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Russula griseocarnosa, an edible and medicinal mushroom abundant in nutrients and notable bioactivities, is predominantly grown in the broad-leaved forest with trees of the family Fagaceae in southern China. This species forms ectomycorrhizal associations with plant roots and cannot be artificially cultivated currently. Previous research indicates a strong correlation between the growth of R. griseocarnosa and factors such as the host plant, climate variables (specifically mean temperature and precipitation from June to October), and the rhizosphere microbiota of its habitat. However, comprehensive studies on the fundamental biology of this species are lacking. The interaction between R. griseocarnosa and its host plant, as well as the mechanisms underlying the microbial community dynamics within its habitat, remain ambiguous. The limited repertoire and diversity of carbohydrate-active enzymes (CAZymes) in R. griseocarnosa relative to saprophytic fungi may contribute to its recalcitrance to cultivation on synthetic media. The specific core enzyme and the substances provided by the host plant to facilitate growth are yet to be elucidated, posing a significant challenge in the artificial cultivation of R. griseocarnosa. The habitat of R. griseocarnosa harbours unique microbial communities, indicating the presence of potentially beneficial microorganisms that could be exploited for artificial propagation and conservation efforts. However, the lack of definitive functional verification experiments hinders the realization of this promising prospect. This review offers a comprehensive overview of the nutritional profile and health benefits of R. griseocarnosa, emphasizing recent developments in its isolation, molecular ecology, and artificial cultivation. Additionally, it explores prospective advancements in R. griseocarnosa research, aiming to enrich our foundational understanding for applied purposes and fostering progress in the realm of ectomycorrhizal edible mushrooms. [ABSTRACT FROM AUTHOR]

Macroautophagy/autophagy has been recognized as a central antiviral defense mechanism in plant, which involves complex interactions between viral proteins and host factors. Rhabdoviruses are single-stranded RNA viruses, and the infection causes serious harm to public health, livestock, and crop production. However, little is known about the role of autophagy in the defense against rhabdovirus infection by plant. In this work, we showed that Rice stripe mosaic cytorhabdovirus(RSMV) activated autophagy in plants and that autophagy served as an indispensable defense mechanism during RSMV infection. We identified RSMV glycoprotein as an autophagy inducer that interacted with OsSnRK1B and promoted the kinase activity of OsSnRK1B on OsATG6b. RSMV glycoprotein was toxic to rice cells and its targeted degradation by OsATG6b-mediated autophagy was essential to restrict the viral titer in plants. Importantly, SnRK1-glycoprotein and ATG6-glycoprotein interactions were well-conserved between several other rhabdoviruses and plants. Together, our data support a model that SnRK1 senses rhabdovirus glycoprotein for autophagy initiation, while ATG6 mediates targeted degradation of viral glycoprotein. This conserved mechanism ensures compatible infection by limiting the toxicity of viral glycoprotein and restricting the infection of rhabdoviruses. Abbreviations: AMPK: adenosine 5'-monophosphate (AMP)-activated protein kinase; ANOVA: analysis of variance; ATG: autophagy related; AZD: AZD8055; BiFC: bimolecular fluorescence complementation; BYSMV: barley yellow striate mosaic virus; Co-IP: co-immunoprecipitation; ConA: concanamycin A; CTD: C-terminal domain; DEX: dexamethasone; DMSO: dimethyl sulfoxide; G: glycoprotein; GFP: green fluorescent protein; MD: middle domain; MDC: monodansylcadaverine; NTD: N-terminal domain; OE: over expression; Os: Oryza sativa; PBS: phosphate-buffered saline; PtdIns3K: class III phosphatidylinositol-3-kinase; qRT-PCR: quantitative real-time reverse-transcription PCR; RFP: red fluorescent protein; RSMV: rice stripe mosaic virus; RSV: rice stripe virus; SGS3: suppressor of gene silencing 3; SnRK1: sucrose nonfermenting1-related protein kinase1; SYNV: sonchus yellow net virus; TEM: transmission electron microscopy; TM: transmembrane region; TOR: target of rapamycin; TRV: tobacco rattle virus; TYMaV: tomato yellow mottle-associated virus; VSV: vesicular stomatitis virus; WT: wild type; Y2H: yeast two-hybrid; YFP: yellow fluorescent protein. [ABSTRACT FROM AUTHOR]

Three prevalent SARS-CoV-2 variants of concern (VOCs) emerged and caused epidemic waves. It is essential to uncover advantageous mutations that cause the high transmissibility of VOCs. However, viral mutations are tightly linked, so traditional population genetic methods, including machine learning–based methods, cannot reliably detect mutations conferring a fitness advantage. In this study, we developed an approach based on the sequential occurrence order of mutations and the accelerated furcation rate in the pandemic-scale phylogenomic tree. We analyzed 3,777,753 high-quality SARS-CoV-2 genomic sequences and the epidemiology metadata using the Coronavirus GenBrowser. We found that two noncoding mutations at the same position (g.a28271−/u) may be crucial to the high transmissibility of Alpha, Delta, and Omicron VOCs although the noncoding mutations alone cannot increase viral transmissibility. Both mutations cause an A-to-U change at the core position −3 of the Kozak sequence of the N gene and significantly reduce the protein expression ratio of ORF9b to N. Using a convergent evolutionary analysis, we found that g.a28271−/u, S:p.P681H/R, and N:p.R203K/M occur independently on three VOC lineages, suggesting that coordinated changes of S, N, and ORF9b proteins are crucial to high viral transmissibility. Our results provide new insights into high viral transmissibility co-modulated by advantageous noncoding and nonsynonymous changes. [ABSTRACT FROM AUTHOR]

An effective immune response against human immunodeficiency virus or simian immunodeficiency virus (SIV) is critical in achieving control of viral replication. Here, we show in SIV-infected rhesus monkeys that an effective and durable SIV-specific cellular and humoral immunity is elicited by a vaccination with chemically inactivated SIV-pulsed dendritic cells. After three immunizations made at two-week intervals, the animals exhibited a 50-fold decrease of SIV DNA and a 1,000-fold decrease of SIV RNA in peripheral blood. Such reduced viral load levels were maintained over the remaining 34 weeks of the study. Molecular and cellular analyses of axillary and inguinal node lymphocytes of vaccinated monkeys revealed a correlation between decreased SIV DNA and RNA levels and increased SIV-specific T-cell responses. Neutralizing antibody responses were augmented and remained elevated. Inactivated whole virus-pulsed dendritic cell vaccines are promising means to control diseases caused by immuno- deficiency viruses., Author(s): Wei Lu (corresponding author) [1]; Xiaoxian Wu [3]; Yaozeng Lu [3]; Weizhong Guo [3]; Jean-Marie Andrieu [1, 2] The lack of functional virus-specific effector T lymphocytes and neutralizing antibodies [...]