How do you prevent cold sores
Unmask the tricks of the herpes viruses
They usually announce themselves hours in advance by tingling, feeling of tension or a slight burning sensation: Cold sores usually appear on the lip of the infected person. But they can also appear on the nose, fingernails, eyes or buttocks. The itchy and painful blisters are caused by type 1 herpes simplex viruses. Normally, the symptoms of the disease are unpleasant, but not dangerous. But especially in certain risk groups such as patients undergoing chemotherapy, newborns or HIV patients, life-threatening complications can arise when a herpes infection breaks out. But even in healthy people, herpes can spontaneously trigger encephalitis, often with irreversible damage.
Once infected with herpes viruses, you will not get rid of them for the rest of your life. Most of the time they are in the idle state. Only when the immune system is weakened, for example in the case of infectious diseases, fever, stress or strong sunlight, the herpes viruses become active again. Most people become infected with herpes before the age of six. “In the first few hours after infection, it is decided in every single infected cell whether the virus will actively multiply or go into dormant state,” says Lars Dölken from the Department of Virology at the University of Würzburg. The doctor and his team want to understand how this decision is made. These findings could provide new starting points for therapies to combat the herpes viruses.
How herpes viruses take control
What happens when the viruses enter the human body? What tricks do they use to evade the immune system? And how do the viruses manage to take command in individual cells? The researchers from Würzburg are looking for answers to these questions. What is certain is that the genetic material of the virus consists of DNA, just like in humans. "As soon as the herpes pathogen has penetrated a human cell, it smuggles its genetic material into the cell nucleus," explains Dölken. In the resting state, the virus hides there so that it cannot be recognized and attacked by the infected person's immune system.
The molecular machinery with which genetic information is read from the DNA and transcribed into so-called RNA molecules is located in the cell nucleus. This RNA then determines which proteins the cell makes, for example to promote cell growth. Herpes viruses are able to take control of this machinery. They use the cells to have their own proteins produced in large quantities and to multiply on a massive scale. “The cell is ultimately destroyed, releasing thousands of new virus particles in the process,” says Dölken.
Cure patients of the virus
If those affected do nothing about the herpes outbreak, the blisters usually go away after about two weeks. But the infection is far from over, because the viruses continue to dormant in individual infected cells. This is where the Würzburg researchers want to start. Her long-term plan is to develop an agent that will trigger an acute outbreak in all cells infected with herpes. That would activate all viruses. "The immune system could then fight the herpes viruses effectively with the support of antiviral drugs," says Dölken. "The latency would go away and we would have cured the patient of the virus."
The scientists hope that this principle would also work for other more serious forms of herpes. There are a total of eight types of herpes virus in humans. These include genital herpes or the Epstein-Barr virus, which is suspected of causing tumor diseases. Herpes viruses also cause diseases such as chickenpox, shingles and glandular fever.
Reading of human DNA disturbed
Dölken and his team have already gained an astonishing insight into the virus' tricky procedure in the cell. When genetic information is read from DNA and converted into RNA, there is usually a defined start and end point on the DNA strand. However, this reading process gets out of control with an infected cell. It no longer stops at the designated points, but just continues. This creates defective RNA products that can no longer be processed into proteins. “The DNA of the virus, on the other hand, is read completely correctly,” explains Dölken. "In this way, the virus increases the production of its own proteins and at the same time weakens the host cell."
Researchers from Yale and Lisbon were also able to observe this phenomenon in tumor cells and in cellular stress reactions. "The causative agent of the cold sore is therefore a model object for us to understand what can go wrong in the cell," says Dölken. Herpes viruses have evolved with humans for millions of years. “This makes them absolute specialists for our cells and our immune system,” says the virologist. “You know the connections much better than we do. Our goal is therefore to know what the viruses know. ”The researchers hope that they will then also have a much better understanding of what happens with tumor diseases - and here too to identify new points of attack for therapies.
Prof. Dr. med. Lars Dölken
Julius Maximilians University of Würzburg
Institute for Virology and Immunobiology
Versbacher Strasse 7
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