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Aggarwal, S.

Publications and source records attributed to Aggarwal, S..

At least 19 recordsLinked to original sources

A MultiOmics time-resolved systems map of gene regulation in Toxoplasma gondii

Understanding how T. gondii builds an invasion-competent cell has been limited by its rapid, asynchronous division cycle, incomplete gene function annotation, and studies that have examined one regulator or complex at a time. Here, we placed acute perturbation of 21 transcriptional and epigenetic factors, promoter occupancy, chromatin accessibility, and molecular validation on a common single-cell clock. The resulting consensus map links the lytic-cycle programs to candidate activating and repressive inputs, organizes genes into 108 co-regulated communities, and nominates regulatory partnerships that would not have emerged from any single data type. The work bridges three longstanding gaps: it resolves perturbation responses in cell-cycle time, distinguishes promoter occupancy from perturbation-linked regulation, and turns a large multidimensional dataset into an experimentally navigable map. We indeed confirmed known factor interactions such as MORC/HDAC3 and recovered combinations such as the Cdc5/SNIP1 and DMAP1/EPL1 as coregulatory nodes (that in other systems have been described to cooperate). Furthermore, we discovered a novel apicomplexan specific combination of AAF1/AP2XI-5 that provides mechanistic insights of the unique AP2 transcription factor family.

microbiology↗

Structural Insights into the Expanded Substrate Scope of a Cysteine-Dependent Hydrolase from Rhodococcus opacus for Polyethylene, Polypropylene, and Polystyrene Biodegradation

Microplastic pollution from homopolymers such as polypropylene (PP), polystyrene (PS), and polyethylene (PE) poses growing health and environmental concerns, highlighting the need for robust polymer-degrading biocatalysts. We previously identified a naturally occurring cysteine-dependent hydrolase (CsdH) from Rhodococcus opacus, featuring a unique Cys160-Lys127-Asp39 catalytic triad and providing a novel mechanism for polyethylene terephthalate (PET) degradation. In this study, we have determined crystal structures of CsdH in complex with PP, PS, PE, and styrene and demonstrated the potential of the enzyme to directly degrade these homopolymers into their respective low molecular weight degradation products using LC-MS. Structural analysis reveals that the enzyme retains a conserved principal access tunnel while undergoing subtle substrate-dependent changes to accommodate different substrates. The enzyme exhibited broad plastic degradation activity with the highest weight loss observed for PE, followed by PP and PS. SEM analysis reveals surface roughness, cracks and grooves, confirming polymer degradation. Further, these results corroborate through FTIR and TGA analysis. These findings establish a strong foundation for enzyme engineering and aim at developing efficient microplastic degradation.

biophysics↗

Age-associated transcriptional programs in tumor-associated macrophages are associated with tumor progression in HPV-negative oral cancer

Aging and tobacco exposure are major determinants of risk and outcome in HPV-negative oral cavity squamous cell carcinoma (OSCC), yet the cellular programs linking host factors to tumor immunity remain poorly defined. We reprocessed and reanalyzed previously published single-cell RNA-seq data from 19 HPV-negative OSCC tumors and we identified a robust age- and smoking-associated expansion of SPP1high tumor-associated macrophages (TAMs), accompanied by a shift toward a myeloid-dominant and lymphocyte-reduced tumor microenvironment. SPP1high TAMs exhibit a distinct transcriptional state enriched for extracellular-matrix remodeling and metabolic programs and reduced antigen-presentation pathways. They also express inflammatory chemokines such as CXCL2 and CXCL3 and down-regulate the cytotoxic mediator TNFSF10, suggesting a broadly protumor TAM phenotype. Ligand-receptor modeling suggests that SPP1high TAMs act as key communication hubs, with dominant SPP1-CD44 signaling to T-cell subsets. Transcription-factor analysis further implicates a POU2F1/POU2F2/SP1 module in maintaining this state. In the TCGA HNSCC cohort, the association between SPP1 expression and overall survival did not reach statistical significance after adjustment for age and tumor purity. These findings demonstrate that aging and tobacco exposure converge to expand an SPP1high TAM population that remodels the extracellular matrix and suppresses antitumor immunity, highlighting the SPP1-CD44 axis and its upstream regulators as potential therapeutic targets in high-risk OSCC.

immunology↗

FLASH Radiotherapy Mitigates Radiation-Induced Lymphopenia and Prevents Immunosuppression via Chk1-STAT3 Axis Modulation in a Preclinical Thoracic Irradiation Model

Background and AimsRadiation-induced lymphopenia (RIL) is a frequent side effect of conventional radiation therapy (CONV RT), due to the high radiosensitivity of circulating lymphocytes. Ultra-high dose rate "FLASH" RT may preferentially spare normal tissue while maintaining tumor control. This study evaluates the impact of single-fraction and multi-fraction thoracic FLASH RT on lymphocyte preservation, apoptosis, and immunosuppressive signaling in mice. MethodsWe compared the immunological impact of thoracic FLASH RT and CONV RT in C57BL/6 mice using single-fraction (17 Gy) and multi-fraction (2 Gy x 5) regimens using the Mobetron (IntraOp). Longitudinal blood sampling was performed at multiple time-points post-irradiation through facial vein bleed with flow cytometry analysis for CD4+, CD8+, CD19+, and NK cells to assess lymphocyte counts, apoptotic lymphocytes through Annexin V staining, and immune suppression by examining regulatory T cells (Tregs) and PD-1/PD-L1 expression. Mechanistic studies included immunofluorescence and Western blot analyses of splenic tissues to evaluate Chk1 and STAT3 signaling pathways. ResultsIn single-fraction RT, FLASH significantly reduced lung and heart fibrosis (p < 0.0001) at 28 weeks post-RT. The FLASH effect was also seen acutely on circulating immune cells, with significantly reduced lymphocyte apoptosis and accelerated recovery of CD4, CD8, CD3, NK, and B cell populations compared to CONV RT in both single-fraction and multi-fraction regimens. Conversely, CONV RT induced long-lasting increases in Tregs and sustained PD-1 and PD-L1 expression on T- and B-cells at 2- and 5-months post-irradiation in both fractionation regimens. Within the spleen, we also found CONV RT induced sustained activation of the Chk1-STAT3 pathway in CD45+ immune cells, which correlates with increased PD-1/PD-L1 expression. ConclusionFLASH RT mitigates RIL, reduces lymphocyte apoptosis, and prevents long-term immunosuppression by reduced activation of the Chk1-STAT3 pathway. These findings suggest FLASH RT may confer immunological advantages over CONV RT to enhance therapeutic efficacy.

cancer biology↗

Synapse-related protein alterations and estradiol deficiency associate with early Parkinsonism in female A53T-α-synuclein transgenic mice fed on a high-fat diet

Substantial evidence highlights the detrimental impact of a fat-rich diet on cognitive and emotional behaviour. Epidemiological studies have linked the consumption of saturated fat with an increased risk of Parkinsons disease (PD), whereas a low-fat or ketogenic diet is reported to improve both motor and non-motor symptoms. Several animal model studies further support these associations. However, the impact of a high-fat diet (HFD) on sex-specific behavioural alterations and the underlying molecular mechanism in PD remains poorly studied. In the present study, we investigated the impact of HFD on PD progression in a sex-specific manner using the A53T transgenic mouse model of PD. Behavioural and pathophysiological analyses revealed a faster onset and progression of PD-like phenotype in female mice exposed to HFD compared with the male mice. Proteomics profiling of brain tissues demonstrated positive enrichment of immune system-related pathways in males, while females exhibited considerable downregulation of synapse-associated pathways under HFD conditions. The reduced estradiol level was identified as a potential factor contributing to synaptic dysfunction and the subsequent early onset of PD in female mice. These findings provide novel insights into the sex-specific consequences of HFD on PD pathogenesis and highlight the role of estrogen-linked synaptic vulnerability in mediating diet-induced PD onset.

neuroscience↗

Decoding human lifespan from neural noise and explaining age-related changes in fractal dimension and gamma oscillations using fractional harmonic oscillator

Predicting human lifespan is a longstanding objective of biomedical research. Traditional statistical models estimate mortality risk or biological age but not lifespan. We propose a two-parameter model based on stochastic fractional harmonic oscillator for neural signals. The model computes maximum human lifespan using 1/f slope, the measure of neural power decay with frequency, which is indicative of neural noise. Using slope rate from electroencephalographic and electrocorticographic datasets, we estimate the mean lifetimes of healthy adults and epileptic patients as 76.9 and 69.7 years, resulting in 89.4% and 96.9% accuracy respectively. Additionally, the present model resolves the inconsistency in age-related changes of fractal dimension (FD) and captures naturally the non-monotonic variation of stimulus-induced gamma power. Thus, the present model provides a simple way to estimate lifespan while explaining age-related changes in slope, FD and power simultaneously, thereby, paving the way for individualized lifetime measurements and unveiling fundamental principles governing life. One line SummaryWe build a two-parameter model for neural signals that predicts mean human lifespan through a single neural observable, that may lead to future individualized lifetime predictions along with unveiling fundamental principles of life.

neuroscience↗

Circulating Biomarkers for Therapeutic Response to Immune Checkpoint Inhibitor Therapy in Patients with Advanced Lung Cancer

Immune checkpoint inhibitors (ICIs) have demonstrated remarkable efficacy in the treatment of advanced lung cancer (ALC), but not all patients benefit. To identify responders, patient selection, categorization, and the identification of specific predictive biomarkers are crucial. Our research aims to identify circulating metabolites that could be used to stratify patients into potential responders prior to the initiation of ICIs and to monitor clinical response in real-time during treatment. In the discovery phase, plasma samples (n = 25) from ALC patients receiving ICIs were analyzed using unbiased metabolomics and validated in a distinct patient cohort (n = 39). Five potential biomarkers were identified (FC > 1.5, p 0.05, AUC 0.81-1), including Thiourea and a combined metabolite panel (CMP) consisting of sphingosine-1-phosphate, gentisic acid, glutathione, and 4-hydroxybutanone. Early on-treatment high plasma levels of Thiourea were significantly associated with 5-year progression-free survival [Hazard ratio (HR) = 0.038, 95% confidence interval (CI) = 0.013-0.107, p<0.001] and overall survival [HR = 0.048, 95% CI = 0.019-0.120, p<0.001]. Low levels of CMP early on treatment were significantly associated with progression-free survival [HR = 8.119, 95% CI: 3.767-17.501, p<0.001] and overall survival [HR = 7.367, 95% CI: 3.517-15.433, 3.517-15.433, p<0.001]. This predictive plasma metabolite panel could serve as promising circulating biomarkers for predicting the therapeutic response of ICIs in ALC patients.

cancer biology↗

Cytokine profiling identifies circulating IL-2, IL23 and sPD-L1 as prognostic biomarkers for treatment outcomes in Non-Small cell Lung Cancer patients undergoing anti-PD1 therapy

BackgroundThis study investigates the predictive potential of circulating cytokines for response and survival outcomes in patients with advanced non-small cell lung cancer (NSCLC) undergoing immune checkpoint inhibitor (ICI) therapy. Materials and MethodsA cohort of 64 patients with advanced NSCLC receiving ICI therapy were included. Baseline serum samples were collected prior to ICI initiation and profiled using a multiplex cytokine panel. Logistic regression, Cox regression, and Kaplan-Meier survival analysis were employed to assess associations between cytokine levels, therapeutic response, progression-free survival (PFS), and overall survival (OS). Gene expression levels of key cytokines were validated in peripheral blood mononuclear cells (PBMCs) using quantitative real-time PCR. ResultsElevated baseline levels of IL-2, IL-23, and sPD-L1 were significantly associated with clinical response to ICI therapy. Among these, sPD-L1 emerged as an independent predictor of response (AUC = 0.87). Multivariate Cox regression showed IL-2 (HR = 0.67), sPD-L1 (HR = 0.15), and IL-23 (HR = 1.18) were significantly associated with PFS and also predictive of OS. Notably, combined profiling of IL-2 and sPD-L1 enhanced predictive power (AUC = 0.95 for both PFS and OS). RT-PCR analysis of PBMCs corroborated these findings, confirming upregulation of IL-2 in responders and elevated IL-23 expression in non-responders. ConclusionBaseline cytokine profiling particularly of IL-2, sPD-L1, and IL-23 provides important prognostic and predictive information in advanced NSCLC patients undergoing ICI therapy. These biomarkers may facilitate more personalized approaches to immunotherapy and guide clinical decision-making.

cancer biology↗

Revealing the impact of Pseudomonas aeruginosa quorum sensing molecule 2'-aminoacetophenone on human bronchial-airway epithelium and pulmonary endothelium using a human airway-on-a-chip

Pseudomonas aeruginosa (PA) causes severe respiratory infections utilizing multiple virulence functions. Our previous findings on PA quorum sensing (QS)-regulated small molecule, 2-aminoacetophenone (2-AA), secreted by the bacteria in infected tissues, revealed its effect on immune and metabolic functions favouring a long-term presence of PA in the host. However, studies on 2-AAs specific effects on bronchial-airway epithelium and pulmonary endothelium remain elusive. To evaluate 2AAs spatiotemporal changes in the human airway, considering endothelial cells as the first point of contact when the route of lung infection is hematogenic, we utilized the microfluidic airway-on-chip lined by polarized human bronchial-airway epithelium and pulmonary endothelium. Using this platform, we performed RNA-sequencing to analyse responses of 2-AA-treated primary human pulmonary microvascular endothelium (HPMEC) and adjacent primary normal human bronchial epithelial (NHBE) cells from healthy female donors and potential cross-talk between these cells. Analyses unveiled specific signaling and biosynthesis pathways to be differentially regulated by 2-AA in epithelial cells, including HIF-1 and pyrimidine signaling, glycosaminoglycan, and glycosphingolipid biosynthesis, while in endothelial cells were fatty acid metabolism, phosphatidylinositol and estrogen receptor signaling, and proinflammatory signaling pathways. Significant overlap in both cell types in response to 2-AA was found in genes implicated in immune response and cellular functions. In contrast, we found that genes related to barrier permeability, cholesterol metabolism, and oxidative phosphorylation were differentially regulated upon exposure to 2-AA in the cell types studied. Murine in-vivo and additional in vitro cell culture studies confirmed cholesterol accumulation in epithelial cells. Results also revealed specific biomarkers associated with cystic fibrosis and idiopathic pulmonary fibrosis to be modulated by 2-AA in both cell types, with the cystic fibrosis transmembrane regulator expression to be affected only in endothelial cells. The 2-AA-mediated effects on healthy epithelial and endothelial primary cells within a microphysiological dynamic environment mimicking the human lung airway enhance our understanding of this QS signaling molecule. This study provides novel insights into their functions and potential interactions, paving the way for innovative, cell-specific therapeutic strategies to combat PA lung infections.

molecular biology↗

IL-1R1 Blockade Enhances CD40 Agonist-Mediated Immune Responses but Fails to Increase Efficacy or Mitigate Hepatotoxicity in Pancreatic Cancer

Pancreatic ductal adenocarcinoma (PDAC) has a poor survival rate and limited treatments. Agonistic CD40 antibodies are promising, but clinical trials have shown only modest efficacy and significant hepatotoxicity. We previously reported that IL-1 pathway blockade enhances agonistic CD40 antibody efficacy against melanoma by depleting polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs; CD11b+Ly6C+Ly6G+). Because PMN-MDSCs also cause liver toxicity, we investigated the impact of IL-1R1 blockade on the efficacy and toxicity of agonistic CD40 antibody therapy in PDAC. Agonistic CD40 antibody therapy induced immune activation and significantly prolonged survival in orthotopic PDAC-bearing mice. IL-1R1 blockade monotherapy downregulated innate and adaptive immune response and exacerbated tumor growth. Although combination therapy upregulated several immune-related pathways and boosted innate and adaptive immune responses. IL-1R1 blockade failed to improve the overall antitumor efficacy of agonistic CD40 antibody therapy and exacerbated liver toxicity. Ly6G+ cell depletion in mice reduced the efficacy of agonistic CD40 antibody therapy, suggesting that Ly6G immune cells (PMN-MDSCs or neutrophils) exhibit an antitumor rather than immunosuppressive role in PDAC. Our findings underscore the complex role of IL-1 signaling in modulating immune responses in PDAC and caution against pursuing IL-1R1 blockade, either as monotherapy or combined with agonistic CD40 antibodies, in clinical trials for PDAC.

cancer biology↗

Dynamics of Bacterial and Viral Transmission in Experimental Microbiota Transplantation

Mouse models are vital tools for discerning the relative contributions of host and microbial genetics to disease, often requiring the transplantation of microbiota between different mouse strains. Transfer methods include antibiotic treatment of recipients and colonization using either co-housing with donors or the transplantation of fecal or cecal donor material. However, the efficiency and dynamics of these methods in reconstituting recipients with donor microbes is not well understood. We thus directly compared co-housing, fecal transplantation, and cecal transplantation methods. Donor mice from Taconic Biosciences, possessing distinct microbial communities, served as the microbial source for recipient mice from Jackson Laboratories, which were treated with antibiotics to disrupt their native microbiota. We monitored bacterial and viral populations longitudinally over the course of antibiotics treatment and reconstitution using 16S rRNA gene sequencing, quantitative PCR, and shotgun sequencing of viral-like particles. As expected, antibiotic treatment rapidly depleted microbial biomass and diversity, with slow and incomplete natural recovery of the microbiota in non-transplanted control mice. While all transfer methods reconstituted recipient mice with donor microbiota, co-housing achieved this more rapidly for both bacterial and viral communities. This study provides valuable insights into microbial transfer methods, enhancing reproducibility and informing best practices for microbiota transplantation in mouse models.

microbiology↗

Branched DNA Processing by a Thermostable CAS-Cas4 from Thermococcus onnurineus: Expanding Biochemical Landscape of Nuclease Activity

The adaptive immune function of CRISPR-Cas systems in bacteria and archaea is mediated through CRISPR-Associated Proteins (Cas). The adaptation module, typically involving Cas1, Cas2, and Cas4, helps integrate viral "spacer" sequences into the host genome. Cas4 proteins are classified into two types based on neighboring genes: CAS-Cas4, flanked by other cas genes, and Solo-Cas4, which exist independently. While CAS-Cas4 proteins are implicated in adaptation, they remain biochemically uncharacterized in archaea, unlike archaeal Solo-Cas4 proteins. This study biochemically characterizes TON_0321, a CAS-Cas4 protein from the Type IV-C CRISPR cassette of Thermococcus onnurineus. TON_0321 exhibits 5' to 3' exonuclease activity and unique structure-dependent endonuclease activity, shedding light on CAS-Cas4 functional diversity. A distinct spatial organization of the catalytic site, angled with the positively charged patch on the protein surface, enables TON_0321 to recognize branching points in DNA substrates. Furthermore, this spatial arrangement facilitates cleavage 2 to 3 nucleotides away from the branch point in the 5' direction, demonstrating structure-specific endonuclease activity.

biochemistry↗

Oxidative Injury to Lung Mitochondrial DNA is a Key Contributorfor the Development of Chemical Lung Injury

The mechanisms and extent to which inhalation of oxidant gases damage the mitochondrial genome contributing to the development of acute and chronic lung injury have not been investigated. C57BL/6 mice exposed to chlorine (Cl2) gas and returned to room air, developed progressive loss of lung DNA glycosylase OGG1, significant oxidative injury to mtDNA, decreased intact lung mitochondrial (mt) DNA, generation of inflammatory pathway by DAMPs causing airway and alveolar injury with significant mortality. Global proteomics identified over 1400 lung proteins with alteration of key mitochondrial proteins at 24 h post Cl2 exposure. Intranasal instillation of a recombinant protein containing mitochondrial targeted OGG1 (mitoOGG1) post exposure, decreased oxidative injury to mtDNA, lung mitochondrial proteome, severity of the acute and chronic lung injury and increased survival. These data show that injury to the mt-genome is a key contributor to the development of acute and chronic lung injury.

physiology↗

Age-related changes in Higuchi's fractal dimension in healthy human EEG are anti-correlated with changes in oscillatory power and 1/f slope

Non-linear dynamical methods such as Higuchis fractal dimension (HFD) are often used to study the complexities of brain activity. In human electroencephalogram (EEG), while power in the gamma band (30-70 Hz) and the slope of the power spectral density (PSD) have been shown to reduce with healthy aging, there are conflicting findings regarding how HFD and other measures of complexity vary with aging. Further, the dependence of HFD on features obtained from PSD (such as gamma power and slope) has not been thoroughly probed. To address these issues, we computed time and frequency resolved HFD for EEG data collected from elderly population (N=217), aged between 50-88 years, for baseline (BL) eyes open state and during a fixation task in which visual grating stimuli that induce strong gamma oscillations were presented. During BL, HFD increased with age for frequencies up to 150 Hz, but surprisingly showed an opposite trend at higher frequencies. Interestingly, this change in HFD was opposite to the age-related change in PSD 1/f slope. Further, stimulus-related changes in HFD were anti-correlated with the changes in oscillatory power. However, age classification using HFD was slightly better than classification using spectral features (power and slope). Further, stimulus and age-related changes in HFD persisted even after normalization with surrogates, showing the effect of non-linear dynamics on HFD. Therefore, HFD could be jointly sensitive to various spectral features as well as some non-linearities not captured using spectral analysis, which could enhance our understanding of brain dynamics underlying healthy aging.

neuroscience↗

Skeletal Muscle Mitochondrial Dysfunction Mediated by Pseudomonas aeruginosa Quorum Sensing Transcription Factor MvfR: Reversing Effects with Anti-MvfR and Mitochondrial-Targeted Compounds

Sepsis and chronic infections with Pseudomonas aeruginosa, a leading "ESKAPE" bacterial pathogen, are associated with increased morbidity and mortality and skeletal muscle atrophy. The actions of this pathogen on skeletal muscle remain poorly understood. In skeletal muscle, mitochondria serve as a crucial energy source, which may be perturbed by infection. Here, using the well-established backburn and infection model of murine P. aeruginosa infection, we deciphered the systemic impact of the quorum sensing (QS) transcription factor MvfR by interrogating five days post-infection its effect on mitochondrial-related functions in the gastrocnemius skeletal muscle and the outcome of the pharmacological inhibition of MvfR function and that of the mitochondrial-targeted peptide, Szeto-Schiller 31 (SS-31). Our findings show that the MvfR perturbs ATP generation, oxidative phosphorylation (OXPHOS), and antioxidant response, elevates the production of reactive oxygen species, and promotes oxidative damage of mitochondrial DNA in the gastrocnemius muscle of infected mice. These impairments in mitochondrial-related functions were corroborated by the alteration of key mitochondrial proteins involved in electron transport, mitochondrial biogenesis, dynamics and quality control, and mitochondrial uncoupling. Pharmacological inhibition of MvfR using the potent anti-MvfR lead, D88, we developed, or the mitochondrial-targeted peptide SS-31 rescued the MvfR- mediated alterations observed in mice infected with the wild-type strain PA14. Our study provides insights into the actions of MvfR in orchestrating mitochondrial dysfunction in the skeletal murine muscle, and it presents novel therapeutic approaches for optimizing clinical outcomes in affected patients.

microbiology↗

Expanding and enriching the LncRNA gene landscape using the GeneCaRNA database

The GeneCaRNA human gene database is a member of the GeneCards Suite. It presents [~]280,000 human non-coding RNA genes, identified algorithmically from [~]690,000 RNAcentrals transcripts. This expands by [~]tenfold the ncRNA gene count relative to other sources. GeneCaRNA thus contains [~]120,000 long non-coding RNAs (LncRNAs, >200 bases long), including [~]100,000 novel genes. The latter have sparse functional information, a vast terra incognita for future research. LncRNA genes are uniformly represented on all nuclear chromosomes, with 10 genes on mitochondrial DNA. Data obtained from MalaCards, another GeneCards Suite member, finds 1,547 genes associated with 1 to 50 diseases. [~]15% of the associations portray experimental evidence, with cancers tending to be multigenic. Preliminary text mining within GeneCaRNA discovers interactions of LncRNA transcripts with target gene products, with 25% being ncRNAs and 75% proteins. GeneCaRNA has a biological pathways section, which at present shows 131 pathways for 38 LncRNA genes, a basis for future expansion. Finally, our GeneHancer database provides regulatory elements for [~]110,000 LncRNA genes, offering pointers for co-regulated genes and genetic linkages from enhancers to diseases. We anticipate that the broad vista provided by GeneCaRNA will serve as an essential guide for further LncRNA research in disease decipherment.

bioinformatics↗

Interferons and tuft cell numbers are bottlenecks for persistent murine norovirus infection

Noroviruses (NoVs) are a leading cause of viral gastroenteritis. Despite global clinical relevance, our understanding of how host factors, such as antiviral cytokines interferons (IFNs), modulate NoV population dynamics is limited. Murine NoV (MNoV) is a tractable in vivo model for the study of host regulation of NoV. A persistent strain of MNoV, CR6, establishes a reservoir in intestinal tuft cells for chronic viral shedding in stool. However, the influence of host innate immunity and permissive cell numbers on viral population dynamics is an open question. We generated a pool of 20 different barcoded viruses (CR6BC) by inserting 6-nucleotide barcodes at the 3 position of the NS4 gene and used this pool as our viral inoculum for in vivo infections of different mouse lines. We found that over the course of persistent CR6 infection, shed virus was predominantly colon-derived, and viral barcode richness decreased over time irrespective of host immune status, suggesting that persistent infection involves a series of reinfection events. In mice lacking the IFN-{lambda} receptor, intestinal barcode richness was enhanced, correlating with increased viral intestinal replication. IL-4 treatment, which increases tuft cell numbers, also increased barcode richness, indicating the abundance of permissive tuft cells to be a bottleneck during CR6 infection. In mice lacking type I IFN signaling (Ifnar1-/-) or all IFN signaling (Stat1-/-), barcode diversity at extraintestinal sites was dramatically increased, implicating different IFNs as critical bottlenecks at specific tissue sites. Of interest, extraintestinal barcodes were overlapping but distinct from intestinal barcodes, indicating that disseminated virus represents a distinct viral population than that replicating in the intestine. Barcoded viruses are a valuable tool to explore the influence of host factors on viral diversity in the context of establishment and maintenance of infection as well as dissemination and have provided important insights into how NoV infection proceeds in immunocompetent and immunocompromised hosts.

microbiology↗

Enhanced stimulus-induced and stimulus-free gamma in open-eye meditators

Visual stimuli induce "narrowband" gamma oscillations (30-70 Hz) that are linked to attention/binding and attenuate with aging and neurodegeneration. In contrast, meditation increases power in a broad frequency range (>25 Hz). However, the effect of meditation on stimulus-induced gamma is unknown. We recorded EEG from meditators and controls performing open-eye meditation while gamma-inducing stimuli were presented before, during and after meditation. We found that stimulus-induced gamma, like stimulus-free gamma, was stronger in meditators. Interestingly, both gamma signatures co-existed during meditation but were unrelated and prominent in occipital and fronto-temporal regions, respectively. Further, power spectral density (PSD) slope, which becomes shallower with aging, was steeper for meditators. Meditation could boost inhibitory mechanisms leading to stronger gamma and steeper PSDs, potentially providing protection against aging and neurodegeneration. One line summaryStimulus-induced and stimulus-free gamma are stronger in open-eye meditators.

neuroscience↗