Mouse study suggests one genetic mutation in 2013 unleashed its ability to attack developing fetal brains
By Dennis Thompson
THURSDAY, Sept. 28, 2017 (HealthDay News) -- A single genetic mutation just a few years back gave the Zika virus the ability to cause severe neurological birth defects like microcephaly, a new study in mice suggests.
Scientists have known about the Zika virus since 1947, when it was discovered in a monkey from the Zika Forest in Uganda. At that point, it was only linked to mild symptoms.
It wasn't until the Zika epidemic of 2015 in Central and South America that Zika became known as a cause of microcephaly, a devastating condition in which a newborn's brain and skull are severely underdeveloped.
How did that happen?
One particular genetic change, which likely occurred in 2013, boosted Zika's ability to damage the neural stem cells that serve as building blocks for a fetus' developing brain, Chinese researchers report.
"The evidence suggests this particular mutation somehow increased the ability of the virus to get into these neural progenitor cells," said Dr. Joseph McCormick, regional dean at the University of Texas School of Public Health in Brownsville. McCormick wasn't involved in the new study.
This discovery is disturbing because it suggests that the virus could have more unwelcome surprises in store for humanity, said Michael Osterholm, director of the University of Minnesota's Center for Infectious Disease Research and Policy.
"The mutation that potentially caused this health outcome in humans is occurring in a virus where additional mutations could still occur, which could bring us other new health challenges," said Osterholm, who had no role in the research.
Zika is transmitted primarily by infected mosquitoes. It can also be spread by having sex with an infected person.
The Chinese team, whose first author is Ling Yuan of the Chinese Academy of Sciences in Beijing, compared three current Zika strains against an older strain isolated in Cambodia in 2010.
The three current strains killed all lab mice exposed to it, producing a series of neurological symptoms. On the other hand, the 2010 strain only killed about 17 percent of mice.
Comparing the strains, researchers found a critical mutation that altered a key protein in the protective coating of newer Zika viruses. This single change greatly enhanced Zika's ability to infect, damage and destroy human precursor brain cells, they said.
An evolutionary analysis revealed that this change likely arose sometime in 2013, just a few months before an explosive outbreak of Zika in French Polynesia. That timing coincides with the first reports linking Zika to microcephaly and Guillain-Barre syndrome, a neural disorder that causes muscle weakness and paralysis in adults.
"They've concluded it looks like the contemporary virus is more virulent than its ancestors," said Dr. Richard Temes, director of the Center for Neurocritical Care at North Shore University Hospital in Manhasset, N.Y. "When patients are infected, it's more likely to lead to neurological disease than the former strains."
Although the analysis "is in many ways a very good explanation of what happened," it needs to be both confirmed and expanded upon, Osterholm said. Research on animals does not always produce the same results in humans.
McCormick agreed. For example, he said, the conclusions leave open the possibility that a genetic trait in some humans might leave them more vulnerable to the threat posed by this Zika mutation.
"Clearly a lot of people got infected with this, and a lot more pregnant women got infected than had microcephalic children," McCormick said. "Is there a human side of this that may make some people with the right genetic background more susceptible to this particular mutation?"
The findings were published Sept. 28 in the journal Science.
For more on Zika, visit the U.S. Centers for Disease Control and Prevention.
SOURCES: Joseph McCormick, M.D., regional dean, University of Texas School of Public Health, Brownsville; Michael Osterholm, Ph.D, MPH, director, Center for Infectious Disease Research and Policy, University of Minnesota; Richard Temes, M.D., director, Center for Neurocritical Care, North Shore University Hospital, Manhasset, N.Y.; Sept. 28, 2017, Science
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