In the study, a team of neuroscientists from the Federal University of Rio de Janeiro in Brazil, infected three-day-old infant mice with the Zika virus and monitored their behavioural and neurological development until adulthood to observe several early and late symptoms.
They found that most of the infected mice developed spontaneous seizures as soon as nine days after birth, and remained more susceptible to chemically-induced seizures in adulthood compared to controls.
This indicates that even though the spontaneous seizures may have been resolved as the animals grew older, the damage caused to the brain is permanent, the researchers said, in a paper published in the journal Science Translational Medicine.
Furthermore, the infected mice demonstrated weight loss that is not recovered in adulthood, cognitive deficits and long-lasting impaired motor function.
The memory and sociability of adult mice were also affected, which may be linked to research that viral exposure shortly before or after birth may be associated to late development of autism and schizophrenia.
These behavioural deficits were also accompanied by persistent viral replication and inflammation in the brain.
The peak of viral replication in the brain was found to be associated with an abundance of molecules that mediate inflammation.
One of these molecules is the Tumor Necrosis Factor Alfa, or simply TNF-a, a molecule closely linked to episodes of acute inflammation in the body.
When administered, infliximab -- a drug that inhibits TNF-a -- prevented seizures in young infected mice by Day 12, suggesting that targeting cerebral inflammation could ameliorate some of the long-term consequences of neonatal Zika infection, the researchers said.
"Young mice responded very well to the TNF-a inhibitor. We found that some animals had a 50 per cent reduction in the number of seizures, on average. Also, adult animals were no longer susceptible to drug-induced seizures," said Julia Clarke from the varsity.
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