The year was 1947. Scientists had isolated a virus from a pyrexial rhesus monkey in Uganda and named it after the forest where the monkey lived — Zika.
Then, a little more than a year ago, in the fall of 2015, health officials in Brazil reported a sharp increase in the number of cases of exceptionally small brains (microcephaly) in human newborns. These cases were connected to infections with the Zika virus.
So what happened during that 70-year gap, and why did most of us feel so blindsided by Zika?
Several reasons can help account for those years, including recent findings by Dr. Daniel Janies and a team of researchers from the Department of Bioinformatics and Genomics at UNC Charlotte, Atheric Pharmaceutical, and ioGenetics, to be published in an upcoming issue of the journal Cladistics.
After the 1947 discovery of Zika in Africa, the virus moved through that country and beyond. In 1948, the Zika virus was found in the Aedes africanus mosquito from the Zika forest. Then, in 1952, the first human cases of Zika were detected in Uganda and the United Republic of Tanzania, confirming Zika could be transmitted to humans. The disease in humans was reported to be mild.
From the 1960s to the 1980s, the virus spread beyond East Africa, moving on to western Africa and equatorial Asia, where the Zika virus was detected in mosquitos in India, Indonesia, Malaysia, and Pakistan.
The year 2007 marked a turning point in Zika's history when the first large Zika outbreak in humans was reported. It occurred in the Pacific island of Yap in the Federated States of Micronesia. Until this outbreak, only 14 cases of Zika had been documented in humans. Now, it is estimated that 73% of Yap's 11,250 residents over three years old were infected with Zika virus.
Neurological complications were reported in 58 cases of Zika infections in Brazil on July 9, 2015. Twenty-nine of those were confirmed as Guillain-Barré Syndrome, a disorder in which the body's immune system attacks part of the nervous system. The first symptoms of this syndrome are tingling sensations in the legs, but the disease can have life-threatening effects on breathing, blood pressure, and heart rate.
In rapid succession, the infection was found in more and more countries worldwide, and its movement was tracked in days, instead of years.
On July 29, 2016, the Zika virus hit the United States. Four cases of mosquito-borne Zika virus disease were confirmed in Florida. The people infected had not traveled outside the U.S., strongly pointing to the presence of the Zika-carrying mosquito was active in Florida.
Twenty-six newborns with microcephaly were reported on October 23, 2015, at different public and private hospitals in Brazil. Microcephaly is defined by the World Health Organization (WHO) as a head circumference below the 5th percentile.
On September 15, 2016, a research paper published in the journal The Lancet showed a strong association between microcephaly and laboratory confirmation of Zika virus infection during pregnancy. When it became clear that Zika could be transmitted from mother to child and cause severe congenital disabilities, the concern for Zika infections elevated to a state of alarm.
What happened between the mild Zika illnesses of the mid-1900s and the thousands of horrific effects of the virus we've witnessed since 2015?
Scientists know that single-stranded RNA viruses like Zika can change over time. Could viral evolution have increased the new potency of Zika infections?
Janies and colleagues used sophisticated genetic analyses to evaluate the ancestral relationships between Zika viruses collected at different places at different times. They hoped to figure out why, when, and how Zika may have gained strength as an infectious agent.
The researchers found some new mutations in the virus as it traveled from island to island across the Pacific. These mutations correlated with the appearance of Guillain-Barré Syndrome and microcephaly in French Polynesia.
Two main key mutations were found in the different viruses; One was in the part of the viral genome that codes the virus's envelope protein, and the other for the ends of the viral genome that are called "untranslated regions."
Mutations in the viral envelope protein caused it to make proteins similar to human proteins. These mutations would make the virus appear less foreign to human cells and trick the cells into allowing them to infect the cell in a move called "epitope mimicry."
As if escaping detection wasn't enough, in a press release from the University of North Carolina at Charlotte, Janies said, "Our team members found that two of the human proteins that Zika is mimicking are involved in the signaling that goes on when the sensory organs are being formed in the fetus."
Specific binding regions on untranslated parts of the Zika viral genome, called "Musashi binding elements," help the virus decide which tissues to invade and infect.
The researchers found that Zika has mutated to be better at binding to human Musashi proteins. These Musashi proteins are present in stem cells, and the study authors said more studies are required to determine if they, too, might be involved in the fetal brain defects seen in Zika infections.
At least for now, the U.S. is not predicted to experience a large outbreak. However, some southern states may experience hot spots where increased numbers of Zika infections occur.
How strong the infections will be remains to be seen. The Zika epidemic is one nasty example of how quickly an innate virus can evolve out of control — with dangerous implications to public health.
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