Researchers have tracked down some of the genetic mutations in the Zika virus and say they hope they can help explain why the virus seems to all of a sudden started causing birth defects.
Their findings support earlier findings that the strain of the virus now spreading across south and central America and the Caribbean is not exactly the same as the seemingly harmless strain first seen in Africa.
Instead, the Zika virus now causing birth defects and paralyzing disorders in its victims descends from a strain that circulated in Asia before jumping across the Pacific, the team at University of California, Los Angeles, and the Chinese Academy of Medical Sciences & Peking Union Medical College said.
"We believe these changes may, at least partially, explain why the virus has demonstrated the capacity to spread exponentially in the human population in the Americas," said Genhong Cheng, a microbiology professor at UCLA.
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"These changes could enable the virus to replicate more efficiently, invade new tissues that provide protective niches for viral propagation, or evade the immune system, leading to viral persistence.”
The team has not actually shown this. What they have done is document several major changes in some of Zika’s genes that can now be examined to see if they change how the virus spreads and affects people.
"It is unclear why the Zika virus strain that already existed in 1966 in Malaysia did not have a significant clinical impact until 50 years later in Oceania," the UCLA team wrote in their report, published in Cell Host & Microbe.
“It confirms a lot of what we suspected,” said Dr. Peter Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine, who was not involved in the research.
"These changes could enable the virus to replicate more efficiently."
“The Zika virus has undergone significant genetic changes in the past 70 years,” Cheng added.
By tracing its genetic mutations, we aimed to understand how the virus is transmitted from person to person and how it causes different types of disease.”
Brazilian researchers are also documenting genetic changes. It may take months before enough scientists have studied the virus to understand which mutations are the most important.
Related: Zika's Been in Brazil Longer Than Anyone Thought
“There is a lot of similarity between the French Polynesian strain and the strains we are seeing in the Americas," added Hotez, who helped sound some of the first alarms about Zika.
Zika was first seen in Uganda in 1947. It didn’t seem to do much to people. It’s closely related to dengue virus, which can cause a deadly hemorrhagic fever. But Zika seemed not to cause any symptoms in most people, and at worst a rash and fever in those who did notice anything.
An epidemic in the Pacific Islands in 2013 and 2014 looked different. People noticed the symptoms of rash, fever and achiness much more.
“It confirms a lot of what we suspected."
And when Zika hit Brazil last year, people noticed they felt much sicker. Then authorities reported a startling rise in the number of cases of a terrible birth defect called microcephaly, marked by a smaller-than-normal brain and head. Zika’s now been found in the brain tissue of fetuses and babies killed by severe birth defects, and they include a range of damage to the brain.
The U.S. Centers for Disease Control and Prevention says there’s no doubt Zika causes these defects. The World Health Organization says it’s pretty clear Zika also causes paralyzing nerve conditions, including Guillain-Barre syndrome and inflammations of the brain and spinal cord.
Related: Mysteries of the Zika Virus Stump Even the Experts
When researchers look back, they find evidence Zika did this in French Polynesia, also. It’s just more noticeable now because it’s spreading across a huge population, and quickly.
Now, Hotez said, researchers can look at the genetic data – taken from just 41 samples of virus – and see if they can link the mutations with seemingly new effects.
“Which of these mutations is involved in the virus’s ability to infect neural progenitor cells, stop the development of the fetal brain, and whether some of those same mutations could also be responsible for Guillain Barre,” Hotez said.
