Zika virus: issues of concern.

The suspected involvement of Zika virus (ZIKV), an arthropod-borne flaviviral agent newly emerged in the Western Hemisphere, in the “epidemics” of microcephaly and Guillain-Barré syndrome (GBS) among patients from Brazil and French Polynesia is a matter of concern (Fauci and Morens, 2016). As a consequence, characterizing the viral neurotropism and neuropathogenicity, along with the host-pathogen interaction dynamics at central nervous system (CNS) level, represent key issues in the neuropathogenetic study of ZIKV infection. This would also be relevant in relation to the occurrence of anti-ZIKV antibodies in the cerebrospinal fluid (CSF) of infected patients, as in the case of other infections caused by neurotropic viruses, where the “intrathecal” production of such antibodies unequivocally proves viral replication and persistence inside the host’s CNS (Bonnan et al., 2015). An “ad hoc” search for these anti-ZIKV antibodies could have been carried out, for instance, in the CSF from the microcephaly-affected foetus in whose brain clear-cut biomolecular and ultrastructural evidence of ZIKV has been recently reported (Mlakar et al., 2016), with a strong cause-effect relationship having been made between viral colonization of foetal brain, on the one hand, and microcephaly development on the other. The same appears to be true when making reference to another recent article reporting the existence of a cause-effect relationship between ZIKV infection and GBS development (Cao-Lormeau et al., 2016). Albeit quite solid and convincing, the results obtained by the aforementioned investigators could have gained additional weight based upon the occurrence, if any, of anti-ZIKV antibodies in the CSF from the GBS-affected patients under study. Indeed, anti-ZIKV antibodies have already been detected in the CSF of microcephaly-affected foetuses and babies in Brazil (Check Hayden, 2016). Of additional concern is the time frame within which transplacental ZIKV infection occurs. Crucial morphogenetic processes are known to take place during the first 4 weeks of embryonic development inside the human uterus, with alteration(s) of these processes which are known to be induced by a long list of “exogenous” factors, including biological noxae leading to several structural (and functional) abnormalities (Barness, 2010). Alongside the “embryonic/foetal developmental stage” at which human ZIKV infection occurs, it would also be important to