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Biology subjects

Crowe, T.

Publications and source records attributed to Crowe, T..

2 recordsLinked to original sources

From Bad to Worse: Carryover Effects Alter Responses to Multiple Stressors

Ecological responses to environmental stressors are increasingly shaped by interactions among anthropogenic and climatic drivers, yet the influence of prior exposure history on subsequent stress responses remains poorly integrated into multiple stressor ecology. Using the blue mussel (Mytilus edulis) as a model system, we experimentally tested whether prior exposure to environmental nanoplastics modifies responses to subsequent stressors, including copper contamination, nutrient enrichment, and salinity fluctuations, individually and in combination. Nanoplastic pre-exposure reduced survival across subsequent treatments and altered stressor interaction outcomes at the community level, shifting responses toward synergistic effects that amplified metabolic costs. These results demonstrate that exposure history can modify both the magnitude and direction of multi-stressor effects, with consequences extending beyond individual performance to ecosystem functioning. By incorporating temporal exposure dynamics into multiple stressor research, our study highlights how ecological responses to global change depend not only on the identity and intensity of stressors, but also on prior environmental conditions shaping subsequent organismal and ecosystem health status and responses.

ecology↗

Ebola's Hidden Target: Virus Transmission to and Accumulation within Skin

Ebola virus (EBOV), the causative agent of Ebola virus disease (EVD), remains one of WHOs top ten threats to global health. Infectious EBOV virions can be found on the surface of skin late during systemic infection and passed from the deceased through skin-to-skin contact. Here, we assess viral load and antigen expression in the skin of EBOV-infected non-human primates (NHP) and mouse adapted-EBOV (ma-EBOV) - infected mice and use the low containment viral model, rVSV/EBOV GP, to mechanistically define skin infection in mice. Viral RNA peaked within the skin proximal to the site of injection in EBOV-infected NHPs on day 6. In contrast, mouse skin sites distal to the site of ma-EBOV injection achieved maximal viral loads by day 3. At late times of infection, viral antigen-positive cells co-localized with markers for endothelial, stromal, and immune cells in the dermis. Epidermal cells within and surrounding hair follicles also harbored viral antigen, suggesting a potential mechanism of virus trafficking to the epidermal surface. Despite robust viral infection, distal skin sites of ma-EBOV-infected mice had low expression of proinflammatory stimulated genes. A similar cellular tropism was observed in the skin of mice infected with rVSV/EBOV GP, with discrete focal areas of intense infection. When virus was applied to the surface of gently abraded skin to remove the stratum corneum, epidermal keratinocytes were robustly infected, followed by systemic viral dissemination. To define cell surface receptors critical for virus trafficking to and replication within the skin, mice lacking the phosphatidylserine receptors were infected intraperitoneally with rVSV/EBOV GP. At day 3 of infection, skin distal to the site of infection of TIM-1 knock out (KO) mice had significantly lower levels of infectious virus than the control mice, suggesting that TIM-1 is essential for efficient distribution of virus to the skin. Our findings reveal that EBOV targets specific skin cell populations at late times of viral infection and that the host receptor TIM-1 is required for optimal viral dissemination.

microbiology↗