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HIV mystery uncovered: How the virus reprograms host cells to create perfect hiding places

For over three decades, HIV has played an elaborate game of hide-and-seek with researchers, making treating—and possibly even curing—the disease a seemingly insurmountable obstacle to achieve.

But scientists at Case Western Reserve University have made a breakthrough discovery that could fundamentally change strategies for treating HIV.

The team identified for the first time how HIV enters a in infected cells that allows the virus to “hide” from the immune system and current treatments.

Enlarged cancer cell nuclei may limit spread rather than signal severity

In tissue biopsies, cancer cells are frequently observed to have nuclei (the cell’s genetic information storage) that are larger than normal. Until now, this was considered a sign that the cancer was worsening, but the exact cause and effect had not been elucidated.

In a new study, a KAIST research team has found that cancer cell nuclear hypertrophy is not a cause of malignancy but a temporary response to replication stress, and that it can, in fact, suppress metastasis. This discovery is expected to lead to the development of new diagnostic and therapeutic strategies for cancer and metastasis inhibition.

The research team, led by Professor Joon Kim of the Graduate School of Medical Science and Engineering, in collaboration with the research teams of Professor Ji Hun Kim and Professor You-Me Kim, confirmed that DNA replication stress (the burden and error signal that occurs when a cell copies its DNA), which is common in , causes the “actin” protein inside the nucleus to aggregate (polymerize), which is the direct cause of the nuclear enlargement.

PA-915 molecule shows long-lasting antidepressant effects without common side effects in mice

Depression and anxiety disorders are among the most widespread mental health disorders, with estimates suggesting that they affect around 264 million and 284 million people worldwide, respectively. Depression is a mood disorder characterized by persistent sadness and a loss of interest in everyday activities, while anxiety disorders are marked by high levels of nervousness, worry and fear, either in specific situations or generalized.

Today, there are several for both depression and , including both pharmacological drugs and specific types of psychotherapy. Yet available therapeutic strategies are not effective for all affected individuals; thus, identifying alternative treatments could be highly advantageous.

Researchers at the University of Osaka, Kobe University School of Medicine, Hamamatsu University School of Medicine and other institutes have recently developed a called PA-915, which could hold some promise for the treatment of depression, anxiety and stress-related disorders. In a paper published in Molecular Psychiatry, they showed that the molecule suppressed both anxiety-like and depression-like behaviors in mice who were placed under high levels of stress.

Forget numbers—your PIN could consist of a shimmy and a shake

In the near future, you may not need to touch a keypad to select a tip or pay for large purchases. All it may take is a swipe, tap or other quick gesture.

The innovation utilizes near-field communication (NFC), the short-range wireless technology embedded in smartphones, and terminals, passports and key fobs. UBC computer scientists say it could help prevent the spread of germs through touchpads, speed up transactions, and improve accessibility for users unable to press buttons.

Researchers debuted the technology in a paper at the User Interface Software and Technology conference.

Is violent AI-human conflict inevitable?

Are you worried that artificial intelligence and humans will go to war? AI experts are. In 2023, a group of elite thinkers signed onto the Center for AI Safety’s statement that “Mitigating the risk of extinction from AI should be a global priority alongside other societal-scale risks such as pandemics and nuclear war.”

In a survey published in 2024, 38% to 51% of top-tier AI researchers assigned a probability of at least 10% to the statement “advanced AI leading to outcomes as bad as human extinction.”

The worry is not about the Large Language Models (LLMs) of today, which are essentially huge autocomplete machines, but about Advanced General Intelligence (AGI)—still hypothetical long-term planning agents that can substitute for human labor across a wide range of society’s economic systems.

Electrically tunable metasurface unlocks real-time THz holography

The terahertz (THz) band of the electromagnetic spectrum holds immense promise for next-generation technologies, including high-speed wireless communication, advanced encryption, and medical imaging. However, manipulating THz waves has long been a technical challenge, since these frequencies interact weakly with most natural materials.

Over the past two decades, researchers have increasingly turned to metasurfaces to tackle this problem. These are ultrathin materials carefully engineered to exhibit specialized properties, providing unprecedented control over THz waves.

Ideally, metasurfaces for THz applications in encryption and holography should be easily configurable, featuring an adjustable response that can be controlled externally. Despite this, tunable metasurface systems often rely on cumbersome or energy-inefficient methods, such as external thermal control.

Cancer-fighting gene plays unexpected role in pancreatic cancer tumor growth

New research from Indiana University School of Medicine scientists has revealed that a well-known cancer-fighting gene also plays an unexpected role in regulating how certain immune cells can support tumor growth. This insight into pancreatic cancer progression could lead to more effective treatments against one of the deadliest forms of cancer.

The study, recently published in Science Advances, focused on M2-like macrophages, a subtype of found in the tumor environment that are known to weaken the body’s ability to fight cancer. The researchers examined how a gene called serine/threonine kinase 11 (STK11) influences these cells. They found that when STK11 is missing in macrophages, those cells switch into a tumor-supporting state.

“STK11 was originally identified as a and extensive studies have examined the gene’s functions and mechanisms in regulating cancer cell growth,” said Kai Yang, PhD, corresponding author of the study, an associate professor of pediatrics and microbiology and immunology at the IU School of Medicine and a researcher with the Indiana University Melvin and Bren Simon Comprehensive Cancer Center.

How gene mutations drive dementia in Parkinson’s disease

Parkinson’s disease causes both movement and cognitive deficits, and for a long time both were thought to be caused by the accumulation of a protein called alpha-synuclein in the brain. But a new Nature Communications study has found that the cognitive deficits arise through a different—and unexpected—mechanism.

The new findings suggest that mutations in a gene called GBA—which are a risk factor for developing Parkinson’s disease—drive by disrupting how neurons communicate with each other in the brain. Patients living with Parkinson’s disease can experience such as difficulty with concentrating and forgetfulness. Over time, many go on to develop dementia, in which they experience profound memory loss among other symptoms.

“Dementia is often the scariest thing for many patients with Parkinson’s disease, more so than ,” says Sreeganga Chandra, PhD, professor of neurology and of neuroscience at Yale School of Medicine (YSM) and the study’s principal investigator. “We are trying to understand the basis of cognitive dysfunction and whether we can find targets to ameliorate it.”

New digital cognitive test for diagnosing Alzheimer’s disease

“The unique aspect of our BioCog test is that unlike other digital tests, it has been evaluated in a primary care population, i.e. patients seeking treatment at a health centre because they are experiencing cognitive problems, such as memory problems. Combining the results of the digital test and the blood test increases the accuracy of diagnosing Alzheimer’s disease. The purpose of the test is to make things easier for primary care doctors,” says one of the authors.

The digital test is done by the patient individually on a tablet computer. The test measures:


Alzheimer’s disease is the most common cause of dementia. As new disease-modifying treatments for Alzheimer’s disease are now becoming available, both early and accurate diagnosis in a resource-efficient assessment process are becoming increasingly important, as not everyone responds to the new drugs. Seeking medical care for cognitive impairment is not necessarily the result of Alzheimer’s disease – it can for example be caused by depression, fatigue or other dementias.

“Primary care does not have the resources, time or specialist knowledge to investigate possible Alzheimer’s disease in the same way as specialised memory clinics. And this is where a digital cognitive test can make the biggest difference,” says the senior author.

Unlike pen-and-paper tests, which are generally used to assess cognitive impairment, digital tests provide a more detailed picture. More aspects and new variables that could not previously be measured as easily are included.

Human genome rearrangement with programmable bridge recombinases

Bridge recombinases were discovered from parasitic mobile genetic elements that hijack bacterial genomes for their own survival. Presented last year in the journal Nature, the same team found these elements encode both a new class of structured guide RNA, which they named a “bridge RNA”, and a recombinase enzyme that rearranges DNA. The researchers repurposed this natural system by reprogramming the bridge RNA to target new DNA sequences, creating the foundation for a new type of precise gene editing tool they called bridge recombinases.

Starting with 72 different natural bridge recombinase systems isolated from bacteria, the team found that about 25% showed some activity in human cells, but most were barely detectable. Only one system, called ISCro4, showed enough measurable activity to enable further optimization. They then systematically improved both the protein and its RNA guide components, testing thousands of variations until they achieved 20% efficiency for DNA insertions and 82% specificity for hitting intended targets in the human genome.

While CRISPR uses a single guide RNA to target one DNA location, bridge RNAs are unique because they can simultaneously recognize two different DNA targets through distinct binding loops. This dual recognition enables the system to perform coordinated rearrangements such as bringing together distant chromosomal regions to excise genetic material or flipping existing sequences in reverse orientation. The system acts as molecular scaffolding that holds two DNA sites together while the recombinase enzyme performs the rearrangement reaction.

As a proof-of-concept, the researchers created artificial DNA constructs containing the same toxic repeat sequences that cause progressive neuromuscular decline in Friedreich’s ataxia patients. While healthy individuals carry fewer than 10 sequential copies of a three-letter DNA sequence, people with the disorder can harbor up to 1,700 copies, which interferes with normal gene function. The engineered ISCro4 successfully removed these repeats from the artificial constructs, in some cases eliminating over 80% of the expanded sequences.

The team also demonstrated that bridge recombinases could replicate existing therapeutic approaches by successfully removing the BCL11A enhancer, the same target disrupted in an FDA-approved sickle cell anemia treatment. And because bridge recombinases can move massive amounts of DNA, the technology could also help model the large-scale genomic rearrangements associated with cancers.


For decades, gene-editing science has been limited to making small, precise edits to human DNA, akin to correcting typos in the genetic code. The researchers are changing that paradigm with a universal gene editing system that allows for cutting and pasting of entire genomic paragraphs, rearranging whole chapters, and even restructuring entire passages of the genomic manuscript.

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