Summary: A new study shows that herpes simplex virus-1 (HSV-1), which is generally known for the cause of fever bubbles, can travel directly to the brain through the nasal cavity and causes severe and permanent neurological symptoms. In animal experiments, the nose HSV 1 infection led to continuing neurological dysfunction, including anxiety and cognitive impairments.
The researchers identified heparanase, a cellular enzyme, as a critical factor to enable HSV-1 to cause severe, permanent neurological damage. Blocking the activity of this enzyme significantly reduced neurological damage to infected animals and shows a possible therapeutic goal.
Key facts:
- Neurological effects: Intranasal HSV-1 infections lead to permanent neurological and cognitive impairments.
- Role of the heparanase: This enzyme facilitates HSV-1-induced brain damage; Block it reduces the neurological consequences.
- Global prevalence: About two thirds of the world's population carry HSV-1 and emphasize the potential far-reaching effects of these results.
Source: University of Illinois
Herpes-Simplex-Virus-1 (HSV-1) is generally known for causing bubbles and wounds. In some cases, however, the virus can hike or to the nervous system, which leads to severe chronic symptoms.
A study by the researchers of the University of Illinois Chicago now determines that herpes infection through the nose can lead to anxiety, motor impairments and cognitive problems. Research is the first to show that the virus can cause behavioral symptoms by using a cellular enzyme. The finding emphasizes the need for prevention and treatment of a virus that is borne by billions of people worldwide.
Research, published in mbiois the latest of the College of Medicine group under the direction of Deepak Shucla, Marion H. Schenk Esq. Professor of ophthalmology for researching the aging eye and the UIC professor of microbiology and immunology.
Shucla's laboratory previously examined how the virus spreads to the eye and brain and can lead to blindness, encephalitis and other diseases. The new research examined the intranasal infection, in which virus particles enter the body through the nose and have more direct access to the nervous system.
“If an infected individual gives the virus over tears, it could reach the nasal cavity in which it could go to the brain more directly,” said Shucla. “I think it is under diagnosed and understandable, but the neurological consequences, as we believe, are much more difficult than they would normally see in fever bubbles or eye infections.”
In animal experiments, the researchers observed high inflammation and neural damage just a few days after the HSV 1 infection. A few months later speaking, the life of man in human, the infected animals, in tests of motor coordination and memory, performed worse and showed more fear-like behavior compared to controls.
“There are definitely nerve damage if you take the intranasal path and the effects are long -term, which is alarming,” said Shucla.
The researchers also examined heparanase, a cellular enzyme that previously examined the group for their role in reinfection of HSV-1 and long-term effects. After infections, animals with a deactivated gene for heparanase did not show the same neuro -Shavioral deficits as checking animals. This suggests that the enzyme conveys some of the harmful effects of the virus in the brain.
“These findings open the door to potential therapeutic approaches to mitigate the effects of neuroinflammation and prevent long-term brain injury caused by viral infections,” said Hemant Borase, a UIC postdoctoral researcher and first author of the study.
Herpes simplex virus-1 is extremely common. The World Health Organization estimates that almost two thirds of the world's population carry the virus.
“The virus reactivates all lives; It is a lifelong infection, ”said Chandrashekhar Patil, professor of scientific assistant to the College of Medicine and co-author of the newspaper. “So I think that this awareness will be really important among the large population that bears this virus.”
Tibor Valyi-Nagy, professor of pathology, is also the co-author of the paper.
Financing: The study was financed by grants from the National Institute of Health.
About this neurology research messages
Author: Brian flood
Source: University of Illinois
Contact: Brian Flood University of Illinois
Picture: The picture is attributed to neuroscience
Original research: Open Access.
“HPSE-mediated pro-inflammatory signal transmission contributes to neuroboral deficits after intranasal HSV 1 infection at” by Deepak Shuckla et al. mbio
Abstract
HPSE-mediated pro-inflammatory signal transmission contributes to neuro-Shavioral deficits after intranasal HSV-1 infection
The herpes simplex virus-1 (HSV-1) is a neurotropic virus that can infect the brain, and uncontrolled infection can lead to a number of diseases, including chronic nerve pain, encephalitis and neuro-havarian anomalies.
These results are often serious and have permanent consequences, which emphasizes the need to identify host factors that contribute to the severity of the disease.
In this study, we report that the intranasal HSV-1 infection in the mouse model, which promotes the viral distribution into the brain, implies the economic paranase (HPSE) as a key mediator for neuroinflammation.
In particular, we observed that HPSE activity during HSV-1 infection in naive animals promotes the high regulation of pro-inflammatory cytokines, improving microglia activity in the brain and contributing to deficits of cognitive impairments, anxiety and motor coordination.
Such effects are significantly less detectable in the case of Heparanase deficiency (HPSE -//-) mice. In addition, we found that moderate activation of great-like receptors (TLRS), especially in HPSE+/+ Mice can contribute to activating the inflammasom path.
This in turn leads to the activation of Caspase-1 (Casp1) and Caspase-3 (Casp3) that can play a role in the loss of nerve function.
Our results position HPSE as a potential therapeutic goal to reduce virus induced neuroinflammation and neuroboric defects.
