The authors review here how viruses, from ancient viruses that integrated the germ line during evolution through old viruses (e.g. papillomaviruses originating from Neanderthals) and more modern sexually-transmitted infections (e.g. simian zoonotic HIV) to emerging viruses (e.g. Ebola and Zika) take advantage of genital tract colonization for horizontal dissemination, viral persistence, vertical transmission and endogenization.
Since the ZIKV outbreak in Brazil in 2015, the scientific community has joined efforts to gather more information on the epidemiology, clinical features and pathogenicity of the virus. Here, you can read a summary of the most important advances made recently and the discussion of promising, innovative approaches to understand and control ZIKV infection.
The structural proteins of epidemic and historical strains of Zika virus differ in their ability to initiate viral infection in human host cellsby Bos et al.
In this study researchers show that ZIKV containing BeH819015 structural proteins is much less efficient in cell-attachment leading to a reduced susceptibility ofepithelial A549 and neuronal SH-SY5Y cells to viral infection.
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.