How does the measles virus spread in the human brain and cause a fatal disease? How does the measles virus spread in the human brain and cause a fatal disease?

How does the measles virus spread in the human brain and cause a fatal disease?

How does the measles virus spread in the human brain and cause a fatal disease?

Researchers from the Mayo Clinic have mapped how the measles virus mutated and spread in the brain of a person who died of a rare and fatal brain disease.
Researchers say new cases of the disease, a complication of the measles virus, may occur with a resurgence of measles among those who are not immunized.

Using the latest tools in genomic sequencing, researchers have reconstructed how a set of viral genomes colonize the human brain.

The virus acquired distinctive mutations that led to the spread of the virus from the frontal cortex outward.

“Our study provides compelling data showing how viral RNA mutated and spread throughout the human organ, the brain, in this case,” said Roberto Cattaneo, Ph.D., a virologist at the Mayo Clinic and co-lead author of the study. “Our findings will help "In studying and understanding how other viruses persist and adapt to the human brain, causing disease. This knowledge may facilitate the generation of effective antiviral drugs."

Measles is one of the most contagious diseases. The measles virus infects the upper respiratory tract where it uses the trachea, or windpipe, as a springboard (bounce mat) to launch and spread through droplets when an infected person coughs or sneezes.

Dr. Cattaneo pioneered studies on how the measles virus spreads throughout the body. He first began studying the measles virus about 40 years ago, and was fascinated by the rare and fatal brain disease called subacute sclerosing panencephalitis (SSPE), which occurs in approximately 1 in 10,000 measles cases.

It may take five to ten years after the initial infection for the measles virus to mutate and spread throughout the brain.

Symptoms of this progressive neurological disease include memory loss, seizures, and inability to move.

Dr. Cattaneo studied this deadly disease for several years until it almost disappeared as more people were vaccinated against measles.

However, measles is making a comeback due to vaccine hesitancy and missed vaccinations, especially during the COVID-19 pandemic.

“We think the incidence of subacute sclerosing panencephalitis will rise again as well,” says study co-author Iris Youssef of the Mayo Clinic Graduate School of Biomedical Sciences. “This is sad because this terrible disease can be prevented by vaccination.” “But we are now in a position to study the disease using modern genetic sequencing technology and learn more about it.”

Cattaneo and Youssef had a unique research opportunity through a collaboration with the Centers for Disease Control, and they studied the brain of a person who contracted measles as a child and succumbed to subacute sclerosing panencephalitis years later as an adult.

They examined 15 samples from different regions of the brain and performed genetic sequencing in each region to piece together the puzzle of how the measles virus mutates and spreads.

The researchers discovered that after the measles virus entered the brain, its genome (the complete set of the virus's genetic material) began to change in harmful ways.

The genome was duplicated, creating other genomes that were slightly different. Then, these genomes were duplicated again, giving rise to more genomes that were also slightly different. The virus did this several times, creating a range of diverse genomes.

"In this group, two specific genomes had a set of characteristics that worked together to promote the spread of the virus from the initial site of infection - the frontal cortex of the brain - to colonize the entire organ," explains Dr. Cattaneo.

The next steps in this research are to understand how certain mutations favor the spread of the virus in the brain. These studies will be performed on cultured brain cells and in clusters of brain-like cells called organoids, which may help create effective antiviral drugs to combat the spread of the virus in the brain.

“Previously undiscovered” antibodies can target types of influenza!

Scientists said that a class of newly discovered antibodies in human blood can neutralize different types of influenza virus, and could be key to developing preventive vaccines against seasonal viruses.
In a new statement, scientists explained that circulating influenza viruses are constantly mutating, so “we need annual influenza virus vaccines to keep pace with ongoing viral evolution.”

There are four types of influenza viruses, known as influenza A, B, C, and D.

Influenza A comes in several subtypes whose differences lie in two proteins that the virus uses to infect cells: hemagglutinin (H) and neuraminidase (N). For example, H1N1 and H3N2 are subtypes of influenza A that routinely infect people.

Within each subspecies there are different "strains" that are constantly modifying their genetic code. 

Making effective influenza vaccines depends on harnessing the protective power of antibodies - immune proteins that attack invading pathogens - but the virus's ability to mutate quickly makes this difficult.

Flu vaccines prime the immune system to produce specific antibodies that attach to the influenza virus and prevent it from infecting cells after it invades the body. Because these strains mutate year after year, people need a new vaccine every year.

In the new study, published in the journal PLOS Biology, scientists describe a new class of antibodies in human blood samples that target multiple forms of influenza A virus.

The research was conducted only in the laboratory, so scientists are not sure exactly how these antibodies contribute to the body's response to the flu vaccine. However, one day, they could be used to develop vaccines that are more effective in protecting people from multiple strains of influenza at the same time.

Through experiments, the study authors identified antibodies that are abundant in human blood, and which can bind to certain H1 and H3 strains of influenza A, whether a hemagglutinin mutation is present or not. This means that it would theoretically be able to provide broad protection against both virus subtypes, perhaps even as circulating strains mutate over time.

The antibodies reacted with H3 strains from the late 1980s to the late 1990s, and H1 strains from the early 2000s until 2015.

This indicates that the patients whose blood samples were taken developed antibodies in response to the H3 virus strains. After subsequent exposure to H1 strains through infection or vaccination, antibodies are primed to target H1 as well.

These findings may have important applications for future vaccine development.
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