Publications by authors named "Lance Presser"

8 Publications

  • Page 1 of 1

Sustainable Laboratory Capacity Building After the 2014 Ebola Outbreak in the Republic of Guinea.

Front Public Health 2021 4;9:659504. Epub 2021 Jun 4.

MRIGlobal, Gaithersburg, MD, United States.

The 2014-2016 West Africa Ebola virus disease outbreak heavily impacted the Republics of Guinea, Sierra Leone, and Liberia. The outbreak uncovered the weaknesses of the public health systems, including inadequately trained and insufficient health personnel as well as limited and poorly equipped health infrastructures. These weaknesses represent significant threats to global health security. In the wake of the outbreak, affected countries made urgent requests for international engagement to help strengthening the public health systems. This work describes the successful multi-year implementation of a laboratory capacity building program in the Republic of Guinea. The program integrated biorisk and quality management systems training, infectious diseases diagnostic training, facility engineering and maintenance training, and mentorship to strengthen Guinea's bio-surveillance capacity. The major outcome of these efforts was an established and local staff-operated public health laboratory that performs disease surveillance and reporting and diagnostic of priority diseases and pathogens of security concerns. This work has improved the Guinea country's capabilities to address country public health issues and preparedness to respond to future infectious disease threats.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fpubh.2021.659504DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8220810PMC
August 2021

Building the Sierra Leone Ebola Database: organization and characteristics of data systematically collected during 2014-2015 Ebola epidemic.

Ann Epidemiol 2021 May 6;60:35-44. Epub 2021 May 6.

National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta.

Purpose: During the 2014-2016 Ebola outbreak in West Africa, the Sierra Leone Ministry of Health and Sanitation (MoHS), the US Centers for Disease Control and Prevention, and responding partners under the coordination of the National Ebola Response Center (NERC) and the MoHS's Emergency Operation Center (EOC) systematically recorded information from the 117 Call Center system and district alert phone lines, case investigations, laboratory sample testing, clinical management, and safe and dignified burial records. Since 2017, CDC assisted MoHS in building and managing the Sierra Leone Ebola Database (SLED) to consolidate these major data sources. The primary objectives of the project were helping families to identify the location of graves of their loved ones who died at the time of the Ebola epidemic through the SLED Family Reunification Program and creating a data source for epidemiological research. The objective of this paper is to describe the process of consolidating epidemic records into a useful and accessible data collection and to summarize data characteristics, strength, and limitations of this unique information source for public health research.

Methods: Because of the unprecedented conditions during the epidemic, most of the records collected from responding organizations required extensive processing before they could be used as a data source for research or the humanitarian purpose of locating burial sites. This process required understanding how the data were collected and used during the outbreak. To manage the complexity of processing the data obtained from various sources, the Sierra Leone Ebola Database (SLED) Team used an organizational strategy that allowed tracking of the data provenance and lifecycle.

Results: The SLED project brought raw data into one consolidated data collection. It provides researchers with secure and ethical access to the SLED data and serves as a basis for the research capacity building in Sierra Leone. The SLED Family Reunification Program allowed Sierra Leonean families to identify location of the graves of loved ones who died during the Ebola epidemic.

Conclusions: The SLED project consolidated and utilized epidemic data recorded during the Sierra Leone Ebola Virus Disease outbreak that were collected and contributed to SLED by national and international organizations. This project has provided a foundation for developing a method of ethical and secure SLED data access while preserving the host nation's data ownership. SLED serves as a data source for the SLED Family Reunification Program and for epidemiological research. It presents an opportunity for building research capacity in Sierra Leone and provides a foundation for developing a relational database. Large outbreak data systems such as SLED provide a unique opportunity for researchers to improve responses to epidemics and indicate the need to include data management preparedness in the plans for emergency response.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.annepidem.2021.04.017DOI Listing
May 2021

Establishing diagnostic training programs in resource-poor settings: The case of Sierra Leone.

Authors:
Lance D Presser

Afr J Lab Med 2020 15;9(1):889. Epub 2020 Jun 15.

Global Engagement Program, MRIGlobal, Gaithersburg, Maryland, United States.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.4102/ajlm.v9i1.889DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7343946PMC
June 2020

Ebola Virus Disease Diagnostics, Sierra Leone: Analysis of Real-time Reverse Transcription-Polymerase Chain Reaction Values for Clinical Blood and Oral Swab Specimens.

J Infect Dis 2016 10 31;214(suppl 3):S258-S262. Epub 2016 Aug 31.

School of Veterinary Medicine, University of California-Davis.

During the Ebola virus outbreak of 2013-2016, the Viral Special Pathogens Branch field laboratory in Sierra Leone tested approximately 26 000 specimens between August 2014 and October 2015. Analysis of the B2M endogenous control Ct values showed its utility in monitoring specimen quality, comparing results with different specimen types, and interpretation of results. For live patients, blood is the most sensitive specimen type and oral swabs have little diagnostic utility. However, swabs are highly sensitive for diagnostic testing of corpses.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/infdis/jiw296DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5769963PMC
October 2016

Legionellosis Outbreak Associated With a Hotel Fountain.

Open Forum Infect Dis 2015 Dec 28;2(4):ofv164. Epub 2015 Dec 28.

Chicago Department of Public Health, Illinois.

Background.  In August 2012, the Chicago Department of Public Health (CDPH) was notified of acute respiratory illness, including 1 fatality, among a group of meeting attendees who stayed at a Chicago hotel during July 30-August 3, 2012. Suspecting Legionnaires' disease (LD), CDPH advised the hotel to close their swimming pool, spa, and decorative lobby fountain and began an investigation. Methods.  Case finding included notification of individuals potentially exposed during July 16-August 15, 2012. Individuals were interviewed using a standardized questionnaire. An environmental assessment was performed. Results.  One hundred fourteen cases were identified: 11 confirmed LD, 29 suspect LD, and 74 Pontiac fever cases. Illness onsets occurred July 21-August 22, 2012. Median age was 48 years (range, 22-82 years), 64% were male, 59% sought medical care (15 hospitalizations), and 3 died. Relative risks for hotel exposures revealed that persons who spent time near the decorative fountain or bar, both located in the lobby were respectively 2.13 (95%, 1.64-2.77) and 1.25 (95% CI, 1.09-1.44) times more likely to become ill than those who did not. Legionella pneumophila serogroup 1 was isolated from samples collected from the fountain, spa, and women's locker room fixtures. Legionella pneumophila serogroup 1 environmental isolates and a clinical isolate had matching sequence-based types. Hotel maintenance records lacked a record of regular cleaning and disinfection of the fountain. Conclusions.  Environmental testing identified Legionella in the hotel's potable water system. Epidemiologic and laboratory data indicated the decorative fountain as the source. Poor fountain maintenance likely created favorable conditions for Legionella overgrowth.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/ofid/ofv164DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4692259PMC
December 2015

Activation of TGF-β1 promoter by hepatitis C virus-induced AP-1 and Sp1: role of TGF-β1 in hepatic stellate cell activation and invasion.

PLoS One 2013 21;8(2):e56367. Epub 2013 Feb 21.

Department of Microbiology and Immunology, H.M. Bligh Cancer Research Laboratories, Rosalind Franklin University of Medicine and Science, Chicago Medical School, Chicago, Illinois, USA.

Our previous studies have shown the induction and maturation of transforming growth factor-beta 1 (TGF-β1) in HCV-infected human hepatoma cells. In this study, we have investigated the molecular mechanism of TGF-β1 gene expression in response to HCV infection. We demonstrate that HCV-induced transcription factors AP-1, Sp1, NF-κB and STAT-3 are involved in TGF-β1 gene expression. Using chromatin immunoprecipitation (ChIP) assay, we further show that AP-1 and Sp1 interact with TGF-b1 promoter in vivo in HCV-infected cells. In addition, we demonstrate that HCV-induced TGF-β1 gene expression is mediated by the activation of cellular kinases such as p38 MAPK, Src, JNK, and MEK1/2. Next, we determined the role of secreted bioactive TGF-β1 in human hepatic stellate cells (HSCs) activation and invasion. Using siRNA approach, we show that HCV-induced bioactive TGF-β1 is critical for the induction of alpha smooth muscle actin (α-SMA) and type 1 collagen, the markers of HSCs activation and proliferation. We further demonstrate the potential role of HCV-induced bioactive TGF-β1 in HSCs invasion/cell migration using a transwell Boyden chamber. Our results also suggest the role of HCV-induced TGF-β1 in HCV replication and release. Collectively, these observations provide insight into the mechanism of TGF-β1 promoter activation, as well as HSCs activation and invasion, which likely manifests in liver fibrosis associated with HCV infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0056367PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578869PMC
August 2013

Hepatitis C virus activates interleukin-1β via caspase-1-inflammasome complex.

J Gen Virol 2012 Feb 12;93(Pt 2):235-246. Epub 2011 Oct 12.

Department of Microbiology and Immunology, H. M. Bligh Cancer Research Laboratories, Rosalind Franklin University of Medicine and Science, Chicago Medical School, 3333 Green Bay Road, North Chicago, IL 60064, USA.

Interleukin-1β (IL-1β) is a potent pro-inflammatory cytokine involved in the pathogenesis of HCV, but the sensors and underlying mechanisms that facilitate HCV-induced IL-1β proteolytic activation and secretion remains unclear. In this study, we have identified a signalling pathway leading to IL-1β activation and secretion in response to HCV infection. Previous studies have shown the induction and secretion of IL-1β through the inflammasome complex in macrophages/monocytes. Here, we report for the first time the induction and assembly of the NALP3-inflammasome complex in human hepatoma cells infected with HCV (JFH-1). We demonstrate that activation of IL-1β in HCV-infected cells involves the proteolytic processing of pro-caspase-1 into mature caspase-1 in a multiprotein inflammasome complex. Next, we demonstrate that HCV is sensed by NALP3 protein, which recruits the adaptor protein ASC for the assembly of the inflammasome complex. Using a small interfering RNA approach, we further show that components of the inflammasome complex are involved in the activation of IL-1β in HCV-infected cells. Our study also demonstrates the role of reactive oxygen species in HCV-induced IL-1β secretion. Collectively, these observations provide an insight into the mechanism of IL-1β processing and secretion, which is likely to provide novel strategies for targeting the viral or cellular determinants to arrest the progression of liver disease associated with chronic HCV infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1099/vir.0.034033-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352344PMC
February 2012

Hepatitis C virus-induced furin and thrombospondin-1 activate TGF-β1: role of TGF-β1 in HCV replication.

Virology 2011 Apr 5;412(2):284-96. Epub 2011 Feb 5.

Department of Microbiology and Immunology, H. M. Bligh Cancer Research Laboratories, Rosalind Franklin University of Medicine and Science, Chicago Medical School, 3333 Green Bay Road, North Chicago, IL 60064, USA.

In this study, we demonstrated the molecular mechanisms of TGF-β1 induction as well as proteolytic activation in HCV (JFH-1)-infected cells. Our studies showed the synthesis and secretion of TGF-β1 in HCV-infected cells which was reduced in the presence of Ca(2+) chelators, an inhibitor of mitochondrial Ca(2+) uptake, and antioxidants. We also showed that the expression of HCV NS proteins NS3/4A, and NS5A can induce TGF-β1 by cell-based luciferase assay. Furthermore, mutational analysis revealed that the functionally active protease domain of NS3 and N-terminus domain of NS5A are required for TGF-β1 activity. Using siRNA approach we demonstrated that HCV-induced furin and thrombospondin-1 (TSP-1) are involved in the proteolytic activation of TGF-β1. Our results also suggest that TGF-β1 positively regulates HCV RNA replication. Collectively, these observations provide insight into the mechanism of TGF-β1 activation, which likely manifest in liver fibrosis associated with hepatitis C infection.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.virol.2010.12.051DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073624PMC
April 2011
-->