Zika virus: from pathogenesis to disease control

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Abstract

Zika virus is a mosquito-borne flavivirus discovered in Uganda in 1947. The virus has emerged in recent years and spread in the Pacific Area and the Americas, where it has caused large human outbreaks. The factors involved in the virus's emergence are still unknown, but probably include its introduction in naïve environments characterised by the presence of high densities of competent Aedes spp. mosquitoes and susceptible human hosts in urban areas. Unique features of Zika virus infection are sexual and transplacental transmission and associated neurological morbidities, i.e. Guillain–Barré syndrome and fetal microcephaly. Diagnosis relies on the detection of viral nucleic acids in biological samples, while detection of a specific antibody response may be inconclusive because of the broad cross-reactivity of antibodies among flaviviruses. Experimental studies have clarified some mechanisms of Zika virus pathogenesis and have identified potential targets for antiviral drugs. In animal models, the virus can infect and efficiently replicate in the placenta and in the brain, and induce fetal demise or neural damage, recapitulating human diseases. These animal models have been used to evaluate candidate vaccines and promising results have been obtained.

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