Abdullah Mahmud-Al-Rafat^{1, 2}, Mahbub -E-Sobhani¹, Andrew W. Taylor-Robinson^3,

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-β 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.

hantavirus, rodent, reservoir, viral persistence, anthropogenic event, glucocorticoid, regulatory T lymphocyte, anti-viral