Comment

Comment by Dr. Krishna Kumari Challa 38 minutes ago

Scientists suspect that this cascade of EBV-generated self-targeting B-cell activation might extend beyond lupus to other autoimmune diseases such as multiple sclerosis, rheumatoid arthritis and Crohn's disease, where hints of EBV-initiated EBNA2 activity have been observed.
The million-dollar question: If about 95% of us are walking around with latent EBV in our B cells, why do some of us—but not all of us—get autoimmunity? The researchers speculate that perhaps only certain EBV strains spur the transformation of infected B cells into antigen-presenting "driver" cells that broadly activate huge numbers of antinuclear B cells.
Many companies are working on an EBV vaccine, and clinical trials of such a vaccine are underway. But that vaccine would have to be given soon after birth, they noted, as such vaccines are unable to rid an already-infected person of the virus.

Shady Younis et al, Epstein-Barr virus reprograms autoreactive B cells as antigen presenting cells in systemic lupus erythematosus, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.ady0210

Part 4

Comment by Dr. Krishna Kumari Challa 40 minutes ago

But at times, somnolent autoreactive B cells become activated, take aim at our own tissues and instigate one of the disorders collectively called autoimmunity. Some awakened autoreactive B cells crank out antibodies that bind to proteins and DNA inside the nuclei of our cells. Such activated "antinuclear antibodies"—the hallmark of lupus—trigger damage to tissues randomly distributed throughout the body, because virtually all our body's cells have nuclei.

The vast majority of EBV-infected people (most of us, that is) have no idea they're still sheltering a virus and never get lupus. But essentially everyone with lupus is EBV-infected, studies have shown. An EBV-lupus connection has long been suspected but never nailed down until now.
Although latent EBV is ubiquitous in the sense that almost everybody carries it, it resides in only a tiny fraction of any given person's B cells. As a result, until the new study, it was virtually impossible for existing methods to identify infected B cells and distinguish them from uninfected ones.
But researchers now developed an extremely high-precision sequencing system that enabled them to do this. They found that fewer than 1 in 10,000 of a typical EBV-infected but otherwise healthy individual's B cells are hosting a dormant EBV viral genome.

Employing their new EBV-infected-B-cell-identifying technology along with bioinformatics and cell-culture experimentation, the researchers found out how such small numbers of infected cells can cause a powerful immune attack on one's own tissues. In lupus patients, the fraction of EBV-infected B cells rises to about 1 in 400—a 25-fold difference.
It's known that the latent EBV, despite its near-total inactivity, nonetheless occasionally nudges the B cell in which it's been snoozing to produce a single viral protein, EBNA2. The researchers showed that this protein acts as a molecular switch—in geneticists' language, a transcription factor—activating a battery of genes in the B cell's genome that had previously been at rest. At least two of the human genes switched on by EBNA2 are recipes for proteins that are, themselves, transcription factors that turn on a variety of other pro-inflammatory human genes.

The net effect of all these genetic fireworks is that the B cell becomes highly inflammatory: It dons its "professional antigen-presenting cell" uniform and starts stimulating other immune cells (called helper T cells) that happen to share a predilection for targeting cell-nuclear components. These helper T cells enlist multitudes of other antinuclear B cells as well as antinuclear killer T cells, vicious attack dogs of the immune system.

When that militia bulks up, it doesn't matter whether any of the newly recruited antinuclear B cells are EBV-infected or not. (The vast majority of them aren't.) If there are enough of them, the result is a bout of lupus.
Part 3

Comment by Dr. Krishna Kumari Challa 42 minutes ago

Once you've been infected by EBV, you can't get rid of it, even if you remain or become symptom-free. EBV belongs to a large family of viruses, including those responsible for chickenpox and herpes, that can deposit their genetic material into the nuclei of infected cells. There the virus slumbers in a latent form, hiding from the immune system's surveillance agents. This may last as long as the cell it's hiding in stays alive; or under certain conditions, the virus may reactivate and force the infected cell's replicative machinery to produce myriad copies of themselves that break out to infect other cells and other people.
Among the cell types in which EBV takes up permanent residence are B cells, immune cells that do a couple of important things after they ingest bits of microbial pathogens. For one, they can produce antibodies: customized proteins that find and bind immune-system-arousing proteins or other molecules (immunologists call them "antigens") on microbial pathogens that have infected an individual, or are trying to.

In addition, B cells are what immunologists call "professional antigen-presenting cells": They can process antigens and display them on their surfaces in a way that encourages other immune cells to raise the intensity of their hunt for the pathogen in question. That's a substantial force multiplier for kick-starting an immune response.

Our bodies harbor hundreds of billions of B cells, which over the course of numerous rounds of cell division develop an enormous diversity of antibodies. In the aggregate, these antibodies can bind an estimated 10 billion to 100 billion different antigenic shapes. This is why we're able to mount a successful immune response to so many different pathogens.

Oddly, about 20% of the B cells in our bodies are autoreactive. They target antigens belonging to our own tissues—not by design, but due to the random way B-cell diversity comes about: through sloppy replication, apparently engineered by evolution to ensure diversification. Fortunately, these B cells are typically in a dopey state of inertia, and they pretty much leave our tissues alone.
Part 2

Comment by Dr. Krishna Kumari Challa 45 minutes ago

Scientists tie lupus to a virus nearly all of us carry

One of humanity's most ubiquitous infectious pathogens bears the blame for the chronic autoimmune condition called systemic lupus erythematosus (lupus), Stanford Medicine investigators and their colleagues have found.

The Epstein-Barr virus (EBV), which usually resides silently inside the bodies of 19 out of 20 people, is directly responsible for commandeering what starts out as a minuscule number of immune cells to go rogue and persuade far more of their fellow immune cells to launch a widespread assault on the body's tissues, the scientists have shown.

The work is published in the journal Science Translational Medicine.

About five million people worldwide have lupus, in which the immune system attacks the contents of cell nuclei. This results in damage to organs and tissues throughout the body—skin, joints, kidneys, heart, nerves and elsewhere—with symptoms varying widely among individuals. For unknown reasons, nine out of 10 lupus patients are women.

With appropriate diagnosis and medication, most lupus patients can live reasonably normal lives, but for about 5% of them the disorder can be life-threatening. 

Existing treatments slow down disease progression but don't 'cure' it.

By the time we've reached adulthood, the vast majority of us have been infected by EBV. Transmitted in saliva, EBV infection typically occurs in childhood, from sharing a spoon with or drinking from the same glass as a sibling or a friend, or maybe during our teen years, from exchanging a kiss. EBV can cause mononucleosis, "the kissing disease," which begins with a fever that subsides but lapses into a profound fatigue that can persist for months.

Practically the only way to not get EBV is to live in a bubble. If you've lived a normal life the odds are nearly 20 to 1 you've got it.

part 1

Comment by Dr. Krishna Kumari Challa 56 minutes ago

Selecting for low activity successfully caused slower movement across the four generations. The researchers analyzed the composition of the microbial community and found that this reduction in activity was linked to higher levels of the bacterium Lactobacillus, which produces the substance indolelactic acid (ILA). They also showed the link was causal. When they independently gave Lactobacillus or ILA to other mice, it was enough to suppress their locomotion.

This work highlights the role of microbiome-mediated trait inheritance in shaping host ecology and evolution," wrote the researchers in a paper.

The novelty in our study lies in experimentally demonstrating that selection on a host trait can lead to changes in that same trait over time purely through microbiome transmission, without any genetic evolution in the host.

 Taichi A. Suzuki et al, Selection and transmission of the gut microbiome alone can shift mammalian behavior, Nature Communications (2025). DOI: 10.1038/s41467-025-65368-w

Part 2

Comment by Dr. Krishna Kumari Challa 58 minutes ago

Gut microbes pass down behavioral traits in mice offspring independent of genes

Gut microbes are essential partners that help digest food, produce vitamins and train the immune system. They can also pass on behavioral traits to their host's offspring, at least in mice. Scientists have discovered that the mouse microbiome can alter the animal's behaviour in just four generations, independent of its genes. The study is published in the journal Nature Communications

Animals and their microbes have coevolved for millions of years. While it was already known that bacteria, viruses and fungi living in the gut can drive inherited changes in some simple creatures, like insects, scientists didn't know till now whether they could be the sole mechanism for passing down a specific trait (like a behavioral tendency) in more complex animals, such as mammals.

The research team designed an experiment in which they strictly controlled the host animal's genes. First, they took gut microbiota from wild-derived mice and gave it to genetically identical germ-free mice in the lab.
Then they set up a selection line, repeatedly choosing the two mice that traveled the least and transferring their microbes into a fresh batch of genetically identical, germ-free mice for the next generation. The scientists focused on locomotor activity (movement) because previous tests had confirmed that it was a behavior strongly influenced by the microbiome. The researchers also ran a control line where two donor mice were chosen at random.

This serial transfer of gut microbes carried on for four generations. By using germ-free mice, the researchers could be sure that any behavioral changes they observed were due to the selection and transfer of the microbial community.
Part 1

Comment by Dr. Krishna Kumari Challa 1 hour ago

The search for life on Mars feels like looking for a needle in a haystack. But it could be narrowed down and made easier by having well-defined targets that, more than others, could be possible homes for life.

Therefore, the scientists behind this latest study think the eight possible karstic caves should be high-priority targets for future human or robotic missions to the planet. Even if no life is there, they could serve as landing sites and natural shelters for astronauts when they are not exploring the surface.

 Ravi Sharma et al, Water-driven Accessible Potential Karstic Caves in Hebrus Valles, Mars: Implications for Subsurface Habitability, The Astrophysical Journal Letters (2025). DOI: 10.3847/2041-8213/ae0f1c

Part 2

Comment by Dr. Krishna Kumari Challa 1 hour ago

Scientists discover caves carved by water on Mars that may have once harbored life

If there is, or ever has been, life on Mars, the chances are it would exist in caves protected from the severe dust storms, extreme temperatures, and high radiation present on its surface. One place to focus our attention could be eight possible cave sites (called skylights) recently discovered by researchers.

In a paper published in The Astrophysical Journal Letters, the team presents the first evidence of a new type of cave on the red planet, formed by water dissolving rock. Most Martian caves discovered so far have been lava tubes, but the study authors argue that they have identified the first documented karstic caves on Mars.

"These skylights are interpreted as the first known potential karstic caves on Mars, representing collapse entrances formed through the dissolution of water-soluble lithologies—defining a new cave-forming class distinct from all previously reported volcanic and tectonic skylights," wrote the researchers in their paper.

On Earth, karstic caves are typically formed when water dissolves soluble rock such as limestone or gypsum, creating and enlarging underground cracks and fractures that grow large enough to become caves. The paper proposes a similar process on Mars, where ancient Martian water may have dissolved carbonate- and sulfate-rich rocks on the crust.

The caves are located in the Hebrus Valles, a northwestern region, and are eight pits that were mapped by previous Mars missions. They are deep and predominantly circular depressions, not impact craters, which typically have raised rims and ejected debris around them.

The researchers studied data from the Thermal Emission Spectrometer (TES) that was onboard NASA's Mars Global Surveyor and discovered that the rocks around the pits are rich in carbonates and sulfates. These are the types of rocks that water can easily dissolve. The team also used high-resolution imagery to create 3D structural models of the pits, which showed that their shapes are consistent with collapse caused by water rather than volcanic or tectonic activity.

Comment by Dr. Krishna Kumari Challa 1 hour ago

Bees learn to read simple 'Morse code'

Researchers  have shown for the first time that an insect—the bumblebee Bombus terrestris—can decide where to forage for food based on different durations of visual cues. Their paper is published in the journal Biology Letters.

In Morse code, a short duration flash or "dot" denotes a letter "E" and a long duration flash, or "dash," means letter "T." Until now, the ability to discriminate between "dot" and "dash" has been seen only in humans and other vertebrates such as macaques or pigeons.

Now researchers  studied this ability in bees. They built a special maze to train individual bees to find a sugar reward at one of two flashing circles, shown with either a long or short flash duration. For instance, when the short flash, or "dot," was associated with sugar, then the long flash, or "dash," was instead associated with a bitter substance that bees dislike.

In each room in the maze, the position of the dot and dash stimulus was changed, so that bees could not rely on spatial cues to orient their choices. After bees learned to go straight to the flashing circle paired with the sugar, they were tested with flashing lights but no sugar present, to check whether bees' choices were driven by the flashing light, rather than by olfactory or visual cues present in the sugar.

It was clear the bees had learned to tell the light apart based on their duration, as most of them went straight to the 'correct' flashing light duration previously associated with sugar, irrespective of spatial location of the stimulus.

Since bees don't encounter flashing stimuli in their natural environment, it's remarkable that they could succeed at this task. The fact that they could track the duration of visual stimuli might suggest an extension of a time processing capacity that has evolved for different purposes, such as keeping track of movement in space or communication.

Alternatively, this surprising ability to encode and process time duration might be a fundamental component of the nervous system that is intrinsic in the properties of neurons. Only further research will be able to address this issue.

Many complex animal behaviors, such as navigation and communication, depend on time-processing abilities. It will be important to use a broad comparative approach across different species, including insects, to shed light on the evolution of those abilities. Processing durations in insects is evidence of a complex task solution using minimal neural substrate.

This has implications for complex cognitive-like traits in artificial neural networks, which should seek to be as efficient as possible to be scalable, taking inspiration from biological intelligence.

 Duration discrimination in the bumblebee Bombus terrestris, Biology Letters (2025). DOI: 10.1098/rsbl.2025.0440. royalsocietypublishing.org/doi … .1098/rsbl.2025.0440

Comment by Dr. Krishna Kumari Challa 23 hours ago

Computers that run on human brain cells
At a company on the shores of Lake Geneva, clumps of living brain cells are waiting for your call. These blobs, about the size of a grain of sand, are available to research teams studying how brains work or exploring the possibility of making computers with brain-cell processors. These neural cells can receive electrical signals and respond to them — much as computers do. For some scientists, the dream is to build supercomputers that share the astonishing power efficiency of the human brain. What they’re not working on, they emphasize, is ‘brains in jars’: the blobs are not sentient or conscious (yet).

https://www.nature.com/articles/d41586-025-03633-0?utm_source=Live+...

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