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|Title:||Temperature-dependent virus lifecycle choices may reveal and predict facets of the biology of opportunistic pathogenic bacteria.|
|Authors:||Egilmez, Halil I.|
Morozov, Andrew Yu
Clokie, Martha R. J.
Galyov, Edouard E.
|Publisher:||Nature Publishing Group|
|Citation:||Scientific Reports, 2018, 8, 9642|
|Abstract:||Melioidosis, a serious illness caused by Burkholderia pseudomallei, results in up to 40% fatality in infected patients. The pathogen is found in tropical water and soil. Recent findings demonstrated that bacterial numbers can be regulated by a novel clade of phages that are abundant in soil and water. These phages differentially infect their bacterial hosts causing lysis at high temperatures and lysogeny at lower temperatures. Thus seasonal and daily temperature variations would cause switches in phage-bacteria interactions. We developed mathematical models using realistic parameters to explore the impact of phages on B. pseudomallei populations in the surface water of rice fields over time and under seasonally changing environmental conditions. Historical records were used to provide UV radiation levels and temperature for two Thailand provinces. The models predict seasonal variation of phage-free bacterial numbers correlates with the higher risk of melioidosis acquisition during the "warm and wet" season. We find that enrichment of the environment may lead to irregular large amplitude pulses of bacterial numbers that could significantly increase the probability of disease acquisition. Our results suggest that the phages may regulate B. pseudomallei populations throughout the seasons, and these data can potentially help improve the melioidosis prevention efforts in Southeast Asia.|
|Rights:||Copyright © the authors, 2018. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
|Description:||Supplementary information accompanies this paper at https://doi.org/10.1038/s41598-018-27716-3|
|Appears in Collections:||Published Articles, Dept. of Infection, Immunity and Inflammation|
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