Purpose of review: Zika virus (ZIKV) was not initially thought to be an important cause of neurologic disease, but with the recent epidemic in the Western Hemisphere, there is a growing body of evidence for possible neurologic complications. This review discusses these in addition to what is known about modes of transmission, testing for the virus, as well as future directions. Recent findings: ZIKV disease has been associated with microcephaly and congenital eye disease in infants, as well as with Guillain-Barré syndrome, uveitis, myelitis, and meningoencephalitis in adults. Summary: Even though most infections are asymptomatic, there are important possible neurologic complications of ZIKV disease in both children and adults of which neurologists should be aware.Neurol Clin Pract 2016;6:515-522 Z ika virus (ZIKV) is an RNA virus of the family Flaviviridae in the genus Flavivirus. It received its name from the Zika Forest in Uganda. In 1947, researchers placed sentinel monkeys on elevated forest platforms to study the natural transmission of yellow fever virus. ZIKV was first isolated from one of these monkeys and subsequently from a pool of Zika Forest-dwelling Aedes africanus mosquitoes. 1,2 ZIKV was first studied in animals, and was shown to be neurotropic after serial brain passage in mice.3 Interestingly, injection of ZIKV into other animals, including cotton rats, guinea pigs, and rabbits, did not cause disease.3 Monkeys were shown to develop asymptomatic infection after subcutaneous inoculation with the mouse brain-passaged virus, but even after intracerebral inoculation, only 1 of 5 monkeys developed fever, and none more extensive illness.
3There was early suggestion that ZIKV could infect humans as serosurveys in Africa showed that 6% of 99 sera samples were positive for ZIKV-specific neutralizing antibodies.3 However, ZIKV was not considered to be an important cause of human disease, as only 14 cases of symptomatic human ZIKV infection were documented between 1947 and 2006. [4][5][6][7][8]