Abstract
As revealed by the recent resurgence of yellow fever virus (YFV) activity in the tropical regions of Africa and South America, YFV control measures need urgent rethinking. Over the last decade, most reported outbreaks occurred in, or eventually reached, areas with low vaccination coverage but that are suitable for virus transmission, with an unprecedented risk of expansion to densely populated territories in Africa, South America and Asia. As reflected in the World Health Organization’s initiative launched in 2017, it is high time to strengthen epidemiological surveillance to monitor accurately viral dissemination, and redefine vaccination recommendation areas. Vector-control and immunisation measures need to be adapted and vaccine manufacturing must be reconciled with an increasing demand. We will have to face more yellow fever (YF) cases in the upcoming years. Hence, improving disease management through the development of efficient treatments will prove most beneficial. Undoubtedly, these developments will require in-depth descriptions of YFV biology at molecular, physiological and ecological levels. This second section of a two-part review describes the current state of knowledge and gaps regarding the molecular biology of YFV, along with an overview of the tools that can be used to manage the disease at the individual, local and global levels.
Highlights
As revealed by the recent resurgence of yellow fever virus (YFV) activity in the tropical regions of Africa and South America, YFV control measures need urgent rethinking
Several hypotheses have been put forward by Sall and colleagues to explain the differences in evolutionary dynamics between YFV and dengue virus (DENV). They suggest that a preponderant role of transovarial transmission (TOT) within mosquitoes in the maintenance of the virus could be implicated as such a mechanism, where the virus may remain quiescent in mosquito eggs for many months, would decrease the replication rate of the virus [108]
Control over YFV infections is a multifaceted issue to which no miraculous solution can be proposed for the time being
Summary
In 1985, the first complete sequence of YFV was determined from complementary DNA (cDNA). The cap structure of flaviviral genomes is thought to be important for cap-dependent translation and to protect the genome from degradation by cellular 50 -30 exonucleases [48]. This (+)ssRNA corresponds to one large open reading frame (ORF), flanked at its 50 and 30 termini by untranslated regions (UTRs) that are required for RNA replication and translation [44,50,51]. The amino-terminal residues correspond to the three structural proteins while the remainder of the ORF encodes the seven NS proteins with the following organisation: 50 cap-C-prM-E-NS1-NS2A-NS2B-NS3-NS4A-2k-NS4B-NS5-30. The 50 UTR of YFV (~110 nts) is much shorter than the 30 UTR (~400–650 nts), the size of which varies among YF strains [28,31]
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