Article Figures & Data
Figures
- FIG 1
Detection of RESTV. The maps shown indicate the locations of RESTV detection, either viral RNA or seropositive evidence, that suggest that RESTV is more widely distributed than previously thought (7, 18, 19, 25). The distribution of RESTV appears to be in close proximity to the equator, similar to that of other Ebolaviruses, although RESTV has never been detected in Africa.
- FIG 2
Phylogenetic analysis of the Filoviridae family. Shown are the results of a Bayesian coalescent analysis of viruses in the Filoviridae family showing that RESTV is most closely related to SUDV (27).
Tables
- TABLE
Protein components of Ebolavirusa
Protein Function % of RESTV residues identified as SDPs NP Protects and packages the viral genome by encapsidation 3.87 GP Class I viral fusion protein, responsible for binding and entry into host cells, activated by proteolysis, creating GP1 and GP2; GP1,2 has extensive roles in modulation of the immune response and alteration of the expression of cell surface adhesion molecules; cleavage of GP1,2 from the plasma membrane creates a soluble variant 4.3 sGP Possible roles in immune evasion and alteration of endothelial permeability 2.43 ssGP Unknown Not determined VP24 Secondary matrix protein, minor component of virions; key player in pathogenicity, inhibits components of immune response 3.59 VP30 Viral nucleocapsid component; key role in transcription depending on its state of phosphorylation 5.86 VP35 Polymerase cofactor in transcription and replication; prevents antiviral response in cells by blocking IRF-3 and protein kinase EIF2AK2/PKR 5.57 VP40 Regulates viral transcription, morphogenesis, packaging, and budding 2.72 Polymerase Replicates the viral genome 2.95 ↵a The percentage of SDP sites in RESTV, compared to EBOV, may offer clues to the lack of RESTV pathogenicity in humans, though higher levels of SDPs do not necessarily indicate a change in protein function or activity. Furthermore, the percentage of difference is likely to fluctuate regularly because of viral mutation and evolution (49, 58, 65–69).
- TABLE 2
Outbreaks of Reston ebolavirusa
Location Yr Organism No. of seropositive humans RESTV outbreaks Philippines 1989–1990 Cynomolgus monkey 3 United States (VA, PA) 1989–1990 Cynomolgus monkey 0 United States (TX) 1989–1990 Cynomolgus monkey 4 Italy 1992–1993 Cynomolgus monkey 0 United States (TX) 1996 Cynomolgus monkey 0 Philippines 1996 Cynomolgus monkey 1 Philippines 2008 Pig 6 China 2011 Pig 0 Philippines 2015 Cynomolgus monkey 0 Locations with seropositive evidence only Philippines 2008–2009 Fruit bat China 2006–2009 Fruit bat Bangladesh 2010–2011 Fruit bat ↵a The 1989 outbreak was characterized by high mortality rates in cynomolgus monkeys, whereas infected pigs were found to be coinfected with PRRSV. No human handlers were reported to show any symptoms of disease (7, 8, 17, 19, 70, 71).
