@article{ajidm2015324,
author={{Mahmud-Al-Rafat, Abdullah and Sobhani, Mahbub-E- and Taylor-Robinson, Andrew W.},
title={Effects of Anthropogenic Events and Viral Persistence on Rodent Reservoirs of Hantavirus Infection: Understanding Host-Pathogen Interactions Facilitates Novel Approaches to Intervention Strategies},
journal={American Journal of Infectious Diseases and Microbiology},
volume={3},
number={2},
pages={77--86},
year={2015},
url={http://pubs.sciepub.com/ajidm/3/2/4},
issn={2328-4064},
abstract={Hantaviruses are primarily rodent-borne pathogens which have received considerable attention recently due to their high mortality rates in humans. In order to find the causes of rapid transmission and emergence of hantavirus-associated diseases anthropogenic changes are a priority. These include deforestation, urbanization, noise pollution, light pollution and electromagnetic fields, all of which have been shown to profoundly affect rodent physiology and immunology. Moreover, anthropogenic events promote human-rodent co-habitation and thereby provide a driver to increase rates of transmission and, by extrapolation, levels of infection in humans. Such environmental disruption acts as a chronic stressor to rodents and causes elevated concentrations of glucocorticoids, which are a major class of immunosuppressive hormone. Glucocorticoids are responsible for altering the immune tolerance of rodents, thereby rendering them susceptible to infection. Glucocorticoids induce regulatory T lymphocytes to reduce inflammatory and antiviral responses and to activate regulatory responses, principally through production of the cytokines interleukin-10 and transforming growth factor-¦Â to support viral persistence. In order to develop a low-cost intervention strategy for hantavirus infection consideration should be given to a systemic approach to therapy. This would both aim to achieve a reduction of anthropogenic stressors and to gain a greater understanding of host-pathogen interactions.},
doi={10.12691/ajidm-3-2-4}
publisher={Science and Education Publishing}
}