Study: Connection between herpes simplex and neurodegeneration

A new study suggests that a protein in cells limits the spread of herpes simplex. The results also suggest a direct connection betweenneurodegenerative diseasessuch as Alzheimer's disease, amyotrophic lateral sclerosis, glaucoma and the herpes virus. The study authors wanted to find out why HSV-1 can be fatal in immunocompromised people but not in healthy people.

What connects herpes simplex with neurodegenerative diseases

Herpes viruses naturally infect the central nervous system and can lead to degenerative brain and eye diseases and encephalitis. However, in most people, the virus is suppressed during a primary infection before it can cause significant damage to the central nervous system. The protein called Optineurin, or OPTN, stops the virus from growing through autophagy. This is the engulfing of the virus particles into tiny vesicles known as autophagosomes. However, the autophagy that takes place is very selective, which accordingly also affects other viruses. The researchers believe that the results of this study will apply to all eight different human herpes viruses. Virus growth was much higher in the brains of laboratory mice without OPTN, killing local neurons, leading to neurodegeneration. This shows that there is faster degeneration of neurons when this protein is not present.

The study results also showed that a lack of OPTN leads to an impairment of the immune response. Some of these problems could include neurodegenerative diseases, which researchers believe further research could reveal. Because herpes simplex remains in neurons, scientists suspect it is linked to neurodegenerative diseases such as Alzheimer's. The immune system also requires inflammation to constantly fight off the virus. Such a continuous immune response can accordingly damage neurons to a certain extent.This studyalso showed that animals without OPTN and infected with HSV-1 lost the ability to recognize objects after 30 days. This could indicate that HSV-1, together with a mutation of OPTN, could accelerate neuronal damage, leading to cognitive impairment.