Project description:Severe fever with thrombocytopenia syndrome (SFTS) is a new tick-borne infectious disease caused by a new SFTS virus (SFTSV). Due to its 12%-50% high fatality rate and the possibility of pandemic transmission, as well as no specific antiviral drugs for the treatment so far, SFTSV has been listed as one of the top 10 priority infectious diseases by the World Health Organization. Currently, there are rare studies of transcriptomic analysis for the patients infected with SFTSV, which makes it difficult to deeply understand the life cyle and pathogenicity of this virus. To explore the differences of transcripts after SFTSV infection, we performed a longitudinal sampling study to systematically investigate the chronological changes of viral load and transcriptomic and epigenetic characterization using white blood cells from SFTSV patients. The results showed significant changes in the expression of some genes from onset to recovery of SFTSV infection. Moreover, these differentially expressed genes showed good consistency in the three patients at different stages of treatment, which may contribute to the pathophysiology of SFTSV and thus lead to a breakthrough in SFTSV therapy. Moreover, by m6A-seq, we found some genes that might be regulated by m6A. This study in transcript changes and RNA modification may open a brand new direction to our understanding of SFTSV and play an important role in the drugs discovery for effective treatment.
Project description:This dataset contains longitudinal transcriptomic profiles of human fibroblasts across in-vitro aging and pharmacological modulation with Metformin and Rapamycin. Longitudinal sampling of human cells is inherently challenging. Thus, we model aging in non-proliferative fibroblast cultures maintained at confluency, which recapitulate key transcriptomic signatures of in-vivo aging. Four female donor fibroblast lines were cultured for six months in a non-proliferative state, with sampling every 30 days to capture pseudo-longitudinal transcriptomic changes. Parallel cultures were treated with the anti-aging compounds Metformin or Rapamycin over the same period to assess their impact on age-associated transcriptional trajectories. We compare transcriptomic aging changes of in-vitro aging to a cohort of donors from 20-90 years. In addition, stable fibroblast lines expressing the neuronal transcription factors Ngn2 and Ascl1 were generated, enabling direct conversion of fibroblasts into induced neurons (iNs) at baseline and after six months of in-vitro aging. This design allows integrative analyses of transcriptomic aging signatures across cell states and pharmacological interventions.