OPTN protein has been found to limit the spread of herpes simplex virus type 1, new research shows
Don't store avocado like this: it's dangerousOPTN protein has been found to limit the spread of herpes simplex virus type 1, new research shows
What do herpes simplex and dementia have in common? Apparently nothing, but new research has found a correlation between the two diseases, as a consequence of the same cause.
The researchers in the new study, however conducted only on animal models at the moment, found that the mutations of the OPTN gene caused an increase in the growth of type 1 herpes, but also the death of local neurons. This resulted in accelerated neurodegeneration. OPTN deficiency has also been associated with impairments in the immune response.
Although these findings are specific to the HSV-1 virus, the researchers believe the findings may apply to up to eight herpes virus infections.
A systematic review
A new study conducted by researchers at the University of Illinois, Chicago, suggests that when the protein optineurin, or OPTN, is present in cells, it limits the spread of HSV-1, the type 1 herpes simplex virus.
In a first-of-its-kind study, researchers also discovered a potential direct connection between neurodegenerative diseases, as the Alzheimer's disease, amyotrophic lateral sclerosis (ALS), glaucoma and the herpes virus.
The team sought to find out why HSV-1 can become fatal for immunocompromised individuals, but not for healthy individuals. Herpes viruses naturally infect the central nervous system and can provoke degenerative disorders of the brain and eyes, as well as encephalitis. However, in most individuals, the virus is suppressed during a primary infection before it can significantly damage the central nervous system.
New research suggests why HSV-1 is suppressed: OPTN, a conserved autophagic receptor, selectively targets HSV-1 proteins for degradation by autophagy. Then, the protein stops the virus from growing and stops it by autophagy by engulfing the virus particles inside tiny vesicles called autophagosomes. The researchers believe the results of this study will apply to all eight different strains of the herpesvirus.
The results
In the study it was found that the growth of the virus was much higher in the brains of animals without OPTN, where local neurons were also compromised, showing a faster degeneration of neurons when OPTN is not present.
Further studies are planned to examine natural mutations in OPTN, such as those reported in patients with glaucoma and ALS, and how they can affect neuronal health and HSV-1 infection. The study also shows that there is an impairment of the immune response when there is a deficiency of OPTN.
According to the research team they may have more data to show that other viruses, like Epstein-Barr virus, Kaposi's sarcoma, chickenpox-zoster, they all share this mechanism as they share homologous proteins.
Hence, since herpesvirus is found in neurons, it is hypothesized that it is linked to neurodegenerative diseases; the immune system requires inflammation to constantly fight the virus, and neurons have some degree of damage due to this ongoing immune response.
The study also showed that subjects without OPTN and infected with HSV-1 lost the ability to recognize objects after 30 days, and this could be an indication of how HSV-1 along with an OPTN mutation could accelerate neuronal damage, which would result in cognitive impairment.
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Photos: Nature
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