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Researchers have found evidence of a possible link between herpes simplex and neurogenic disorders-ScienceDaily




A new study by researchers at the University of Illinois at Chicago suggests that the presence of the protein optineurin (OPTN) in cells limits the spread of herpes simplex virus type 1 HSV-1.

Dr. Deepak Shukla of Marion H. Schenck, in his “first of its kind” study, has potential among neurodegenerative diseases such as Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), glaucoma, and herpesvirus. He said he also found a direct relationship. Esq. Professor of Ophthalmology for the Study of Presbyopia, and Vice-Chair for the Study of UIC.

A research treatise led by Shukla, “OPTN is a host-specific limiting factor for neuroinvasive HSV-1 infection,” was recently published in the journal. Nature Communications.

Researchers have sought to find out why HSV-1 can be fatal to immunocompromised people, but not to healthy people. The herpes virus naturally infects the central nervous system and can cause degenerative diseases of the brain and eyes, and encephalitis. However, in most cases, the virus is suppressed during a primary infection before it causes serious damage to the central nervous system.

New studies suggest why HSV-1 is suppressed: the conserved autophagy receptor OPTN selectively targets the HSV-1 protein for autophagy degradation, the study said. Co-author Tejabhiram Yadavalli, a visiting researcher in the Department of Ophthalmology and Vision at UIC, explained Science.

“OPTN blocks the growth of the virus and autophagy blocks the virus particles. It involves the virus particles in small vesicles called autophagosomes. The autophagy that occurs is very selective. This is another Viruses also make sense, “says Shukla.

Researchers believe that the results of this study apply to all eight different human herpesviruses.

In this study, mice depleted of the OPTN gene were infected with HSV-1 in the eye. Viral proliferation was much higher in the brains of animals without OPTN, killing local neurons and eventually leading to animal death. This indicates that neurons degenerate faster in the absence of OPTN. Additional studies are planned to investigate naturally occurring mutations in OPTN, such as those reported in glaucoma and ALS patients, and how they affect neuronal health and HSV-1 infection. Shukla explained.

“There are recipes that can cause disasters in terms of neurodegeneration when mutating OPTN and herpes,” says Shukla.

“This study also shows that a lack of OPTN impairs the immune response. OPTN is needed to signal the proper influx of immune cells to the site of infection. Without it, problems arise. “Chandrashekhar Patil, a co-author of the study and a visiting researcher in the Department of Ophthalmology and Visual Science at UIC, said.

Some of those problems may involve neurodegenerative diseases, and researchers believe that further research may indicate.

“Other viruses such as Epstein-Barr, Kaposi’s sarcoma, and varicella-zoster share a homologous protein, so I think there is data to show that they all share this mechanism,” Shukra said.

Herpesviruses are permanently present in neurons and are speculated to be associated with neurodegenerative diseases. According to Dr. Tibor Valyi-Nagy, director of neuropathology at UIC and professor of pathology, a collaborator in the study, the immune system constantly needs inflammation to fight the virus, and neurons need this continuity. Has some damage due to a strong immune response.

The study also showed that animals infected with HSV-1 after 30 days without OPTN lost their ability to recognize objects. Shukla said this may indicate that having HSV-1 with mutations in OPTN may accelerate neuronal damage that leads to cognitive impairment.

“Part of our translational research is how we can fix OPTN problems so that they don’t have neurodegenerative problems,” says Shukla.

Additional authors are Joshua Ames, Rahul Suryawanshi, James Hopkins, Alexander Agelidis, Chandrashekhar Patil, Brian Fredericks, All UIC, and Henry Tseng of the Duke University Medical Center.

This study includes grants from the National Institutes of Health and the National Eye Institute (K08-EY021520-02, RO1 EY029426, P30 EY001792, and RO1 EY024710) and unlimited Research to Prevent Blindness at the Butner Pioneer Award, Duke Health Scholars, and Research to Prevent Blindness. Supported by funding.





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