Abstract. Along the southeastern coast of the United States of America (USA), the marsh rice rat (Oryzomys palustris) is the primary host for the hantavirus genotype Bayou. According to the socio-ecological model for a territorial, polygamous species, females should be distributed across space and time by habitat resources and predation risks, whereas males should space themselves according to the degree of female aggregation and reproductive synchrony. To investigate how females affect the male-male transmission paradigm of Bayou virus, rodents were captured, marked, released, and re-captured in two macrohabitat types across a 30-month period. Microhabitat cover variables were quantified around the individual trap stations. A geodatabase was created from habitat and rodent capture data and analysed in a geographical information system. The ratio of breeding to non-breeding females was ~1:1, with breeding females overly dispersed and non-breeding females randomly dispersed. Spatial analyses revealed both macro-and microhabitat preferences in females. Compared to sero-negatives, higher proportions of seropositive adult males were found consistently within closer proximities to breeding females but not to non-breeding females, indicating that male locations were not driven simply by habitat selection. Activities to acquire dispersed receptive females could be an important driver of Bayou virus transmission among male hosts. To date, socio-ecological theory has received little attention as an investigative framework for studying pathogen dynamics in small, solitary mammals. Herein, we describe an interdisciplinary effort providing a novel approach to elucidate the complexity of hantavirus trafficking and maintenance in rodent populations of a coastal marsh ecosystem.
Lewy body disorders are associated with hallmark inclusions containing aggregated forms of alpha‐synuclein. When alpha‐synuclein aggregates in the synapse, it may be transported along axonal microtubular tracks to the soma for degradation or deposition into insoluble inclusions. However, during this transportation, alpha‐synuclein aggregates may also adhere to the microtubules and impede the axonal transport of other cellular constituents. Axonal transport is known to depend upon the stability of the microtubule tracks, but the specific impact of alpha‐synucleinopathy on microtubular dynamicity is unclear. Here, we assessed markers of microtubule stabilization in olfactory bulb and amygdala samples harvested postmortem from men and women with Lewy body disorders and age‐matched control subjects. Unexpectedly, we observed that women showed higher levels of detyrosinated alpha‐tubulin (marker of microtubule stability) as well as higher levels of tyrosinated alpha‐tubulin (marker of non‐stabilized microtubules) compared to men. Second, the impact of microtubule stability on inclusion body formation is also poorly understood. Thus, we measured inclusion counts in primary hippocampal cultures treated with novel heterocyclic microtubule stabilizers and challenged with preformed alpha‐synuclein fibrils. As expected, the microtubule stabilizers reduced pathologically phosphorylated (pSer129) alpha‐synuclein+ inclusion counts, and the microtubule destabilizer nocodazole prevented this reduction in pathological inclusions. These collective data suggest that microtubule stability may influence the emergence of alpha‐synucleinopathy in experimental Lewy body disease.
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