Researchers in Japan have linked the measles virus to subacute sclerosing panencephalitis, or SSPE, a rare but severe neurological condition that can emerge years after a measles infection.
You might have contracted the measles as a child if you are of a specific age. Thanks to vaccinations, many people born after the 1970s have never had it. The disease is brought on by the similar thing virus, which is currently one of the most contagious diseases. According to the World Health Organization, there will be 128,000 measles-related deaths worldwide in 2021, with an expected nine million cases of disease.
Through a number of proteins that protrude from its surface, a virus infects cells. Usually, a surface protein helps a virus connect to a cell before another surface protein initiates a reaction that allows the virus into the cell, causing an infection. As a result, the type of cell can have a significant impact on what a virus can or cannot infect.
A protein known as fusion protein, or F protein, is crucial for the measles virus to infiltrate a cell. Previous research by the ensure performance that certain mutations in the F protein put it in a “hyperfusongenic” state, enabling it to fuse onto neuronal synapses and spread disease all through the brain.
In their most recent investigation, the group examined the measles viral genome from SSPE patients and discovered that a number of mutations had accumulated in the F protein. It is interesting to note that some mutations increased infection activity while others decreased it.
“This was surprising to see, but we found an explanation. When the virus infects a neuron, it infects it through ‘en bloc transmission,’ where multiple copies of the viral genome enter the cell,” continues Shirogane. “In this case, the genome encoding the mutant F protein is transmitted simultaneously with the genome of the normal F protein, and both proteins are likely to coexist in the infected cell.”
In another instance, the scientists discovered that an entirely separate group of F protein mutations causes a decrease in fusion activity.
To their astonishment, this mutation can, in fact, work in conjunction with regular F proteins to boost fusion activity. As a result, even mutant F proteins that don’t seem to be able to infect neurons can nonetheless spread to the brain.
The team hopes that their results will help develop therapeutics for SSPE, as well as elucidate the evolutionary mechanisms common to viruses that have similar infection mechanisms to measles such as novel coronaviruses and herpesviruses.
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