Juliet Bryant

Dr. Juliet Bryant


Research Focus & Metrics

Academic Career Length

27Years (2000-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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18 May 2007 in PLOS Pathogens
Verified
Journal Article
Open access
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JBJuliet Bryant
Juliet Bryant
EHEdward Holmes
Edward Holmes
ABAlan Barrett
Alan Barrett
Yellow fever virus (YFV) remains the cause of severe morbidity and mortality in South America and Africa. To determine the evolutionary history of this important reemerging pathogen, we performed a phylogenetic analysis of the largest YFV data set compiled to date, representing the prM/E gene region from 133 viral isolates sampled from 22 countries over a period of 76 years. We estimate that the currently circulating strains of YFV arose in Africa within the last 1,500 years and emerged in the Americas following the slave trade approximately 300–400 years ago. These viruses then spread westwards across the continent and persist there to this day in the jungles of South America. We therefore illustrate how gene sequence data can be used to test hypotheses of viral dispersal and demographics, and document the role of human migration in the spread of infectious disease. Throughout the 18th and 19th centuries, yellow fever was one of the most dreaded of diseases in New and Old world port cities. Large-scale epidemics of yellow fever helped shape colonial expansion in both the Americas and in Africa, and the medical and scientific developments associated with control of the virus have been a favored topic of historians for many years. The most commonly cited hypothesis of the origin of yellow fever virus (YFV) in the Americas is that the virus was introduced from Africa, along with Aedes Aegypti mosquitoes, in the bilges of sailing vessels during the slave trade. Although the hypothesis of a slave trade introduction is often repeated, it has not been subject to rigorous examination using gene sequence data and modern phylogenetic techniques for estimating divergence times. Herein we have assembled a comprehensive data set of gene sequences for YFV, which we used to infer the time-scale and evolutionary history of YFV. These data show that the spread of YFV to the Americas corresponds closely with the routes and timing of the slave trade. Overall, this study demonstrates how molecular epidemiological studies can provide new insight into debates on the origin and spread of infectious disease.

14 May 2013 in Proceedings of the National Academy of Sciences
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Journal Article
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NNNguyet Nguyen
Nguyet Nguyen
DKDuong Thi Hue Kien
Duong Thi Hue Kien
TTTrung Vu Tuan
Trung Vu Tuan
NQNguyen Than Ha Quyen
Nguyen Than Ha Quyen
CTChau N. B. Tran
Chau N. B. Tran
CSCameron P. Simmons
Cameron P. Simmons
Dengue is the most prevalent arboviral disease of humans. The host and virus variables associated with dengue virus (DENV) transmission from symptomatic dengue cases ( n = 208) to Aedes aegypti mosquitoes during 407 independent exposure events was defined. The 50% mosquito infectious dose for each of DENV-1–4 ranged from 6.29 to 7.52 log10 RNA copies/mL of plasma. Increasing day of illness, declining viremia, and rising antibody titers were independently associated with reduced risk of DENV transmission. High early DENV plasma viremia levels in patients were a marker of the duration of human infectiousness, and blood meals containing high concentrations of DENV were positively associated with the prevalence of infectious mosquitoes 14 d after blood feeding. Ambulatory dengue cases had lower viremia levels compared with hospitalized dengue cases but nonetheless at levels predicted to be infectious to mosquitoes. These data define serotype-specific viremia levels that vaccines or drugs must inhibit to prevent DENV transmission.

19 May 2020 in Science Immunology
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Journal Article
Open access
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JBJuliet Bryant
Juliet Bryant
AAAndrew S. Azman
Andrew S. Azman
MFMatthew J. Ferrari
Matthew J. Ferrari
BABenjamin F. Arnold
Benjamin F. Arnold
MBMaciej F. Boni
Maciej F. Boni
DLDaniel T. Leung
Daniel T. Leung
Defining acceptable performance characteristics for SARS-CoV-2 serological tests requires factoring in how the results will be used.

26 October 2016 in Proceedings Of The Royal Society B-Biological Sciences
Verified
Journal Article
Open access
EPEmily E. Puckett
Emily E. Puckett
JPJane Park
Jane Park
MCMatthew Combs
Matthew Combs
MBMichael J. Blum
Michael J. Blum
JBJuliet Bryant
Juliet Bryant
JMJason Munshi-South
Jason Munshi-South
Native to China and Mongolia, the brown rat ( Rattus norvegicus ) now enjoys a worldwide distribution. While black rats and the house mouse tracked the regional development of human agricultural settlements, brown rats did not appear in Europe until the 1500s, suggesting their range expansion was a response to relatively recent increases in global trade. We inferred the global phylogeography of brown rats using 32 k SNPs, and detected 13 evolutionary clusters within five expansion routes. One cluster arose following a southward expansion into Southeast Asia. Three additional clusters arose from two independent eastward expansions: one expansion from Russia to the Aleutian Archipelago, and a second to western North America. Westward expansion resulted in the colonization of Europe from which subsequent rapid colonization of Africa, the Americas and Australasia occurred, and multiple evolutionary clusters were detected. An astonishing degree of fine-grained clustering between and within sampling sites underscored the extent to which urban heterogeneity shaped genetic structure of commensal rodents. Surprisingly, few individuals were recent migrants, suggesting that recruitment into established populations is limited. Understanding the global population structure of R. norvegicus offers novel perspectives on the forces driving the spread of zoonotic disease, and aids in development of rat eradication programmes.

1 June 2000 in The American Journal of Pathology
Verified
Journal Article
Closed access
JKJeanne Kahn
Jeanne Kahn
FMFuad Mehraban
Fuad Mehraban
GIGladys Ingle
Gladys Ingle
XXXiaohua Xin
Xiaohua Xin
JBJuliet Bryant
Juliet Bryant
MGMary E. Gerritsen
Mary E. Gerritsen

24 March 2011 in PLOS ONE
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Journal Article
Open access
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ADAnh Ha Lien Do
Anh Ha Lien Do
HDH Rogier van Doorn
H Rogier van Doorn
MNMy Ngoc Nghiem
My Ngoc Nghiem
JBJuliet Bryant
Juliet Bryant
THThanh Hang Thi Hoang
Thanh Hang Thi Hoang
MJMenno D De Jong
Menno D De Jong
The dominant viral etiologies responsible for acute respiratory infections (ARIs) are poorly understood, particularly among hospitalized children in resource-limited tropical countries where morbidity and mortality caused by ARIs are highest. Improved etiological insight is needed to improve clinical management and prevention. We conducted a three-year prospective descriptive study of severe respiratory illness among children from 2 months to 13 years of age within the largest referral hospital for infectious diseases in southern Vietnam. Molecular detection for 15 viral species and subtypes was performed on three types of respiratory specimens (nose, throat swabs and nasopharyngeal aspirates) using a multiplex RT-PCR kit (Seeplex™ RV detection, Seegene) and additional monoplex real-time RT-PCRs. A total of 309 children were enrolled from November 2004 to January 2008. Viruses were identified in 72% (222/309) of cases, including respiratory syncytial virus (24%), influenza virus A and B (17%), human bocavirus (16%), enterovirus (9%), human coronavirus (8%), human metapneumovirus (7%), parainfluenza virus 1–3 (6%), adenovirus (5%), and human rhinovirus A (4%). Co-infections with multiple viruses were detected in 20% (62/309) of patients. When combined, diagnostic yields in nose and throat swabs were similar to nasopharyngeal aspirates. Similar to other parts in the world, RSV and influenza were the predominant viral pathogens detected in Vietnamese hospitalized children. Combined nasal and throat swabs are the specimens of choice for sensitive molecular detection of a broad panel of viral agents. Further research is required to better understand the clinical significance of single versus multiple viral coinfections and to address the role of bacterial (co-)infections involved in severe respiratory illness.