Normally, the measles virus only infects immune and epithelial cells, leaving cells of the nervous system alone. But measles can also lead to a neurological disorder called subacute sclerosing panencephalitis, or SSPE. This complication of measles infections is rare, but it can happen years after the acute phase is over, and can be fatal. Researchers have now learned how the virus gains the ability to disrupt the nervous system.
This study, reported in Science Advances, has shown that the measles virus may persist in the body, and acquire mutations over time. If mutations happen in one particular viral protein, it can affect how the virus infects cells. Mutant and normal forms of the measles virus can then interact, and enable the virus to infect the brain.
Measles is caused by one of the most contagious viruses ever to have affected humans. While vaccinations have dramatically reduced the incidence of measles infections, the virus is experiencing a resurgence. The COVID-19 pandemic caused a major disruption to the distribution and use of typical vaccines, like the one many kids receive for measles. Vaccine hesitancy is also a growing public health problem in some countries including the United States, and people are starting to get measles more often, though the US once came close to eradicating the disease.
"Despite its availability, the recent COVID-19 pandemic has set back vaccinations, especially in the global South," noted corresponding study author Yuta Shirogane, an assistant professor at Kyushu University.
The measles virus is encased by a lipid bilayer, which carries a receptor that binds to the hemagglutinin (H) protein and fusion (F) proteins. The H protein binds to a target cell receptor, then the conformation of the F protein changes, which fuses the membranes of the virus and target cell to cause infection.
Previous work by this team has shown that mutations in the F protein lead to a "hyperfusongenic" state that allows it to infect the brain. After assessing mutations in measles virus samples that were isolated from SSPE patients, the researchers identified various mutations affecting the F protein. Some mutations increased infection activity while others decreased it.
"It is almost counter to the 'survival of the fittest' model for viral propagation. In fact, this phenomenon where mutations interfere and/or cooperate with each other is called 'Sociovirology.' It's still a new concept, but viruses have been observed to interact with each other like a group. It's an exciting prospect," noted Shirogane.
The researchers are hopeful that these findings will open up new treatment options for SSPE patients, and help us learn more about other viruses.
Sources: Kyushu University, Science Advances