University of Nebraska-Lincoln researchers have recently discovered a mutation in the Zika virus that helps explain the severity of the virus’ outbreak in 2015-16.
Asit Pattnaik, a professor in the School of Veterinary Medicine and Biomedical Sciences, three graduate students in the school and other researchers conducted research on a mutation which results an addition of glycans, or sugars, to one of the viral proteins. Their research started around May 2016.
Pattnaik said the glycan mutation was discovered through comparison of nucleic acid sequences in the original Zika virus isolated in Africa and the virus isolated in the United States and Asia. A majority of the African viruses did not have the sequence that adds sugars onto the envelope protein of the virus, but all of the viruses from America contained sugars on the protein.
Thomas M. Petro, oral biology professor at the University of Nebraska Medical Center, was one of the authors of the study conducted by Pattnaik’s team. For the past 15 years, he has been studying two other viruses that infect the brain.
“In both of those cases, we found that when the virus invades the brain, the immune response to the virus is powerful enough that there are neurological complications, mainly due to the immune response to the virus,” Petro said.
Petro said it came as no surprise to him that there would be development of neurological problems since the Zika virus is able to reach the brain.
Bikash Sahoo, a graduate student in integrative biomedical sciences, was one of the students who worked on the study. He said there are similarities and differences between the viruses with and without the sugars in them.
“In adults, the parental virus has been shown to be associated with Guillain-Barré syndrome,” Sahoo said. “In most cases the infection is asymptomatic, although mild fever, rash or conjunctivitis can be seen in some cases.”
Sahoo said another difference is that the original virus infects the brain cells of fetuses, causing brain cells to die, resulting in a condition known as microcephaly. This birth defect causes the fetus to be born with a reduced brain size. The mutated virus with the sugar envelope is not able to reach the brain as easily as the original.
According to Pattnaik, the original Zika virus presumably did not contain the recently discovered mutation. The glycan mutation is thought to have developed during several passes of the Zika virus in mosquitoes, laboratories or both.
As a continuation of the study, the team will be studying other mutations to generate a less pathogenic virus and hopefully create potential viral vaccines. This new discovery may also help prevent neuroinvasion of the Zika virus, even in those with persistent infection of the virus.