets, undergo procedures to shrink their stomachs, or pony up for expensive new drugs like Ozempic. Now, researchers have revealed a gentler and potentially cheaper option: A vibrating pill that stimulates nerve endings in the stomach to tell the brain it’s time to stop eating. 

The capsule—reported last week in Science Advancesslashes food intake in pigs without causing obvious side effects. Scientists now hope to develop it into an obesity treatment for humans. 

The stomach stretches when we eat a meal, stimulating nerve endings in the organ’s wall that send messages to the brain. These signals make us feel full, encouraging us to push away from the dinner table. Researchers have tried to come up with obesity treatments that harness this effect. One approach involves inserting a fluid-filled balloon into the stomach that produces a sense of fullness. Another option is an implanted device that stimulates the vagus nerve, which transmits impulses from the stomach to the brain. 

However, the balloons can become less effective over time as the stomach becomes inured to constant stretching, and some patients have died after receiving them. The nerve-stimulating devices require surgery, and they don’t seem to result in much weight loss. 

So in the new study, a team led by Harvard University biomedical engineer Shriya Srinivasan and Massachusetts Institute of Technology gastroenterologist and biomedical engineer Giovanni Traverso devised an alternative: a 31-by-10-millimeter pill that carries a tiny motor and battery. A gel plug in the pill keeps the motor from switching on. But the gel dissolves rapidly when it contacts stomach fluid, allowing the motor to start turning. When that happens, the pill shakes for about 38 minutes, roughly the amount of time it would stay in the stomach. The researchers hypothesized that these vibrations would stimulate the stretch-sensing nerve endings and signal satiety. 

To test the pill, the team inserted it into the stomachs of young pigs that were about the same size and weight as humans. When the scientists measured the electrical activity of a portion of the vagus nerve, they found that the vibrations spurred a very similar firing pattern as expanding the animals’ stomachs with air, suggesting that the pill was tickling the organ’s nerve endings. As the device pulsates in the folds of the stomach lining, it also rotates, which appears to provide further stimulation. 

Srinivasan, Traverso, and colleagues determined that the pill induced in the pigs many of the same changes in hormone levels as eating a meal, including an increase in insulin and a decrease in the hunger-promoting hormone ghrelin. The scientists also monitored how much food the pigs gobbled with one of the pills in their stomachs. They found that the animals ate about 40% less than controls that hadn’t received a pill. 

For most of the experiments, the scientists tethered the pill inside the animals’ stomachs. But they also measured how fast the devices passed through the animals’ digestive system, finding that they were excreted after about 4 days. 

Tom Hildebrandt, a clinical psychologist at the Icahn School of Medicine at Mount Sinai who studies weight loss treatments, says he is “hopeful but cynical” about the approach. Because similar capsules are already in use for disease diagnosis, the pill is likely to be “low-risk” he says. Still, researchers need to answer several questions before they can transform the pill into a useful weight loss option. For example, no one knows what a vibrating pill will feel like in a person’s stomach, he says. “A pig can’t tell you how uncomfortable it is.”  

Traverso and Srinivasan say they hope to refine the pill and delve deeper into its effects on the body. For instance, they weren’t able to demonstrate that it induces weight loss because the pigs they studied were still growing. To resolve the issue, the researchers want to study the pill in dogs, whose stomachs are more similar to those of humans. If they find the funding for this research, Traverso says, “we could be [testing] in humans in 2 to 3 years.” 


Researchers are closing in on ways to produce CAR T cells in the body, raising hopes that the notoriously expensive and bespoke cancer therapies might one day become more accessible. 

In CAR-T treatment, immune cells called T cells are removed from the person receiving treatment, engineered to target cancer cells and reintroduced to their body. The process has yielded dramatic recoveries from advanced forms of some blood cancers, but its high price and technical difficulty have placed it out of reach for many people. 

Results presented at the American Society of Hematology annual meeting in San Diego, California on 11 December suggest that people undergoing treatment might eventually just get an injection of a virus that infects T cells. The virus would then insert the genes needed to guide the T cells to tumour cells. 

The key lies in finding ways to genetically engineer T cells to express chimeric antigen receptors (CARs), proteins that recognize cancer — without meddling with the genomes of other cells, says Els Verhoeyen, an INSERM research director at the International Centre for Infectious Disease Research in Lyon, France, who develops viruses for use in gene therapies. To do so, she and other researchers have been modifying viruses to recognize molecules found only on the surface of T cells. 

At the haematology conference, two companies presented the results of their efforts to use viruses to engineer T cells still inside the bodies of monkeys. Teams from both Interius BioTherapeutics in Philadelphia, Pennsylvania and Umoja Biopharma in Seattle, Washington, generated CAR-T treatments that target other immune cells called B cells, mimicking the action of approved CAR-T therapies that treat cancers caused by abnormal B cells. 

In both companies’ experiments, the treatment was sufficient to deplete the monkeys’ B cells. Interius reported that B-cell counts were reduced by at least 75% in 15 out of 16 animals treated. The two companies plan to request authorization next year from the US Food and Drug Administration to begin trials on people. 

The hope is that the technique could expand the use of CAR-T therapies: the current cost of the treatment and necessary hospital care can together exceed half a million US dollars. 

A host of challenges awaits that approach as well, however. For one, regulators will want to see evidence that the process truly targets only T cells and leaves other cells untouched, says Verheoyen. 

Researchers have also tried to generate CAR T cells from cells that have been donated by an unrelated person, and engineered to evade detection by the recipient’s immune system. If successful, that would allow cells from a single donor to be used to treat many people. That approach still holds promise, but the results from these therapies have thus far been disappointing, driving greater interest in approaches that can generate CAR-T cells directly in the body, says Andrew Scharenberg, chief executive of Umoja. 

Less than a block away from Umoja, near the eastern shore of Lake Union in Seattle, sits Sana Biotechnology, a company that has been developing a virus designed by Verhoeyen to generate CAR T cells in the body. Earlier this year, Sana announced that it was scaling back that programme to concentrate on other projects, including CAR-T therapies made from donor cells. 

It was a difficult decision, says Steve Harr, chief executive of the company. But the other programmes were further along, whereas “there’s a lot of scientific work to do,” to sort out the logistics of commercializing a CAR-T therapy made in the body, he says. 

“There was more risk,” to inside-the-body CAR-T, he says. “But I still like it. We’ll do it over time.” 


Lalita Panicker is Consulting Editor, Views and Editor, Insight, Hindustan Times, New Delhi 

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