People who have had the virusherpes simplex are twice as likely to develop dementia at some point in their lives than those who have never been infected. A new study from Uppsala University confirms previous research on the possibility that herpes may be a possible risk factor for dementia.
The researchers studied 1,000 70-year-olds from Uppsala over a 15-year period. The study found that people who had been infected with the herpes simplex virus at some point in their lives were twice as likely to develop dementia, compared to those who had never been infected.
There research was published in the Journal of Alzheimer's Disease.
People infected with the herpes simplex virus are twice as likely to develop dementia
The herpes simplex virus is very common and up to 80% of Swedish adults may be infected. The infection is lifelong, but symptoms can come and go at different times of life. Many people never experience any symptoms related to the infection.
“The peculiarity of this study is that the participants are more or less the same age, which makes the results even more reliable since age differences, which would otherwise be linked to the development of dementia, cannot confound the results,” explains Erika Vestin, student doctor at Uppsala University.
Worldwide, 55 million people suffer from dementia. Advanced age and the presence of the apolipoprotein ε4 risk gene are already known risk factors. Research has previously been conducted to see whether the herpes simplex virus could also be a possible risk factor for dementia, which is now confirmed in this study.
“It is exciting that the results confirm previous studies. More and more evidence is emerging from studies that, like our results, point to the herpes simplex virus as a risk factor for dementia,” continues Vestin.
Important conclusions of the study include the need to further investigate whether already known drugs against the herpes simplex virus can reduce the risk of dementia and the possibility of developing new vaccines.
“The findings could further push dementia research towards treating the disease at an early stage using common anti-herpes virus drugs or towards preventing the disease before it occurs,” adds Vestin.
The results of an additional study conducted by a team of researchers from the Geisel School of Medicine at Dartmouth and the Thayer School of Engineering and published in Cell Reports Medicine offer new insights into how antibodies work in the fight against herpes simplex virus infections (HSV). The research could lead to possible new treatments for neonatal herpes.
Herpes simplex virus infections are common and typically affect the skin and nervous system. They are caused by two related but distinct viruses: type 1 (HSV-1) which most commonly causes infections around the mouth and affects up to 80-90% of older adults, and type 2 (HSV-2) which most commonly causes infections genital infections and are found in 20-30% of adults.
While these viruses often lie dormant in the body and usually pose no serious health risks, HSV can be more dangerous for those with weak immune systems. In some cases, HSV can cause corneal blindness and brain infections and may also have an association with neurodegeneration and Alzheimer's disease. Neonatal herpes simplex virus infections are particularly devastating – serious infections can spread to internal organs and the brain – and are one of the deadliest neonatal infections.
“Despite three decades of trying, the scientific community has not been able to develop an effective herpes vaccine, and I think the main problem has been that we haven't fully understood what we need, in terms of antibodies and their specific functions, to fight herpes. protect against this disease,” says David Leib, Ph.D., chair and professor of microbiology and immunology at Geisel, who was a corresponding author on the study along with Margaret Ackerman, Ph.D., professor of engineering at Thayer
As they often have in the past, Leib and Ackerman collaborated on the project, combining the expertise and resources of their labs and co-supervising the work of Matthew Slein, a Ph.D. candidate in the Leib and Ackerman labs, and Iara Backes, an M.D.-Ph.D. student at Geisel, who was co-first author of the study.
In their experiments, the research team used a neonatal mouse model to mimic human neonatal infections, designing antibodies with different properties to explore how they mediate protection.
“What Matt and Iara discovered was something unexpected,” says Leib. “It is not only the neutralizing capacity of antibodies, i.e. their ability to bind directly to the virus and prevent it from entering the cell, that is important. Effector functions, which allow antibodies to interface with other parts of the immune system, also play a critical role, which has been largely overlooked in the past.”
Slein and Backes also discovered key differences between HSV-1 and HSV-2 infections and that each requires different antibody properties for optimal protection. Importantly, their findings point to a better way to design vaccines and may help explain why many vaccine candidates have failed to provide protection in clinical trials in the past.
“Another important aspect of the work that Matt and Iara have done is that we now have some really good monoclonal antibodies that we have produced in the lab that could potentially be used directly as a drug to treat acute neonatal herpes infections, which are vital diseases. -threatening to newborns,” Leib says.
“Monoclonal antibodies have been used to treat cancer and other diseases and show promise as a therapy for infectious diseases,” he says. “This would be a wonderful development, as antiviral drugs such as acyclovir have been shown to be only partially effective in treating these very sick children.”
Pregnant women with a previous history of herpes simplex virus type 1 (HSV-1) infection maintain active antibodies against the virus, and researchers have found that this protection can pass to the nervous system of their offspring.
Using a mouse model of HSV-1 and autopsy samples of adult and fetal human tissue, researchers at Dartmouth College's Geisel School of Medicine found that antibodies to HSV-1 produced by adult women or female mice could travel to the nervous system of their animals. unborn children, preventing the development and spread of the infection during childbirth.
The work, published this week in mBio, an open-access online journal of the American Society for Microbiology, suggests that immunizing pregnant women against HSV and similar infections could prevent serious brain diseases linked to these conditions in fetuses and newborns, said the study's senior author. David A. Leib, Ph.D., professor of microbiology and immunology in the medical school.
“Our findings highlight the previously underappreciated role of maternal antibodies in protecting the nervous system of the fetus and newborn from infection,” Leib said. “Maternal antibodies have a powerful protective role in the neonatal nervous system against HSV.”
While HSV-1 is commonly associated with cold sores on the skin, the infection can also cause eye infections and is the most common form of infectious corneal blindness in the United States, Leib said. It can also enter the brain and cause inflammation (encephalitis).
HSV-1 infection in newborns – who can contract the virus from infected mothers as they pass through the birth canal – can be serious and cause brain damage or death. Neonatal HSV infection affects about 1 in 3,200 to 1 in 10,000 live births, Leib said. Even with antiviral intervention, HSV causes significant brain disease in newborns.
In a series of laboratory experiments, the researchers found that herpes simplex antibodies remain in the trigeminal ganglion (a group of nerve cells that receives signals from the eyes and face and is a key site of HSV infection) very time after the active viral infection has disappeared. eliminated and that these maternal antibodies can travel to the fetal trigeminal ganglia. The researchers then demonstrated that the antibodies completely protected newborn mice from herpes simplex infection.
“What this tells us is that women who become pregnant and who have a pre-existing herpes simplex infection have a mature immune response to that virus and will pass those antibodies on to their baby,” Leib said.
“If that baby were to be infected during birth, it will be protected because the mother's antibodies enter its nervous system before birth.” In contrast, if herpes simplex infection is acquired during pregnancy, the risk of serious outcomes for the newborn can reach 50%.
Maternal antibodies that provide neural protection to newborns “have never been observed before and are very important for pathogens that infect newborns because often there is some kind of neurological consequence that can impact their entire life,” he said. added study lead author Yike Jiang, a physician. /Ph.D. student of medical school.
Several herpes simplex vaccines tested in clinical trials for prevention of adult-to-adult transmission have failed, Leib noted, but none have been tested for prevention of so-called “vertical transmission” of the virus from adult to child.
Ongoing studies in his lab are evaluating whether any of the vaccines can protect against vertical transmission. Maternal immunization can also be an effective strategy against other pathogens that affect newborns, she said, such as the Zika virus.
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