PLoS Neglected Tropical Diseases News

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A Peer-Reviewed Open-Access Journal
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Partnering to promote research where it matters

20 April 2017 - 9:00pm

by Michael Eisenstein

The yin and yang of leishmaniasis control

20 April 2017 - 9:00pm

by Shaden Kamhawi

Building on the success of soil-transmitted helminth control - The future of deworming

20 April 2017 - 9:00pm

by Peter Mark Jourdan, Antonio Montresor, Judd L. Walson

Guinea worm eradication: Progress and challenges— should we beware of the dog?

20 April 2017 - 9:00pm

by David Molyneux, Dieudonné P. Sankara

Neglected tropical diseases: A DFID perspective

20 April 2017 - 9:00pm

by Charlotte Watts

The <i>PLOS Neglected Tropical Diseases</i> decade

20 April 2017 - 9:00pm

by Peter Hotez, Donald A. P. Bundy

Cystic and alveolar echinococcosis: Successes and continuing challenges

20 April 2017 - 9:00pm

by Christine M. Budke, Adriano Casulli, Peter Kern, Dominique A. Vuitton

The role of 'omics' in the quest to eliminate human filariasis

20 April 2017 - 9:00pm

by Sara Lustigman, Alexandra Grote, Elodie Ghedin

Parasite genomics—Time to think bigger

20 April 2017 - 9:00pm

by Carlos Talavera-López, Björn Andersson

How to determine if a model is right for neglected tropical disease decision making

20 April 2017 - 9:00pm

by Bruce Y. Lee, Sarah M. Bartsch

Mathematical and computational modeling can transform decision making for neglected tropical diseases (NTDs) if the right model is used for the right question. Modeling can help better understand and address the complex systems involved in making decisions for NTD prevention and control. However, all models, modelers, and modeling are not the same. Thus, decision makers need to better understand if a particular model actually fits their needs. Here are a series of questions that a decision maker can ask when determining whether a model is right for him or her.

Human African trypanosomiasis control: Achievements and challenges

20 April 2017 - 9:00pm

by Serap Aksoy, Phillipe Buscher, Mike Lehane, Philippe Solano, Jan Van Den Abbeele

Sleeping sickness, also known as human African trypanosomiasis (HAT), is a neglected disease that impacts 70 million people living in 1.55 million km2 in sub-Saharan Africa. Since the beginning of the 20th century, there have been multiple HAT epidemics in sub-Saharan Africa, with the most recent epidemic in the 1990s resulting in about half a million HAT cases reported between 1990 and 2015. Here we review the status of HAT disease at the current time and the toolbox available for its control. We also highlight future opportunities under development towards novel or improved interventions.

A decade of arboviral activity—Lessons learned from the trenches

20 April 2017 - 9:00pm

by Ann M. Powers, Stephen H. Waterman

Progress and projections in the program to eliminate trachoma

20 April 2017 - 9:00pm

by Paul M. Emerson, Pamela J. Hooper, Virginia Sarah

<i>PLOS Neglected Tropical Diseases</i>: Ten years of progress in neglected tropical disease control and elimination … More or less

20 April 2017 - 9:00pm

by Peter Hotez, Serap Aksoy

This year PLOS Neglected Tropical Diseases (PLOS NTDs) celebrates its tenth anniversary following the publication of the first issue in 2007 [1]. When PLOS NTDs was founded, the framework of the neglected tropical diseases (NTDs) as an alternative to “other diseases” (as they were then referred to in the Millennium Development Goals) was just getting started—especially for Africa [2, 3]. In the decade since, PLOS NTDs has overseen enormous successes in NTD control and elimination. Here, we want to briefly review the ten year progress made towards the control or elimination of the diseases now identified by the WHO as NTDs. Many of the details are highlighted in PLOS NTDs papers cited here, but the summary information is based on the recently released Global Burden of Disease (GBD) Study 2015 (also launched with Gates Foundation support) that summarized past-decade changes in disease prevalence, mortality, or disability rates (from the years 2005 to 2015) [4–6], as well as the GBD Study 2013 that summarizes disease prevalence changes over a longer time horizon from 1990 to 2013 [7].

Glycosome biogenesis in trypanosomes and the de novo dilemma

20 April 2017 - 9:00pm

by Sarah Bauer, Meredith T. Morris

Trypanosomatid parasites, including Trypanosoma and Leishmania, are the causative agents of lethal diseases threatening millions of people around the world. These organisms compartmentalize glycolysis in essential, specialized peroxisomes called glycosomes. Peroxisome proliferation can occur through growth and division of existing organelles and de novo biogenesis from the endoplasmic reticulum. The level that each pathway contributes is debated. Current evidence supports the concerted contribution of both mechanisms in an equilibrium that can vary depending on environmental conditions and metabolic requirements of the cell. Homologs of a number of peroxins, the proteins involved in peroxisome biogenesis and matrix protein import, have been identified in T. brucei. Based on these findings, it is widely accepted that glycosomes proliferate through growth and division of existing organelles; however, to our knowledge, a de novo mechanism of biogenesis has not been directly demonstrated. Here, we review recent findings that provide support for the existence of an endoplasmic reticulum (ER)-derived de novo pathway of glycosome biogenesis in T. brucei. Two studies recently identified PEX13.1, a peroxin involved in matrix protein import, in the ER of procyclic form T. brucei. In other eukaryotes, peroxins including PEX13 have been found in the ER of cells undergoing de novo biogenesis of peroxisomes. In addition, PEX16 and PEX19 have been characterized in T. brucei, both of which are important for de novo biogenesis in other eukaryotes. Because glycosomes are rapidly remodeled via autophagy during life cycle differentiation, de novo biogenesis could provide a method of restoring glycosome populations following turnover. Together, the findings we summarize provide support for the hypothesis that glycosome proliferation occurs through growth and division of pre-existing organelles and de novo biogenesis of new organelles from the ER and that the level each mechanism contributes is influenced by glucose availability.