Abstract
The sudden appearance of overt human Zika virus infections that cross the placenta to damage fetal tissues, target sexual organs, and are followed in some instances by Guillain-Barré syndrome raises questions regarding whether these outcomes are caused by genetic mutations or if prior infection by other flaviviruses affects disease outcome. Because dengue and Zika viruses co-circulate in the urban Aedes aegypti mosquito–human cycle, a logical question, as suggested by in vitro data, is whether dengue virus infections result in antibody-dependent enhancement of Zika virus infections. This review emphasizes the critical role for epidemiologic studies (retrospective and prospective) in combination with the studies to identify specific sites of Zika virus infection in humans that are needed to establish antibody-dependent enhancement as a possibility or a reality.
Highlights
The sudden appearance of overt human Zika virus infections that cross the placenta to damage fetal tissues, target sexual organs, and are followed in some instances by Guillain-Barré syndrome raises questions regarding whether these outcomes are caused by genetic mutations or if prior infection by other flaviviruses affects disease outcome
Three studies have shown that monoclonal antibodies to the dengue virus (DENV) fusion loop epitope reliably enhanced Zika virus infection in Fc receptor–bearing K-562 human myelogenous leukemia cells or the U-937 human monocytic cell line [1,2,3]
Broadly neutralizing DENV monoclonal antibodies directed at a conformational quaternary epitope on the virion formed at the interface of 2 envelope dimer epitopes (EDE1 and EDE2) potently neutralized Zika virus in a picomolar range similar to the neutralization of DENV [2]
Summary
The sudden appearance of overt human Zika virus infections that cross the placenta to damage fetal tissues, target sexual organs, and are followed in some instances by Guillain-Barré syndrome raises questions regarding whether these outcomes are caused by genetic mutations or if prior infection by other flaviviruses affects disease outcome. By using a simple protocol (Table), it should be possible to gather evidence using a case-control format comparing the frequency of a secondary flavivirus antibody response in convalescent-phase serum samples of persons experiencing any defined acute Zika virus disease syndromes, such as exanthematous fever, congenital Zika syndrome, or GBS (i.e., case-patients) with the prevalence of past DENV infection in Zika virus–infected age-, sex-, residence-, and ethnicity-matched persons from the same exposure group (i.e., controls). Such a comparison should be undertaken promptly in several different Zika virus–endemic locales.
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