Tag: 7/10/25

The HIV Dormancy Mystery Could Unlock the Path to a Cure

Colourised scanning electron micrograph of HIV (yellow) infecting a human T9 cell (blue). Credit: NIH

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 dormant state in infected cells that allows the virus to “hide” from the immune system and current treatments. 

The researchers believe the finding, just published in Nature Microbiology, challenges decades of scientific assumptions and opens a new approach to possibly eliminating the deadly virus. 

“This discovery rewrites what we thought we knew about how HIV goes into this stealth mode in the human body,” said study lead Saba Valadkhan, an associate professor in the Department of Molecular Biology and Microbiology at the Case Western Reserve School of Medicine. “We’ve shown that HIV actually orchestrates its own survival by reprogramming host cells to create the perfect hiding place.”

The team discovered that HIV uses a clever survival trick that explains why it’s been impossible to cure. After HIV invades a cell, it sneaks its genetic code into the cell’s DNA, then tricks the cell into going to sleep, which also puts the virus to sleep, making both completely invisible. This tactic makes the infected cell invisible to the immune system and unreachable by even today’s most advanced HIV drugs. The virus stays hidden in these dormant cells until the right moment to “wake up” and spread again, creating an undetectable reservoir that ensures HIV never goes away completely.

“What we’ve uncovered is that HIV doesn’t just randomly go dormant – it actively manipulates the host cell to create conditions for its own survival,” said study collaborator Jonathan Karn, Distinguished University Professor and chair of the Department of Molecular Biology and Microbiology. “This gives us specific targets to attack.”

The findings may extend far beyond HIV treatment. The researchers believe similar dormancy actions could be triggered by other viruses – including herpes, hepatitis and other retroviruses – potentially leading to new therapies for many viral diseases. 

“We may have uncovered new tactic viruses use to trick the host cells to do their bidding,” Valadkhan said.

This discovery is also important for protecting public health worldwide because viruses like HIV – which can permanently insert themselves into a person’s DNA – could potentially be used as future viral threats and pandemic preparedness.

Source: Case Western Reserve University

Poor Sleep May Accelerate Brain Ageing

Poor sleep may accelerate brain ageing, a new study shows. Photo by Andrea Piacquadio

People who sleep poorly are more likely than others to have brains that appear older than they actually are. This is according to a comprehensive brain imaging study from Karolinska Institutet, published in the journal eBioMedicine. Increased inflammation in the body may partly explain the association.

Poor sleep has been linked to dementia, but it is unclear whether unhealthy sleep habits contribute to the development of dementia or whether they are rather early symptoms of the disease. In a new study, researchers at Karolinska Institutet have investigated the link between sleep characteristics and how old the brain appears in relation to its chronological age. 

The study includes 27 500 middle-aged and older people from the UK Biobank who underwent magnetic resonance imaging (MRI) of the brain. Using machine learning, the researchers estimated the biological age of the brain based on over a thousand brain MRI phenotypes. 

Low-grade inflammation 

The participants’ sleep quality was scored based on five self-reported factors: chronotype (being a morning/evening person), sleep duration, insomnia, snoring, and daytime sleepiness. They were then divided into three groups: healthy (≥ 4 points), intermediate (2-3 points), or poor (≤ 1 point) sleep. 

“The gap between brain age and chronological age widened by about six months for every 1-point decrease in healthy sleep score,” explains Abigail Dove, researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, who led the study. “People with poor sleep had brains that appeared on average one year older than their actual age.” 

To understand how poor sleep can affect the brain, the researchers also examined levels of low-grade inflammation in the body. They found that inflammation could explain just over ten per cent of the link between poor sleep and older brain age. 

“Our findings provide evidence that poor sleep may contribute to accelerated brain ageing and point to inflammation as one of the underlying mechanisms,” says Abigail Dove. “Since sleep is modifiable, it may be possible to prevent accelerated brain ageing and perhaps even cognitive decline through healthier sleep.” 

Several possible explanations 

Other possible mechanisms that could explain the association are negative effects on the brain’s waste clearance system, which is active mainly during sleep, or that poor sleep affects cardiovascular health, which in turn can have a negative impact on the brain. 

Participants in the UK Biobank are healthier than the general UK population, which could limit the generalisability of the findings. Another limitation of the study is that the results are based on self-reported sleep. 

The study was conducted in collaboration with researchers from the Swedish School of Sport and Health Sciences, and Tianjin Medical University and Sichuan University in China, among others. It was funded by the Alzheimer’s Foundation, the Dementia Foundation, the Swedish Research Council, the Loo and Hans Osterman Foundation for Medical Research, and the Knowledge Foundation. The researchers report no conflicts of interest. 

Source: Karolinska Institutet

Pancreatic Alpha Cells also Secretly Produce Significant Amounts of GLP-1

New study uncovers natural hormone shift that could transform type 2 diabetes treatment

A 3D map of the islet density routes throughout the healthy human pancreas. Source: Wikimedia CC0

A new study from Duke University School of Medicine is challenging long-standing views on blood sugar regulation — and pointing to a surprising new ally in the fight against type 2 diabetes. 

Published in Science Advances, the research reveals that pancreatic alpha cells, once thought to only produce glucagon – a hormone that raises blood sugar to maintain energy when fasting or exercising – also generate GLP-1, a powerful hormone that boosts insulin release from beta cells and helps regulate glucose. GLP-1 is the same hormone mimicked by blockbuster drugs like semaglutide. 

Using mass spectrometry, Duke researchers found that human alpha cells may naturally produce far more bioactive GLP-1 than previously believed. 

Led by Duke scientist Jonathan Campbell, PhD, the team of obesity and diabetes researchers analysed pancreatic tissue from mice and from humans across a range of ages, body weights, and diabetes statuses. They found that human pancreatic tissue produces much higher levels of bioactive GLP-1 and that this production is directly linked to insulin secretion. 

“Alpha cells are more flexible than we imagined,” said Campbell, an associate professor in the Division of Endocrinology in the Department of Medicine and a member of the Duke Molecular Physiology Institute. “They can adjust their hormone output to support beta cells and maintain blood sugar balance.” 

This flexibility could change the approach to treating type 2 diabetes, where beta cells in the pancreas can’t make enough insulin to keep blood sugar at a healthy level. By boosting the body’s own GLP-1 production, it may offer a more natural way to support insulin and manage blood sugar.  

Switching gears 

In mouse studies, when scientists blocked glucagon production, they expected insulin levels to drop. Instead, alpha cells switched gears – ramping up GLP-1 production, improving glucose control, and triggering stronger insulin release.  

“We thought that removing glucagon would impair insulin secretion by disrupting alpha-to-beta cell signaling,” Campbell said. “Instead, it improved it. GLP-1 took over, and it turns out, it’s an even better stimulator of insulin than glucagon.” 

To test this further, researchers manipulated two enzymes: PC2, which drives glucagon production, and PC1, which produces GLP-1. Blocking PC2 boosted PC1 activity and improved glucose control. But when both enzymes were removed, insulin secretion dropped and blood sugar spiked – confirming the critical role of GLP-1. 

Implications for diabetes treatment 

While GLP-1 is typically made in the gut, the study confirms that alpha cells in the pancreas can also release GLP-1 into the bloodstream after eating. This helps to lower blood sugar by increasing insulin and reducing glucagon levels. 

Common metabolic stressors, like a high-fat diet, can increase GLP-1 production in alpha cells – but only modestly. That opens the door to future research: If scientists can find ways to safely boost GLP-1 output from alpha cells they may be able to naturally enhance insulin secretion in people with diabetes.  

But measuring GLP-1 accurately hasn’t been easy. The team developed a high-specificity mass spectrometry assay that detects only the bioactive form of GLP-1 – the version that actually stimulates insulin — not the inactive fragments that often muddy results. 

“This discovery shows that the body has a built-in backup plan,” Campbell said. “GLP-1 is simply a much more powerful signal for beta cells than glucagon. The ability to switch from glucagon to GLP-1 in times of metabolic stress may be a critical way the body maintains blood sugar control.” 

Source: Duke University

Innovative UK Project to Test Drones for Cardiac Arrest Response

Credit: University of Surrey

A project to test how drones can be integrated into the UK’s 999 emergency response system to rapidly deliver defibrillators to patients experiencing out-of-hospital cardiac arrest (OHCA) has been launched by the University of Surrey, Air Ambulance Charity Kent Surrey Sussex, South East Coast Ambulance Service NHS Foundation Trust. 

With survival rates for OHCA in the UK currently below 10%, a key challenge is the delay in delivering life-saving defibrillation. While public Automated External Defibrillators (AEDs) are widely available, getting them to a patient in time is often difficult. This 16-month project will explore using drones to rapidly deliver AEDs to the scene of an emergency. 

This research is the first step towards integrating drone technology into our emergency response systems. Our ultimate goal is to develop and test the procedures needed to seamlessly introduce drone delivery of AEDs into the 999-emergency system 

Dr Scott Munro, Lecturer in Paramedic Practice at the University of Surrey and co-lead on the project

The initiative, which has been funded by the National Institute for Health and Care Research (NIHR), will be divided into two sections: in the first, researchers will develop and refine the drone delivery process through a series of simulations, coordinating 999 call taking, Air Traffic Control, ambulance dispatch and drone operators.  

In the second part, interviews will be conducted with a diverse group of people -including OHCA survivors, family members, responders and members of the public – to understand the public’s perception of drone technology, including any barriers or concerns, and to ensure ease of use for responders. 

This project is a great example of how NIHR’s RfPB programme supports life-saving innovation. Using drones to deliver defibrillators could help emergency teams reach patients faster, improve survival after cardiac arrest, and bring cutting-edge technology directly to the NHS frontline, while working with the public to ensure it’s used safely and effectively. 

Professor Kevin Munro, Director of the NIHR Research for Patient Benefit (RfPB) Programme

Rapid intervention is vital in managing out-of-hospital cardiac arrests. As demand continues to grow, the opportunity to integrate this technology into future healthcare systems represents real progress in ensuring ambulance services can work with the communities they serve to strengthen the chain of survival and give patients the best chance of a positive outcome Being a partner in this research, we are eager to explore how this new initiative could strengthen our cardiac arrest care pathway. 

Dr Craig Mortimer, Research Manager at South East Coast Ambulance Service NHS Foundation Trust (SECAmb)

Source: University of Surrey

Webber Wentzel Secures Landmark Constitutional Court Ruling Reforming South Africa’s Parental Leave Laws

Photograph by Drew Hays on Unsplash

Webber Wentzel’s Pro Bono team represented Mr and Mrs van Wyk in a landmark case that has resulted in the Constitutional Court confirming that South Africa’s statutory four months of parental leave may be shared between both parents. The ruling marks a significant step toward gender equality in the workplace and family law.

The case challenged the unequal parental leave provisions under section 25 of the Basic Conditions of Employment Act (BCEA), which granted birthing mothers up to four months of maternity leave while limiting fathers to only 10 days.

Webber Wentzel argued that section 25 of the BCEA unfairly discriminated against fathers and placed an undue burden on birthing mothers by not allowing families to decide who should be the primary caregiver. The court agreed and criticised the 10-day leave for fathers by rejecting the cultural norms that reinforce gendered parenting roles as inconsistent with constitutional values.

The application was supported by the Commission for Gender Equality (CGE) and Sonke Gender Justice (Sonke). CGE advocated for equal parental leave for adoptive and surrogacy-commissioning parents, which the court partially granted. Sonke’s request for an equal 16-week leave for both parents was not granted.

The Constitutional Court, in a unanimous judgment delivered by the Honourable Justice Tshiqi, confirmed that sections 25, 25A, 25B and 25C of the BCEA, along with corresponding provisions of the Unemployment Insurance Fund Act (UIF Act), are unconstitutional. The Court held that these provisions violate the rights to equality and human dignity under sections 9 and 10 of the Constitution.

The Minister of Employment and Labour accepted that differentiation exists between birthing mothers and other categories of parents is automatically unfair as it is based on grounds specified in section 9(3) of the Constitution. Further, the Minister acknowledges that there is a need for reform in the current legislation pertaining to the parental leave regime contained in the BCEA.

As a result of the ruling in the Constitutional Court, the 4 months of maternal and the 10 days of parental leave will be combined into a total of 4 months and 10 days, which parents may now share as they choose. If no agreement is reached, the leave will be split equally. Where only one parent is employed, that parent will be entitled to the 4 consecutive months of parental leave.

The Constitutional Court also confirmed that the same parental leave provisions apply to adoptive parents and commissioning parents in a surrogacy arrangement.

The Constitutional Court has suspended the declaration of invalidity of the relevant BCEA and UIF Act provisions for a period of 36 months, to allow the legislature to remedy the necessary constitutional defects.  In the interim, the following principles will apply:

  • A single parent or a parent who is the only employed parent is entitled to four months’ consecutive parental leave.
  • Parents who are both employed may share the allocated parental leave of four months and 10 days between them, concurrently or consecutively.
  • An adoptive parent of a child younger than two years is entitled to four months’ consecutive parental leave.
  • If an adoption order is granted in respect of two parents, they may share the allocated parental leave of four months and 10 days between them, concurrently or consecutively.
  • A commissioning parent is entitled to four months’ consecutive parental leave.
  • Where there are two commissioning parents, they may share the allocated parental leave of four months and 10 days between them, concurrently or consecutively.

Employers are encouraged to review and, where necessary, update their leave policies and employment contracts to reflect the new parental leave framework.

“This judgment is a powerful affirmation of the constitutional rights to equality and dignity,” said Nkosinathi Thema, senior associate, Webber Wentzel. “It recognises that caregiving is not the exclusive responsibility of mothers and that both parents should have the freedom to decide how best to care for their child.”

The Webber Wentzel team comprised Ayanda Khumalo, Nkosinathi Thema and Lize-Mari Doubell. Counsel Nasreen Rajab-Budlender SC, Liam Minné and Sanan Mirzoyev appeared on a pro bono basis.

The judgment can be read here.

Ends…

Founded in 1868, Webber Wentzel is a leading full-service law firm providing clients with innovative solutions to their most complex legal and tax issues across Sub-Saharan Africa. With over 450 lawyers, their multi-disciplinary expertise is consistently ranked top tier in leading directories and awards, both in South Africa and on the African continent. Their collaborative alliance with Linklaters and their deep relationships with outstanding law firms across Africa provide clients with market-leading support wherever they do business.