Latest news with #HSV1
Gizmodo
08-07-2025
- Health
- Gizmodo
The Next Big Cancer Treatment Could Be Herpes
Scientists are developing all sorts of potential new treatments to tackle the most difficult cancer cases—including some that will make you thankful for the existence of herpes and other viruses. Clinical trial data out today shows that a modified version of the herpes simplex virus 1 (HSV-1) can help keep late-stage skin cancer at bay. Researchers at the University of Southern California and others conducted the study, a Phase I/II trial of people with advanced, treatment-resistant melanoma. About a third of patients given the modified virus, in combination with immunotherapy, saw their tumors substantially shrink, while some even experienced a complete regression of their cancer. A larger, definitive trial of the experimental therapy, code-named RP1, is already underway, and the Food and Drug Administration will decide on an approval later this month. Scientists have been intrigued about the promise of cancer-fighting, or oncolytic, viruses for over a century, according to study author Gino In, a medical oncologist at USC's Keck School of Medicine. But it's only recently that this potential has started to look within reach. 'Most progress has been made just in the last few decades, thanks to advances and progression in gene editing technologies, which have allowed researchers to specifically design oncolytic viruses that are more effective and safer,' In told Gizmodo. HSV-1, the primary cause of cold sores, has emerged as a particularly promising candidate for cancer treatment. HSV-1 is a relatively large virus, meaning scientists can replace or add new genes without too much trouble. And though it does use our cells to replicate, like any virus, it doesn't insert its DNA into a cell's genome directly, eliminating the risk of certain mutations (an important consideration for safety). A typical HSV-1 infection also isn't life-threatening and can be treated with antiviral medications if needed, further limiting its potential danger. These properties have allowed scientists to create strains of the virus that can selectively target cancer cells. The first herpes-based cancer therapy (T-VEC) was approved in the U.S. in 2015 for some cases of metastatic melanoma. But researchers like In are especially excited by the new generation of these treatments. A Cancer-Fighting Version of Herpes Shows Promise in Early Human Trial RP1 is the brainchild of biotech company Replimune, and it's one of several cancer-fighting viruses that the company is currently developing. Compared to the typical HSV-1 virus, RP1 has been weakened, meaning it shouldn't be able to cause severe infections. It's also been modified to not only target cancer cells, but to also boost the immune system's natural tumor-killing ability. 'These changes make RP1 both safer and better at killing cancer cells than natural HSV-1,' In explained. And while RP1 might be a viable treatment on its own, Replimune is also testing whether it can be even more effective when paired with other existing immunotherapies. This latest study involved 140 patients from the company's IGNYTE trial of RP1 conducted across several sites, including at USC. The participants had late-stage melanoma that was unresponsive to earlier immunotherapy treatment. They received both RP1 and nivolumab, an immunotherapy drug commonly used for melanoma, every two weeks for up to four months. If patients responded to the initial treatment, they continued taking nivolumab alone for up to two years. By the study's end, a third of patients saw their tumors decrease in size by at least 30%, the researchers found, and almost one in every six patients had their tumors disappear entirely. Importantly, this shrinkage was seen in tumors directly injected with RP1 as well as uninjected tumors throughout the body—indicating its immune-boosting potential worked as hoped. The combination therapy also appeared to be safe, with most patients only experiencing minor adverse events like fatigue or other flu-like symptoms. The findings were presented earlier this year at the annual meeting of the American Society of Clinical Oncology and are set to be published soon in the Journal of Clinical Oncology. 'This study provides an important new approach for patients with immunotherapy-refractory melanoma; this is very important since about half of all melanoma patients do not benefit from immunotherapy,' said In. 'So it provides a new type of treatment, one that is both effective and well tolerated.' Experimental Therapy Fights Brain Cancer with Modified Herpes Virus Early trials are primarily intended to vet an experimental treatment's safety and optimal dosing, not its effectiveness. But given the general outlook of these normally untreatable cases, there's certainly reason to be optimistic here. Last year, Replimune launched a Phase III trial that will test RP1 combined with nivolumab in around 400 people with treatment-resistant melanoma. But even before this study concludes, RP1 could become available to the public. In January, the FDA agreed to consider the combination therapy for accelerated approval, a process that allows a novel treatment to be tentatively approved with less direct evidence of its effectiveness (further trial data is still required to secure a full approval). The FDA's decision on RP1 is scheduled for July 22. In and the USC team will continue to study their data to better understand how RP1 works. But they expect RP1 to become a new option for these resistant melanoma cases, and In notes that RP1 is also being tested for other kinds of cancer. If things keep going right, virus-based therapies like RP1 could soon become the next frontier of cancer treatment.
The Independent
27-06-2025
- Health
- The Independent
The shocking speed at which cold sore virus hijacks human DNA
A new study is the first to prove that the Herpes Simplex Virus (HSV-1) deliberately reshapes the human genome and reorganises infected cells within an hour of infection. The virus compacts and densifies human DNA to access host genes essential for its reproduction, a previously unknown mechanism of manipulation. Researchers discovered that blocking a single host cell enzyme, topoisomerase I, completely prevented the virus from rearranging the human genome and stopped infection in cell culture. This finding offers a potential new therapeutic target to control HSV-1, which affects nearly four billion people worldwide. HSV-1, while often causing benign cold sores, can lead to severe complications in rare cases and has been linked to dementia in older adults.
The Independent
27-06-2025
- Health
- The Independent
Cold sore virus takes over human DNA within just one hour, study finds
The cold sore-causing Herpes Simplex Virus (HSV-1) hijacks human cells and reconfigures its DNA within just an hour after infection, according to a new study that may help tackle the pathogen. Viruses are dependant on their hosts for replication, and upon infecting cells they tend to take over its cellular machinery to make new copies of themselves. Scientists have now found that the herpes virus not only hijacks its host's genome, but tends to reorganise the entire internal structure of the cells it infects within an hour after infection. Two out of every three people under the age of 50 live with HSV-1, and once infected, they have the virus for life. Although most cases are asymptomatic or manifest as mostly benign but recurrent cold sores, in rare cases the virus can cause blindness or life-threatening disease in newborns or those with compromised immunity. herpes infection and dementia in older adults. The new study, published in the journal Nature Communications, found that HSV-1 reshapes the human genome's structure, making it compact and dense so that the virus can access host genes most useful for it to reproduce. This finding could lead to new treatments to control the virus, which infects nearly four billion people worldwide, researchers say. "HSV-1 is an opportunistic interior designer, reshaping the human genome with great precision and choosing which bits it comes into contact with. It's a novel mechanism of manipulation we didn't know the virus had to exploit host resources," said Esther González Almela, first author of the study. While previous studies have suggested that HSV infection leads to compacting and reshaping host chromosomes, it remained unclear whether it was a side effect of the cold sore virus infection or caused directly by the pathogen itself. The latest study is the first to prove that HSV-1 reshapes the human genome deliberately and within hours of infection. Researchers also found that blocking a single host cell enzyme – topoisomerase I – completely blocked the cold sore virus' crucial ability to rearrange the human genome. "In cell culture, inhibiting this enzyme stopped the infection before the virus could make a single new particle," said Pia Cosma, another author of the study. "That gives us a potential new therapeutic target to stop infection,' Dr Cosma said. In the study, scientists used super-resolution microscopy to peer into ultra small cell structures just 20 nanometres wide, which is around 3,500 times thinner than a strand of hair. They combined this with another technique that reveals which bits of DNA are touching inside the nucleus. These techniques showed that the herpes virus' hostile takeover begins within the first hour, with the virus hijacking a key human enzyme – RNA-polymerase II – to synthesise its own proteins. Just three hours after infection, the virus causes a sizeable fraction of molecules involved in human DNA replication to abandon the cell nucleus and enter viral replication compartments. The wholesale theft causes a collapse of any activity across the host genome, which then gets crushed into a dense shell just 30 per cent of its original volume. Scientists hope the latest findings can help address the global health challenge posed by HSV-1 due to its prevalence and ability to cause recurrent outbreaks.
Daily Mail
19-06-2025
- Health
- Daily Mail
EXCLUSIVE Experts finally find treatment for incurable viral infection suffered by 122million Americans
Half of Americans are suffering from an incurable disease that causes painful - and embarrassing - blisters and sores around the mouth. About 122million people have herpes simplex virus 1 (HSV-1), the oral strain of herpes. It's spread though close skin-to-skin contact and differs from the sexually transmitted herpes simplex virus 2 (HSV-2), which causes genital blisters and sores. There is no cure for HSV-1, but antiviral medications can manage outbreaks and reduce the risk of transmission. Now, however, researchers from Spain, have discovered how the virus acts on a person's DNA, opening the door for a possible cure. The team found that the virus 'hijacks' a certain enzyme in the body that allows herpes to replicate itself, but if that enzyme is blocked, it brings 'the hostile takeover to a halt.' The researchers are hopeful that the study's findings, which provide the first proof herpes actually reshapes a person's DNA within only hours of infection, may help address the public health burden of HSV-1. Globally, nearly 4billion people have this type of herpes and experts are becoming more concerned as drug-resistant strains are developing, which could lead to more transmission. And unmanaged herpes can lead to devastating complications, traveling to the brain and triggering inflammation, which can increase the risk of dementia. Researchers in Spain analyzed human cells and infected them with HSV-1, and found almost immediately that it reshapes cell DNA so it can access more genes and spread rapidly throughout the body. However, blocking the enzyme topoisomerase I, which controls DNA replication, stopped HSV-1 from rearranging genes during infection, stopping it from spreading. Blocking the enzyme can be done with drugs called topoisomerase inhibitors, which are usually used in chemotherapy regimens to stop DNA from replicating and forming more cancer cells. This could be the first-ever method of slowing the spread of HSV-1. The researchers said while more evidence supporting a possible treatment is needed, the study could be the first step in preventing worldwide herpes outbreaks. Professor Pia Cosma, corresponding study author and researcher at the Centre for Genomic Regulation (CRG) in Barcelona, said: 'In cell culture, inhibiting this enzyme stopped the infection before the virus could make a single new particle. 'That gives us a potential new therapeutic target to stop infection.' Herpes is most commonly transmitted from a carrier to a person without herpes by touching a cold sore, which actively produces or 'sheds' the virus. However, it can cause genital herpes by spreading through oral sex. HSV-1 leads to painful blisters around the lips and mouth, skin and genitals. When the virus infects a person, it may travel up to a cluster of sensory nerves in the brain and remain dormant there for months or even years after the initial infection. But in times of stress, severe fatigue, or changes to the immune system, the virus can reactivate, multiply, and travel back to the skin through nerve fibers. These stressful times can result in new blisters in the same area as the initial infection. The new study, published Thursday in Nature Communications, looked at human A549 cells, which are caused by the cancer lung carcinoma. The cells were then infected with HSV-1 representing one, three and eight hours post infection. Researchers found after eight hours, HSV-1 had occupied 70 percent of the cells, suggesting it would take less than a day for the virus to completely overtake cell DNA and spread. Dr Esther Gonzalez Almela, first study author, said: 'HSV-1 is an opportunistic interior designer, reshaping the human genome with great precision and choosing which bits it comes into contact with. 'It's a novel mechanism of manipulation we didn't know the virus had to exploit host resources.' The researchers then tried to suppress topoisomerase I, which relaxes DNA and makes it easier for it to replicate. They found this 'hindered viral replication.' The team wrote that suppressing the enzyme stops HSV-1 from progressing, suggesting it could be most beneficial for those in later stages of infection. Topoisomerase inhibitors are sold under names like etoposide, irinotecan and topotecan to slow the growth of lung, colorectal, ovarian and testicular cancers, among others. Some are also used to treat multiple sclerosis, a progressive neurological disorder that attacks the spinal cord, by reducing central nervous system inflammation. They can be given as either pills or intravenously for anywhere from $8 to $61 depending on the method.
Yahoo
01-06-2025
- General
- Yahoo
Study Links Herpes Virus To Alzheimer's Risk, But Experts Urge Caution
A new study published in the scientific journal BMJ Open has found that herpes simplex virus type 1 (HSV-1), which causes cold sores, is associated with an increased risk of Alzheimer's disease. However, experts emphasize that the findings show correlation, not causation, and more research is needed. The study, conducted by researchers at Gilead Sciences Inc., analyzed health insurance data from 344,628 U.S. adults aged 50 and older diagnosed with Alzheimer's or related dementia between 2006 and 2021, each matched with a control of similar age, sex, and region without neurological disorders. Of those with Alzheimer's, 0.44% had a prior HSV-1 diagnosis, compared to 0.24% of controls, suggesting an 80% higher relative risk for Alzheimer's among those with HSV-1. The absolute numbers, however, remain small. Additionally, individuals treated with antiviral medication for HSV-1 showed a 17% lower risk of developing Alzheimer's compared to untreated counterparts. 'Despite the large sample size, this research has limitations partly due to only using health records and administrative claims data,' said Dr. Sheona Scales, Director of Research at Alzheimer's Research UK, in a statement to the Science Media Centre. 'Most people infected with HSV-1 don't have any symptoms, so some infections might not have been recorded.' Dr. David Vickers of the University of Calgary was more critical, stating, 'This pharma-funded research exaggerates the role of HSV-1, failing to appreciate its absence in 99.56 percent of [Alzheimer's disease] cases.' The World Health Organization estimates two-thirds of people under 50 globally carry HSV-1, a neurotropic virus that can infect nerve cells and often lies dormant after initial infection, sometimes reactivating to cause cold sores. Previous studies have detected HSV-1 DNA in postmortem Alzheimer's brains and shown it can trigger amyloid-beta plaque accumulation, a hallmark of the disease, in lab settings. A 2024 Journal of Virology study found HSV-1 can enter mouse brains, causing persistent inflammation, noting evidence for its role in Alzheimer's as 'overwhelming.' 'We're not saying viruses explain everything. But they may be central to it. This is no longer a fringe theory – it's the next phase of Alzheimer's research, and we're pursuing it,' Dr. Bryce Vissel of St. Vincent's Hospital Sydney told the Australian Science Media Centre. However, Professor Tara Spires-Jones of the University of Edinburgh cautioned, 'It is important to note that HSV-1 infection, which is extremely common in the population, is by no means a guarantee that someone will develop Alzheimer's.' The study's reliance on insurance data raises concerns, as HSV-1 is often underdiagnosed, potentially skewing results. It also lacks data on infection frequency or severity, which could influence risk. 'The study's data source makes its findings ungeneralisable, and it overstates a minor infection as a 'public health priority' to justify unnecessary treatment,' Vickers added. Other factors, like genetics, lifestyle, or healthcare access, may also contribute to Alzheimer's risk among HSV-1 carriers. Some experts see potential in antiviral treatments. 'With many GPs and the population being unaware of the dementia related benefits of treating HSV infections and preventing VZV activation through vaccination, it is time to call for actions informing those working in primary care as well as the population at large,' said Professor Cornelia van Duijn of the University of Oxford. Dr. Richard Oakley of Alzheimer's Society advised, 'If you are worried about a cold sore or your general health, be sure to seek the appropriate help from a health professional.' 'More research is needed to understand the best way to protect our brains from Alzheimer's disease as we age,' Spires-Jones said. For now, experts recommend focusing on proven brain health strategies like exercise, sleep, and a balanced diet.
