"Nutrient-fungi-host" tripartite interaction in cancer progression.

The human microbiome exhibits a profound connection with the cancer development, progression, and therapeutic response, with particular emphasis on its components of the mycobiome, which are still in the early stages of research. In this review, we comprehensively summarize cancer-related symbiotic and pathogenic fungal genera. The intricate mechanisms through which fungi impact cancer as an integral member of both gut and tissue-resident microbiomes are further discussed. In addition, we shed light on the pivotal physiological roles of various nutrients, including cholesterol, carbohydrates, proteins and minerals, in facilitating the growth, reproduction, and invasive pathogenesis of the fungi. While our exploration of the interplay between nutrients and cancer, mediated by the mycobiome, is ongoing, the current findings have yet to yield conclusive results. Thus, delving into the relationship between nutrients and fungal pathogenesis in cancer development and progression would provide valuable insights into anticancer therapy and foster precision nutrition and individualized treatments that target fungi from bench to bedside.

Dynamically adjustable SVEIR(MH) model of multiwave epidemics: Estimating the effects of public health measures against COVID-19.

The COVID-19 pandemic was characterized by multiple subsequent, overlapping outbreaks, as well as extremely rapid changes in viral genomes. The information about local epidemics spread and the epidemic control measures was shared on a daily basis (number of cases and deaths) via centralized repositories. The vaccines were developed within the first year of the pandemic. New modes of monitoring and sharing of epidemic data were implemented using Internet resources. We modified the basic SEIR compartmental model to include public health measures, multiwave scenarios, and the variation of viral infectivity and transmissibility reflected by the basic reproduction number R0 of emerging viral variants. SVEIR(MH) model considers the capacity of the medical system, lockdowns, vaccination, and changes in viral reproduction rate on the epidemic spread. The developed model uses daily infection reports for assessing the epidemic dynamics, and daily changes of mobility data from mobile phone networks to assess the lockdown effectiveness. This model was deployed to six European regions Baden-Württemberg (Germany), Belgium, Czechia, Lombardy (Italy), Sweden, and Switzerland for the first 2 years of the pandemic. The correlation coefficients between observed and reported infection data showed good concordance for both years of the pandemic (ρ = 0.84-0.94 for the raw data and ρ = 0.91-0.98 for smoothed 7-day averages). The results show stability across the regions and the different epidemic waves. Optimal control of epidemic waves can be achieved by dynamically adjusting epidemic control measures in real-time. SVEIR(MH) model can simulate different scenarios and inform adjustments to the public health policies to achieve the target outcomes. Because this model is highly representative of actual epidemic situations, it can be used to assess both the public health and socioeconomic effects of the public health measures within the first 7 days of the outbreak.

Revealing the characteristics of ZIKV infection through tissue-specific transcriptome sequencing analysis.

BACKGROUND: Recently, Zika virus (ZIKV) re-emerged in India and was potentially associated with microcephaly. However, the molecular mechanisms underlying ZIKV pathogenesis remain to be explored. RESULTS: Herein, we performed a comprehensive RNA-sequencing analysis on ZIKV-infected JEG-3, U-251 MG, and HK-2 cells versus corresponding uninfected controls. Combined with a series of functional analyses, including gene annotation, pathway enrichment, and protein-protein interaction (PPI) network analysis, we defined the molecular characteristics induced by ZIKV infection in different tissues and invasion time points. Data showed that ZIKV infection and replication in each susceptible organ commonly stimulated interferon production and down-regulated metabolic-related processes. Also, tissue-specific immune responses or biological processes (BPs) were induced after ZIKV infection, including GnRH signaling pathway in JEG-3 cells, MAPK signaling pathway in U-251 MG cells, and PPAR signaling pathway in HK-2 cells. Of note, ZIKV infection induced delayed antiviral interferon responses in the placenta-derived cell lines, which potentially explains the molecular mechanism by which ZIKV replicates rapidly in the placenta and subsequential vertical transmission occurs. CONCLUSIONS: Together, these data may provide a systemic insight into the pathogenesis of ZIKV infection in distinct human tissue-derived cell lines, which is likely to help develop prophylactic and therapeutic strategies against ZIKV infection.