Zika virus and neurology: proving cause and effect.

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‘Zika fever’ was first reported in Uganda and Tanzania in 1952. Caused by the Zika flavivirus it consisted of a mild and self-limiting illness of rash, low-grade fever, conjunctivitis, headache and myalgia. Two strains of Zika virus were subsequently identified (African and Asian) with transmission via mosquito or sexual contact. Since 2007 there have been several epidemics of the Asian strain including in French Polynesia (2013–2014; 20,000 cases) and Brazil (2015–2016; 30,000 cases), and these outbreaks have been associated with increased incidence of Guillain–Barre syndrome (GBS) in adults and microcephaly in infants. Proving a causative link between an infectious agent and subsequent neurological damage is not straightforward. This month’s journal club examines three papers that attempt to provide evidence connecting Zika virus to neurological sequelae. The first is a case–control study of GBS during the Zika virus epidemic in French Polynesia. The second is a prospective cohort study reporting foetal growth defects in pregnant women in Brazil, some of whom had been infected with Zika virus. The third is a cellular paper looking at neural expression of AXL, a receptor that could mediate Zika virus entry into cells.