Zika virus: neurologic complications

Kelsey Peters (Ms. Peters of Indiana University School of Medicine has no relevant financial relationships to disclose.)
Karen L Roos MD FAAN (Dr. Roos of Indiana University School of Medicine has no relevant financial relationships to disclose.)
Originally released September 11, 2016; expires September 11, 2019

Overview

First discovered in 1947, Zika virus is a single-stranded RNA, mosquito-borne flavivirus that is closely related to dengue, West Nile, and yellow fever viruses. Initially, few documented cases of human Zika infection occurred, and the virus was contained within Africa and Asia. Infection was thought to be largely asymptomatic or cause no more than a mild febrile illness. Common clinical manifestations of Zika infection include maculopapular rash, conjunctivitis, arthralgia, frontal headache, malaise, and fever. Within the past decade, Zika has expanded globally to the Western Pacific and South and Central America. The first documented case of autochthonous transmission in the Americas occurred on May 7, 2015, in Northeast Brazil. Since then, researchers have noticed a rise in both the incidence of Guillain-Barre syndrome in adults and microcephaly, cerebral calcifications, and ventriculomegaly in infants born to mothers infected during pregnancy. The association between Zika infection and these severe neurologic sequelae contradict what was once believed to be a relatively benign virus and is the focus of this article.

Key points

 

• Zika virus is a mosquito-borne flavivirus that is asymptomatic in 80% of those infected and, when symptomatic, generally results in a mild febrile illness.

 

• Studies have shown that the virus is highly neurotropic in both mice and in vitro cell studies with human embryonic cortical neural progenitor cells.

 

• The incidence of microcephaly is 20 times higher in Brazil than in years past since the epidemic began in 2015.

 

• The incidence of Guillain-Barre has also been linked to antecedent Zika infection in French Polynesia during the 2013–2014 outbreak and now in Brazil.

Historical note and terminology

In 1947, researchers studying yellow fever in Uganda isolated a new virus from the blood of a caged rhesus macaque. They named this virus Zika, after the forest in which it was discovered (Dick et al 1952). Before the first major outbreak in 2007 in Yap State, Micronesia, only 14 cases of human infection had been documented in the literature (Lanciotti et al 2008; Duffy et al 2009; Hayes 2009). The virus then spread to French Polynesia in 2013–2014, where approximately 10% of the population was symptomatic (Zanluca and Dos Santos 2016). The virus arrived in Brazil in March 2015 and has since spread to approximately 33 additional countries (Zanluca et al 2015; Petersen et al 2016). Association of Zika infection with Guillain-Barre syndrome first occurred during the 2013–2014 outbreak in French Polynesia, whereas the first association of the virus with microcephaly occurred during the 2015 outbreak in Brazil (Broutet et al 2016).

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