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    Home > Active Ingredient News > Immunology News > Does a virus infecting the nasal cavity "climb" into the brain? Science sub-paper uncovers the mechanism of protection of the olfactory system.

    Does a virus infecting the nasal cavity "climb" into the brain? Science sub-paper uncovers the mechanism of protection of the olfactory system.

    • Last Update: 2020-07-18
    • Source: Internet
    • Author: User
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    When the nose is infected by the virus, nervous system cells act as "mediators" to stimulate the immune system response.infected olfactory neurons can "pass" the virus to microglia, and then T cells can detect the virus infection and remove the virus in a way that does not kill neurons.photo source: pixabay source NIH / NINDS translation page Stroke, NINDS) researchers have found a special front-line defense that limits infection to the olfactory bulb and protects neurons in the olfactory bulb from damage caused by infection.neurons in the nose respond to inhaled odors and send this information to the olfactory bulb area of the brain.the location of nasal neurons and exposure to the external environment make them easy targets for air borne virus infection. However, viral respiratory tract infections rarely spread from olfactory bulb to other parts of the brain, causing potentially fatal encephalitis. The study was published in the journal Science immunology.a team led by Dr. Dorian mcgavern, a senior researcher at NINDS, used a special virus that can be traced with a fluorescence microscope, and found that the virus infection on the nose was blocked before it spread from the olfactory bulb to the central nervous system.Dr mcgavern said: "airborne viruses have always challenged our immune system, but we rarely see (this type of) viral infection leading to neurological diseases.this means that the immune system in this region must be very good at protecting the brain. The additional experiments showed that microglia, the immune cells in the central nervous system, play an important role in helping the immune system to recognize viruses, and to some extent limit the damage of viruses to neurons.this protection of neurons is crucial because, unlike cells in most other tissues, most types of neurons do not regenerate.because of this, the central nervous system has evolved a variety of defense mechanisms to prevent the invasion of pathogens.however, when airborne viruses are inhaled, they cross the nasal passages and interact with the olfactory epithelial tissue responsible for our sense of smell.the axonal projections of neurons on the edge of the olfactory system are distributed on the bones in the nasal cavity and enter the brain to expose the brain to the smell in the air.similarly, neurons in olfactory epithelial cells provide a simple way for viruses to bypass the traditional central nervous system disorders, that is, a direct pathway to the brain.Dr mcgavern said: "if the virus infects neurons in the nasal airway, the virus may enter the brain and eventually lead to encephalitis or meningitis.and we wanted to understand the immune response that evolved at the junction of the olfactory neurons (which terminate in the olfactory bulb) and other parts of the brain."Dr. mcgavern's team has demonstrated that CD8 T cells are important in protecting the brain after nasal tissue infection.CD8 T cells are part of the immune system responsible for fighting the virus. using advanced microscopes, his team observed in real time how CD8 T cells protect the brain from rhinovirus infection. interestingly, CD8 T cells do not seem to interact directly with the major types of infected neurons, but with microglia. microglia are immune cells of the central nervous system. Their functions are somewhat like garbage trucks. Their duties include removing cell debris and dead cell materials. when viral infection occurs, microglia seem to absorb viral substances from their surroundings and present them to the immune system as if they were infected themselves. in this way, infected olfactory neurons can "deliver" viral particles to microglia and then be detected by T cells. the T cells then respond by releasing antiviral molecules that remove the virus from neurons in a way that does not kill the cells. because microglia are a renewable cell type, this interaction is reasonable from an evolutionary point of view. Dr mcgavern said: "the immune system has developed strategies to protect neurons at all costs. in this study, we demonstrated that microglia can withstand the attack of the virus on neurons by contacting T cells, and then make the human antiviral program work. "due to the current new epidemic situation, respiratory tract virus infection has received great attention. Dr mcgavern pointed out that although the new coronavirus was not studied in these experiments, some symptoms produced by it suggest that the mechanism described in this study may be at work. "an interesting symptom of infection with the new coronavirus is that many people lose their sense of smell and taste. this indicates that the virus is not only a respiratory pathogen, but also may target olfactory neurons or destroy olfactory neurons. "it is worth noting that either the new coronavirus, the virus used in this study, or any other similar virus infecting olfactory neurons in large areas may destroy our sense of smell. however, unlike other neurons in the central nervous system, these sensory neurons from the nose to the end of the brain can regenerate after the infection is cleared. Dr mcgavern explained: "the immune response we described does not protect olfactory neurons or olfactory neurons. but this does not necessarily cause long-term problems, because once the virus is eliminated, these damaged olfactory neurons will be replaced. protecting the brain and central nervous system from encephalitis or meningitis is the most important thing, and our sense of smell is usually restored over time. "Dr. mcgavern continued that, given the importance of microglia in stimulating antiviral responses, factors leading to their failure or loss of function may increase the possibility of infection in the central nervous system. source link:
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