Journal Article > CommentaryFull Text
Nature. 9 February 2022; Volume 602 (Issue 7896); 207-210.; DOI:10.1038/d41586-022-00324-y
Swaminathan S, Pecoul B, Abdullah H, Christou C, Gray G, et al.
Nature. 9 February 2022; Volume 602 (Issue 7896); 207-210.; DOI:10.1038/d41586-022-00324-y
Journal Article > LetterFull Text
Nature. 17 June 2015; Volume 524 (Issue 7563); 97-101.; DOI:10.1038/nature14594
Carroll MW, Matthews DA, Hiscox JA, Elmore MJ, Pollakis G, et al.
Nature. 17 June 2015; Volume 524 (Issue 7563); 97-101.; DOI:10.1038/nature14594
West Africa is currently witnessing the most extensive Ebola virus (EBOV) outbreak so far recorded. Until now, there have been 27,013 reported cases and 11,134 deaths. The origin of the virus is thought to have been a zoonotic transmission from a bat to a twoyear-old boy in December 2013 (ref. 2). From this index case the virus was spread by human-to-human contact throughout Guinea, Sierra Leone and Liberia. However, the origin of the particular virus in each country and time of transmission is not known and currently relies on epidemiological analysis, which may be unreliable owing to the difficulties of obtaining patient information. Here we trace the genetic evolution of EBOV in the current outbreak that has resulted in multiple lineages. Deep sequencing of 179 patient samples processed by the European Mobile Laboratory, the first diagnostics unit to be deployed to the epicentre of the outbreak in Guinea, reveals an epidemiological and evolutionary history of the epidemic from March 2014 to January 2015. Analysis of EBOV genome evolution has also benefited from a similar sequencing effort of patient samples from Sierra Leone. Our results confirm that the EBOV from Guinea moved into Sierra Leone, most likely in April or early May. The viruses of the Guinea/Sierra Leone lineage mixed around June/July 2014. Viral sequences covering August, September and October 2014 indicate that this lineage evolved independently within Guinea. These data can be used in conjunction with epidemiological information to test retrospectively the effectiveness of control measures, and provides an unprecedented window into the evolution of an ongoing viral haemorrhagic fever outbreak.
Journal Article > CommentaryAbstract
Nature. 27 October 2011; Volume 478 (Issue 7370); DOI:10.1038/478458a
Guerrier G, Baron E, Fakri R, Mouniaman I
Nature. 27 October 2011; Volume 478 (Issue 7370); DOI:10.1038/478458a
The burden of war-related mental disorders is well documented among US veterans (Nature 477, 390–393; 2011), but not among civilians in Iraq. This oversight must be rectified so that adequate medical support can be provided to the Iraqi people. US combat troops will soon depart Iraq, leaving Iraqis to cope with the consequences of the 2003 invasion. Although the number of violent deaths is falling, civilians have been killed almost every day this year, most of them in coordinated bomb attacks. Roadside blasts cause long-term disabilities and societal effects among injured civilians. However, these have been largely neglected by the media and no systematic surveillance has been undertaken.
Journal Article > ResearchFull Text
Nature. 4 May 2016; Volume 533 (Issue 7601); 100-104.; DOI:10.1038/nature17949
Ruibal P, Oestereich L, Ludtke A, Becker-Ziaja B, Wozniak DM, et al.
Nature. 4 May 2016; Volume 533 (Issue 7601); 100-104.; DOI:10.1038/nature17949
Despite the magnitude of the Ebola virus disease (EVD) outbreak in West Africa, there is still a fundamental lack of knowledge about the pathophysiology of EVD. In particular, very little is known about human immune responses to Ebola virus. Here we evaluate the physiology of the human T cell immune response in EVD patients at the time of admission to the Ebola Treatment Center in Guinea, and longitudinally until discharge or death. Through the use of multiparametric flow cytometry established by the European Mobile Laboratory in the field, we identify an immune signature that is unique in EVD fatalities. Fatal EVD was characterized by a high percentage of CD4(+) and CD8(+) T cells expressing the inhibitory molecules CTLA-4 and PD-1, which correlated with elevated inflammatory markers and high virus load. Conversely, surviving individuals showed significantly lower expression of CTLA-4 and PD-1 as well as lower inflammation, despite comparable overall T cell activation. Concomitant with virus clearance, survivors mounted a robust Ebola-virus-specific T cell response. Our findings suggest that dysregulation of the T cell response is a key component of EVD pathophysiology.
Journal Article > ResearchFull Text
Nature. 1 December 2015; Volume 528 (Issue 7580); S68-S76.; DOI:10.1038/nature16046
Phillips AN, Shroufi A, Vojnov L, Cohn J, Roberts TR, et al.
Nature. 1 December 2015; Volume 528 (Issue 7580); S68-S76.; DOI:10.1038/nature16046
There are inefficiencies in current approaches to monitoring patients on antiretroviral therapy in sub-Saharan Africa. Patients typically attend clinics every 1 to 3 months for clinical assessment. The clinic costs are comparable with the costs of the drugs themselves and CD4 counts are measured every 6 months, but patients are rarely switched to second-line therapies. To ensure sustainability of treatment programmes, a transition to more cost-effective delivery of antiretroviral therapy is needed. In contrast to the CD4 count, measurement of the level of HIV RNA in plasma (the viral load) provides a direct measure of the current treatment effect. Viral-load-informed differentiated care is a means of tailoring care so that those with suppressed viral load visit the clinic less frequently and attention is focussed on those with unsuppressed viral load to promote adherence and timely switching to a second-line regimen. The most feasible approach to measuring viral load in many countries is to collect dried blood spot samples for testing in regional laboratories; however, there have been concerns over the sensitivity and specificity of this approach to define treatment failure and the delay in returning results to the clinic. We use modelling to synthesize evidence and evaluate the cost-effectiveness of viral-load-informed differentiated care, accounting for limitations of dried blood sample testing. We find that viral-load-informed differentiated care using dried blood sample testing is cost-effective and is a recommended strategy for patient monitoring, although further empirical evidence as the approach is rolled out would be of value. We also explore the potential benefits of point-of-care viral load tests that may become available in the future.
Journal Article > ResearchFull Text
Nature. 7 February 2008; Volume 451 (Issue 7179); DOI:10.1038/nature06509
Ferrari MJ, Grais RF, Bharti N, Conlan AJK, Bjørnstad ON, et al.
Nature. 7 February 2008; Volume 451 (Issue 7179); DOI:10.1038/nature06509
Although vaccination has almost eliminated measles in parts of the world, the disease remains a major killer in some high birth rate countries of the Sahel. On the basis of measles dynamics for industrialized countries, high birth rate regions should experience regular annual epidemics. Here, however, we show that measles epidemics in Niger are highly episodic, particularly in the capital Niamey. Models demonstrate that this variability arises from powerful seasonality in transmission-generating high amplitude epidemics-within the chaotic domain of deterministic dynamics. In practice, this leads to frequent stochastic fadeouts, interspersed with irregular, large epidemics. A metapopulation model illustrates how increased vaccine coverage, but still below the local elimination threshold, could lead to increasingly variable major outbreaks in highly seasonally forced contexts. Such erratic dynamics emphasize the importance both of control strategies that address build-up of susceptible individuals and efforts to mitigate the impact of large outbreaks when they occur.
Journal Article > ResearchFull Text
Nature. 18 May 2006; Volume 441 (Issue 7091); DOI:10.1038/441283a
Usdin M, Guillerm M, Chirac P
Nature. 18 May 2006; Volume 441 (Issue 7091); DOI:10.1038/441283a
Journal Article > LetterAbstract
Nature. 27 April 2014; Volume 507 (Issue 7493); DOI:10.1038/507431d
Pecoul B, Balasegaram M
Nature. 27 April 2014; Volume 507 (Issue 7493); DOI:10.1038/507431d
Journal Article > CommentaryFull Text
Nature. 3 August 2015; Volume 524 (Issue 7563); DOI:10.1038/524027a
Liu J
Nature. 3 August 2015; Volume 524 (Issue 7563); DOI:10.1038/524027a
Journal Article > LetterFull Text
Nature. 2 January 2019; Volume 565 (Issue 7738); DOI:10.1038/s41586-018-0818-3
Weill FX, Domman D, Njamkepo E, Almesbahi AA, Naji MAM, et al.
Nature. 2 January 2019; Volume 565 (Issue 7738); DOI:10.1038/s41586-018-0818-3
Yemen is currently experiencing, to our knowledge, the largest cholera epidemic in recent history. The first cases were declared in September 2016, and over 1.1 million cases and 2,300 deaths have since been reported1. Here we investigate the phylogenetic relationships, pathogenesis and determinants of antimicrobial resistance by sequencing the genomes of Vibrio cholerae isolates from the epidemic in Yemen and recent isolates from neighbouring regions. These 116 genomic sequences were placed within the phylogenetic context of a global collection of 1,087 isolates of the seventh pandemic V. cholerae serogroups O1 and O139 biotype El Tor2-4. We show that the isolates from Yemen that were collected during the two epidemiological waves of the epidemic1-the first between 28 September 2016 and 23 April 2017 (25,839 suspected cases) and the second beginning on 24 April 2017 (more than 1 million suspected cases)-are V. cholerae serotype Ogawa isolates from a single sublineage of the seventh pandemic V. cholerae O1 El Tor (7PET) lineage. Using genomic approaches, we link the epidemic in Yemen to global radiations of pandemic V. cholerae and show that this sublineage originated from South Asia and that it caused outbreaks in East Africa before appearing in Yemen. Furthermore, we show that the isolates from Yemen are susceptible to several antibiotics that are commonly used to treat cholera and to polymyxin B, resistance to which is used as a marker of the El Tor biotype.