Zika infection caused an epidemic in Brazil beginning in 2015 and has since been reported in most Latin American and Caribbean countries as well as some southern U.S. states and Puerto Rico. In a review and separate analysis, two research groups present updates and gaps in our knowledge of Zika-related microcephaly.
While most Zika infections occur via Aedes mosquitoes (globally prevalent in tropical and subtropical areas, putting as many as 3.6 billion individuals at risk), sexual transmission has been documented, and the virus can persist in semen for several months. Transmission can also occur through blood transfusions.
Most cases of Zika infection are asymptomatic or present as a self-limited febrile illness, often accompanied by rash, conjunctivitis, and malaise. In pregnant women the virus can infect the fetus, targeting neuronal progenitor cells and causing subsequent brain malformations, most commonly microcephaly and calcifications.
Zika infection caused an epidemic in Brazil beginning in 2015
However, the spectrum of the disease appears wide, and some infants who appear healthy at birth may exhibit developmental delay or other neurological complications. Diagnosis of Zika infection is complicated by cross reactivity with antibodies to related viruses (dengue and chikungunya) that share the same geographic distribution.
Among the many things we still don’t understand about Zika infection is the geographic and temporal variability in risk for microcephaly seen across the Brazilian epidemic. Surveillance from 2015 through 2016 identified >41,000 cases of infection in pregnant women and 1950 confirmed cases of infection-related microcephaly in their offspring.
However, the risk for microcephaly was 50 per 10,000 live births during the 2015 epidemic but only 3 to 15 per 10,000 live births in 2016. In addition, notable geographic variation yielded the highest rate of microcephaly cases in the northeast region of Brazil.
