Researchers are developing killer cells that kill herpes viruses
Herpes viruses are common in humans. When talking about herpes, the virus herpes simplex is primarily meant. In Germany, around 85 to 90 percent of the population carry this virus, but only 20 to 40 percent reveal it through symptoms. A team of researchers from the Helmholtz Zentrum München has now taken a closer look at a related virus, the herpes virus 6 (HHV-6). The scientists have successfully identified the components of the virus and they now know where so-called killer T cells can attack to switch off the virus.
Herpes virus 6 is also widespread in humans. Many carriers do not even know that they are infected. However, it can lead to diseases in people with a weak immune system. A team of researchers at the Helmholtz Zentrum München and the German Center for Infection Research (DZIF) has developed a possible approach for new therapies to combat herpes viruses. The results of their work were recently published in the specialist journal "PLOS Pathogens".
About the herpes virus 6
In most cases, people get infected with the human herpes virus 6, or HHV-6 for short, in early childhood. This virus is similar to the herpes simplex virus, which causes the annoying cold sore. HHV-6 shows other effects. Infection with HHV-6 can trigger the infectious disease three-day fever in infancy or early childhood. The virus then remains in the body for life.
What diseases can cause HHV-6?
The virus does not cause symptoms in healthy people. However, it is believed that HHV-6 may contribute to the development of autoimmune diseases and chronic fatigue syndrome. The fact is that patients with a severely weakened immune system, for example after major operations, have difficulty controlling the virus. Severe damage to various organs can be the possible consequence.
The toolbox of the immune system helps
Scientists at the Helmholtz Zentrum München deal in depth with the virus and how a healthy immune system keeps HHV-6 at bay. "We study the toolbox of the immune system," explains Dr. Andreas Moosmann in a press release on the study results. He heads a DZIF research group in the gene vectors department. "And we discovered a few interesting new tools that we have already been able to replicate," said Moosmann.
Killer T cells from the toolbox
Specifically, the scientists investigated which structures of the virus preferentially attack the killer T cells. The T cells are part of the natural cellular immune defense. If components of pathogens (antigens) are recognized in the organism, the body sends these T cells to the body's defense in order to fight foreign substances. An important type of T cells are the effector cells (CD8 + T cells), which kill infected or changed cells in the body. Once the infection has been defeated, these effector cells can develop into so-called memory cells, which serve as a kind of memory for the immune system.
Vulnerabilities of the viruses exposed
The research team discovered 16 structures of the virus on which killer cells can dock and attack. In extensive analyzes, the scientists reduced 300 possible points of attack to a circle of 20. Against these points, the researchers succeeded in producing killer T cells, 16 of which could actually bind their target and destroy the infected cell. "Obviously, very different virus proteins can serve as target structures for the immune system," explains Moosmann.
Mimicking natural processes
"We regularly observe T cells against these structures in healthy people," says the doctor. After serious operations such as transplants, such killer cells could keep the virus at bay. This is currently being checked in a large number of patients.
Prevent an outbreak with killer T cells
In the long term, Andreas Moosmann and his team want to use this knowledge for new treatments. "An outbreak of the virus could possibly be prevented by giving patients HHV-6-specific killer T cells," summarizes the expert. However, there is still a good deal of work ahead of the researchers. Until then, the classic home remedies for herpes must still help. (vb)