Journal Article > ReviewFull Text
Lancet Infect Dis. 10 June 2016; Volume 16 (Issue 7); DOI:10.1016/S1473-3099(16)30063-9
Cnops L, van Griensven J, Honko AN, Bausch DG, Sprecher A, et al.
Lancet Infect Dis. 10 June 2016; Volume 16 (Issue 7); DOI:10.1016/S1473-3099(16)30063-9
Quantitative measurement of viral load is an important parameter in the management of filovirus disease outbreaks because viral load correlates with severity of disease, survival, and infectivity. During the ongoing Ebola virus disease outbreak in parts of Western Africa, most assays used in the detection of Ebola virus disease by more than 44 diagnostic laboratories yielded qualitative results. Regulatory hurdles involved in validating quantitative assays and the urgent need for a rapid Ebola virus disease diagnosis precluded development of validated quantitative assays during the outbreak. Because of sparse quantitative data obtained from these outbreaks, opportunities for study of correlations between patient outcome, changes in viral load during the course of an outbreak, disease course in asymptomatic individuals, and the potential for virus transmission between infected patients and contacts have been limited. We strongly urge the continued development of quantitative viral load assays to carefully evaluate these parameters in future outbreaks of filovirus disease.
Journal Article > CommentaryFull Text
Lancet Infect Dis. 19 September 2016; Volume 16 (Issue 10); DOI:10.1016/S1473-3099(16)30339-5
Cnops L, van Griensven J, Honko AN, Bausch DG, Sprecher A, et al.
Lancet Infect Dis. 19 September 2016; Volume 16 (Issue 10); DOI:10.1016/S1473-3099(16)30339-5
Journal Article > ResearchFull Text
Cell. 18 June 2015; Volume 161 (Issue 7); DOI:10.1016/j.cell.2015.06.007
Park DJ, Dudas G, Wohl S, Goba A, Whitmer SL, et al.
Cell. 18 June 2015; Volume 161 (Issue 7); DOI:10.1016/j.cell.2015.06.007
The 2013-2015 Ebola virus disease (EVD) epidemic is caused by the Makona variant of Ebola virus (EBOV). Early in the epidemic, genome sequencing provided insights into virus evolution and transmission and offered important information for outbreak response. Here, we analyze sequences from 232 patients sampled over 7 months in Sierra Leone, along with 86 previously released genomes from earlier in the epidemic. We confirm sustained human-to-human transmission within Sierra Leone and find no evidence for import or export of EBOV across national borders after its initial introduction. Using high-depth replicate sequencing, we observe both host-to-host transmission and recurrent emergence of intrahost genetic variants. We trace the increasing impact of purifying selection in suppressing the accumulation of nonsynonymous mutations over time. Finally, we note changes in the mucin-like domain of EBOV glycoprotein that merit further investigation. These findings clarify the movement of EBOV within the region and describe viral evolution during prolonged human-to-human transmission.