image: Zika infection during pregnancy can lead to birth defects such as microcephaly, and a new study shows it can cause other complications in infant mice such as seizures and motor deficits that persist into adulthood. This material relates to a paper that appeared in the 6 June, issue of <i>Science Translational Medicine</i>, published by AAAS. The paper, by I. Nem de Oliveira Souza at Federal University of Rio de Janeiro in Rio de Janeiro, Brazil; and colleagues was titled, "Acute and chronic neurological consequences of early-life Zika virus infection in mice." view more
Credit: Image by Fernanda Barros-Aragão, based on Nem de Oliveira Souza<i> et al., Sci Transl Med</i>, 2018
Scientists have discovered that Zika virus infection in infant mice results in seizures and long-term deficits in brain structure and behavior that persist into adulthood. Their sobering findings support the idea that Zika virus could markedly alter brain development in infants infected after birth, but reveal that inhibiting a signaling protein may reduce the severity of some brain abnormalities. Research has established that Zika virus infections in pregnant women can seriously harm the developing fetal nervous system, resulting in birth defects such as eye damage and microcephaly - a condition characterized by an abnormally small head. Zika infection in newborn infants could lead to a host of other conditions such as epilepsy that are not as immediately apparent, but direct animal evidence for these changes is still lacking. Seeking further insight, Isis Nem de Oliveira Souza and colleagues investigated the short- and long-term neurological consequences of Zika infection in newborn mice. They infected three-day-old infant mice with the virus and monitored their behavioral and neurological development until adulthood. The authors 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. Furthermore, the infected mice demonstrated reduced motor function and muscle strength during behavioral tests in infancy, and displayed short-term memory impairment in adulthood. These behavioral deficits were also accompanied by persistent viral replication and inflammation in the brain. Finally, administering a drug that inhibits the proinflammatory molecule TNF-α prevented seizures in young infected mice, suggesting that targeting cerebral inflammation could ameliorate some of the long-term consequences of neonatal Zika infection.
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Journal
Science Translational Medicine