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Varroa destructor is a major pathogenic driver of the Western honeybee colony losses globally. Understanding the developmental regulation of V. destructor is critical to develop effective control measures. Development is a complex biological process regulated by numerous genes and long non-coding RNAs (lncRNAs); however, the underlying regulation of lncRNAs in the development of V. destructor remains unknown. In this study, we analyzed the RNA sequencing (RNA-Seq) data derived from the four stages of female V. destructor in the reproductive phase (i.e., egg, protonymph, deutonymph, and adult). The identified differentially expressed mRNAs and lncRNAs exhibited a stage-specific pattern during developmental transitions. Further functional enrichment established that fat digestion and absorption, ATP-binding cassette (ABC) transporters, mitogen-activated protein kinase (MAPK) signaling pathway, and ubiquitin-proteasome pathway play key roles in the maturation of female V. destructor. Moreover, the lncRNAs and mRNAs of some pivotal genes were significantly upregulated at the deutonymph stage, such as cuticle protein 65/6.4/63/38 and mucin 5AC, suggesting that deutonymph is the key stage of metamorphosis development and pathogen resistance acquisition for female V. destructor. Our study provides novel insights into a foundational understanding of V. destructor biology.

Toxoplasma gondii is a protozoan parasite with a remarkable neurotropism. We recently showed that T. gondii infection can alter the global metabolism of the cerebral cortex of mice. However, the impact of T. gondii infection on the metabolism of the cerebellum remains unknown. Here we apply metabolomic profiling to discover metabolic changes associated with T. gondii infection of the mouse cerebellum using ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Multivariate statistics revealed differences in the metabolic profiles between the infected and control mouse groups and between the infected mouse groups as infection advanced. We also detected 10, 22, and 42 significantly altered metabolites (SAMs) in the infected cerebellum at 7, 14, and 21 days post infection (dpi), respectively. Four metabolites [tabersonine, arachidonic acid (AA), docosahexaenoic acid, and oleic acid] were identified as potential biomarker or responsive metabolites to T. gondii infection in the mouse cerebellum. Three of these metabolites (AA, docosahexaenoic acid, and oleic acid) play roles in the regulation of host behavior and immune response. Pathway analysis showed that T. gondii infection of the cerebellum involves reprogramming of amino acid and lipid metabolism. These results showcase temporal metabolomic changes during cerebellar infection by T. gondii in mice. The study provides new insight into the neuropathogenesis of T. gondii infection and reveals new metabolites and pathways that mediate the interplay between T. gondii and the mouse cerebellum.

Toxoplasma gondii is an obligate intracellular parasite causing severe diseases in immunocompromised individuals and congenitally infected neonates, such as toxoplasmosis encephalitis and toxoplasmic chorioretinitis. This study aimed to determine whether serum metabolic profiling can (i) identify metabolites associated with oocyst-induced T. gondii infection and (ii) detect systemic metabolic differences between T. gondii -infected mice patients and controls. We performed the first global metabolomics analysis of mice serum challenged with 100 sporulated T. gondii Pru oocysts (Genotype II). Sera from acutely infected mice (11 days post-infection, dpi), chronically infected mice (33 dpi) and control mice were collected and analysed using LC-MS/MS platform. Following False Discovery Rate filtering, we identified 3871 and 2825 ions in ESI + or ESI ? mode, respectively. Principal Component Analysis (PCA) and Partial Least Squares Discriminant Analysis (PLS -DA) identified metabolomics profiles that clearly differentiated T. gondii -infected and -uninfected serum samples. Acute infection significantly influenced the serum metabolonme. Our results identified common and uniquely perturbed metabolites and pathways. Acutely infected mice showed perturbations in metabolites associated with glycerophospholipid metabolism, biosynthesis of amino acid, and tyrosine metabolism. These findings demonstrated that acute T. gondii oocyst induces a global perturbation of mice serum metabolonme, providing new insights into the mechanisms underlying systemic metabolic changes during early stage of T. gondii oocyst infection.

Toxoplasma gondii has a complex two-host life-cycle between intermediate host and definitive host. Understanding proteomic variations across the life-cycle stages of T. gondii may improve the understanding of molecular adaption mechanism of T. gondii across life-cycle stages, and should have implications for the development of new treatment and prevention interventions against T. gondii infection. Here, we utilized LC–MS/MS coupled with iTRAQ labeling technology to identify differentially expressed proteins (DEPs) specific to tachyzoite (T), bradyzoites-containing cyst (C) and sporulated oocyst (O) stages of the cyst-forming T. gondii Prugniuad (Pru) strain. A total of 6285 proteins were identified in the three developmental stages of T. gondii. Our analysis also revealed 875, 656, and 538 DEPs in O vs. T, T vs. C, and C vs. O, respectively. The up- and down-regulated proteins were analyzed by Gene Ontology enrichment, KEGG pathway and STRING analyses. Some virulence-related factors and ribosomal proteins exhibited distinct expression patterns across the life-cycle stages. The virulence factors expressed in sporulated oocysts and the number of up-regulated virulence factors in the cyst stage were about twice as many as in tachyzoites. Of the 79 ribosomal proteins identified in T. gondii, the number of up-regulated ribosomal proteins was 33 and 46 in sporulated oocysts and cysts, respectively, compared with tachyzoites. These results support the hypothesis that oocyst and cystic stages are able to adapt to adverse environmental conditions and selection pressures induced by the host's immune response, respectively. These findings have important implications for understanding of the developmental biology of T. gondii, which may facilitate the discovery of novel therapeutic targets to better control toxoplasmosis.