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In the Americas, wild yellow fever (WYF) is an infectious disease that is highly lethal for some non-human primate species and non-vaccinated people. Specifically, in the Brazilian Atlantic Forest, Haemagogus leucocelaenus and Haemagogus janthinomys mosquitoes act as the major vectors. Despite transmission risk being related to vector densities, little is known about how landscape structure affects vector abundance and movement. To fill these gaps, we used vector abundance data and a model-selection approach to assess how landscape structure affects vector abundance, aiming to identify connecting elements for virus dispersion in the state of São Paulo, Brazil. Our findings show that Hg. leucocelaenus and Hg. janthinomys abundances, in highly degraded and fragmented landscapes, are mainly affected by increases in forest cover at scales of 2.0 and 2.5 km, respectively. Fragmented landscapes provide ecological corridors for vector dispersion, which, along with high vector abundance, promotes the creation of risk areas for WYF virus spread, especially along the border with Minas Gerais state, the upper edges of the Serra do Mar, in the Serra da Cantareira, and in areas of the metropolitan regions of São Paulo and Campinas.

White Spot Syndrome Virus (WSSV) is one of the main threats to farming Litopenaeus vannamei , the most important crustacean commercialized in aquaculture worldwide. Here, we performed RNA-seq analyses in hepatopancreas and muscle from WSSV-negative (healthy) and WSSV-positive (unhealthy) L. vannamei, previously exposed to the virus, to obtain new insights about the molecular basis of resistance to WSSV. We detected 71% of our reads mapped against the recently described L. vannamei genome. This is the first report mapping RNA-seq transcripts from shrimps exposed to WSSV against the species reference genome. Differentially expressed gene (DEG) analyses were performed for four independent comparisons, and 13,338 DEGs were identified. When the redundancies and isoforms were disregarded, we observed 8351 and 6514 DEGs, respectively. Interestingly, after crossing the data, we detected a common set of DEGs for hepatopancreas and healthy shrimps, as well as another one for muscle and unhealthy shrimps. Our findings indicate that genes related to apoptosis, melanization, and the Imd pathway are likely to be involved in response to WSSV, offering knowledge about WSSV defense in shrimps exposed to the virus but not infected. These data present potential to be applied in further genetic studies in penaeids and other farmed shrimp species.