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Prior to 2007, Zika virus (ZIKV) was generally considered an arbovirus of limited importance, causing a mild self-limiting febrile illness in tropical Africa and Southeast Asia. Now, a large, ongoing outbreak of ZIKV that started in Brazil in early 2015 is spreading rapidly across the Americas and has been potentially linked to congenital malformations (including microcephaly) and Guillain–Barré syndrome (GBS). In England, as of 4 February 2016, five adults have been diagnosed with ZIKV infection following travel to countries currently experiencing a ZIKV outbreak.
ZIKV was first isolated from a monkey employed as a sentinel animal in a yellow fever study in the Zika forest, near Entebbe, Uganda, in 1947.1 ZIKV is an RNA arbovirus belonging to the Flaviviridae family, which also includes dengue, Japanese encephalitis and West Nile viruses. The virus is transmitted by female Aedes mosquitoes, especially, Aedes aegypti, which is also an effective vector of dengue and chikungunya virus. Unlike many other mosquito vectors (eg, Anopheles spp. that transmit malaria), Aedes are predominantly day-biting mosquitoes. While the majority of human infections with ZIKV are likely to be acquired via mosquitoes, the virus has been detected in semen2 and blood donors who were asymptomatic at the time of donation,3 raising the possibility of sexual transmission and transmission through blood transfusion, respectively.
Up to 80% of individuals infected with ZIKV remain asymptomatic and the remainder usually develop a mild self-limiting febrile illness lasting 4–7 days associated with maculopapular rash, arthralgia, conjunctivitis, itching, myalgia and headache. The infection is seldom severe enough to warrant hospitalisation and ZIKV-related deaths are very rarely reported and are mostly associated with underlying comorbidities. Most recently, a teenager with sickle cell disease in Colombia died after developing acute respiratory distress syndrome and hepatic necrosis.4 There is no vaccine to prevent ZIKV …
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