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New study shows how the herpes virus kidnaps the immune system for survival

New study shows how the herpes virus 'hijacks' the immune system for survival (image credits: iStock)

Herpes is a common viral infection that causes painful bubbles and ulcers. It is caused by the herpes simplex virus-1 (HSV-1) and can lead to flu-like symptoms, deafness, pain and a burning feeling in affected areas. While the body's immune system can suppress the virus, a new study by Dr. Anna Cliffe from the University of Virginia found that the herpes virus can kidnap the same immune system that is fighting against it – the reactivation of reactivation.

Herpesinfection

According to the World Health Organization (WHO), more than 60 percent of people under the age of 50 have the herpes virus. As soon as the virus gets into the body, it stays in the nerve cells for life. Many people may never have symptoms because the immune system rests the virus. However, certain triggers such as stress, sunburn, infections or a weakened immune system can cause it to flare up, which leads to painful outbreaks.

Common symptoms of herpes

While some people with herpes may not show any symptoms, others can occur:

    Painful blowing or wounds on the mouth, lips or face
  • Tingling, itching or burning feeling before a bladder appears
  • Swollen lymph nodes
  • Fever and flu -like symptoms
  • Daubiness or nerve pain near the affected areas
  • New research illuminates the reactivation

    Dr. Anna Cliffe from the UVA department for microbiology, immunology and cancer biology explains how the virus reactivates. She said: “Our results identify the first viral protein that is required for the herpes simplex virus to wake up from the break, and surprisingly, this protein does this by triggering answers that should work against the virus. This is important because we may have new opportunities to prevent the virus from waking up and activity in the nervous system that could have negative consequences in the long term. “

    How the virus kidnaps the immune system

    The study focused on a viral protein called Ul12.5. The researchers found that this protein acts as a “double agent”. Instead of simply hiding from the immune system like most viruses, the herpes virus actually activates the body's antiviral alarm. Then manipulates this alarm to reactivate yourself in the body.

    Traditionally, it is known that viruses withdraw or suppress immune responses to survive. However, this study suggests that HSV-1 uses something different Tut-Sie to recognize stress in the body. If it captures cellular damage, infections or other threats, it takes a keyword to reactivate new hosts and spread to new hosts.

    The researcher Patryk Krakowiak said to Student finds: “We were surprised to provide HSV-1 not only passively waiting for the right conditions, but also actively and take control of the process. Our results suggest that the virus can be used in order to use cellular stress – be it from neuron damage, infections or other threats – as a hint to escape its host and find a new one. “

    This groundbreaking research emphasizes what scientists knew beforehand about how viruses and the immune system interact. Understanding how HSV-1 reactivates could open new doors for treatment. If researchers can find paths to block the viral protein Ul12.5, they may be able to prevent the reactivation of herpes – reduce the outbreaks and the transmission.

    While scientists continue to examine the herpes virus, this discovery could pave the way for better treatments and possibly a vaccine in the future.

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