Suramin inhibits Zika virus replication by interfering with virus attachment and release of infectious particlesby Albulescu et al.
The authors of this article describe inhibition of ZIKV replication by suramin, originally an anti-parasitic drug. They suggest that the inhibitory effect of suramin on ZIKV attachment and virion biogenesis and its broadspectrum activity warrant further evaluation of this compound as a potential therapeutic.
The key message from this study is that the large uncertainty around the risk estimate needs to be further investigated because of a) the possible existence of co-factors that are yet to be validated, b) the assumptions that the authors needed to make in the absence of good data for the proportion of women who were infected during pregnancy.
Substrate selectivity of Dengue and Zika virus NS5 polymerase towards 2'-modified nucleotide analoguesby Potisopon et al.
In addition to representing the first ZIKV full-length NS5 activity report at the molecular level, this study should help the design of pan-flavivirus drugs aiming at the control of many Flavivirus members of this large family of emerging arboviruses, as well as understand the basis of re-purposing drugs against emerging viral diseases.
The results outlined in the article contribute to a better understanding of the ZIKVMTase, a central player in viral replication and host innate immune response, and lay the basis for the development of potential antiviral drugs.
The article concludes that infection with Flaviviridae can increase centrosome numbers and impair spindle positioning, thus potentially contributing to microcephaly in the case of Zika.
African and Asian Zika virus strains differentially induce early antiviral responses in primary human astrocytesby Hamel et al.
This study describes for the first time the specific antiviral gene expression in infected primary human astrocytes, the major glial cells within the central nervous system.
This pioneering study suggests that the study of blood donors during outbreaks of emerging pathogens has become a key element of epidemiological surveillance.
A study performed by the Institut National de la Santé et de la Recherche Médicale (INSERM) team of Dr Ali Amara (U944, Paris, France) and published in Cell Reports sheds new light on the mechanisms allowing ZIKV to infect cells within the human nervous system. Amara et al. showed that the protein Axl is expressed in a number of brain glial cells and that the entry of ZIKV into these cells requires another protein, Gas6, to act as a bridge between the ZIKV particles and the glial cells.
By using the bacterium-free ‘Infectious Subgenomic Amplicons’ (ISA) method, this study provides the scientific community with two simple and performing reverse genetics systems for ZIKV.
The article argues that the off-label use of drugs that may protect against Zika virus-induced brain damage has to be balanced with their risk during pregnancy.