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Tsai W-Y, Tseng AC, Chen G-H, Hsieh S-C, Balmaseda A, Nerurkar VR, Harris E, Wang W-K
Microbiology spectrum
2025-07-01
PMID: 40401969
Antibodies, Viral
Child
Child, Preschool
Female
HIPC 2 (2015)
Humans
Infant
Male
Nicaragua
Viral Envelope Proteins
West Nile Fever
West Nile virus
Zika Virus
Zika Virus Infection
Abstract:
[{'@Label': 'UNLABELLED', '#text': 'Since its introduction to the Western Hemisphere in 1999 in New York City, West Nile virus (WNV) has spread throughout the continental USA and moved into Canada, Mexico, Caribbean, and Central and South Americas. While WNV has caused ~7 million human infections and >59,000 cases in the USA and >6,000 cases in Canada, only few human cases have been reported in Latin America. Due to the cross-reactivity of anti-envelope antibodies, the detection of WNV infection by serology to explore its epidemiology in Latin America, where multiple flaviviruses co-circulate, remains a challenge. Previously, we reported that anti-premembrane (prM) antibodies can distinguish between four flavivirus (WNV, dengue, Zika, and yellow fever viruses) infections. In this study, we examined 73 samples from 40 Zika cases from a pediatric cohort in Nicaragua using Western blot analysis and detected anti-prM antibodies to WNV in three participants in samples collected between 2016 and 2017, suggesting previous WNV infection prior to ZIKV infection. Analysis of available archived samples revealed anti-WNV prM antibodies in the earliest samples (2007-2009), which were further confirmed by plaque reduction neutralization test, suggesting that they were infected by WNV prior to 2007-2009. Our report of WNV infection in three Nicaraguan children, corresponding to a seropositive rate of 7.5%, highlights the transmission of WNV in humans in Central America prior to 2007. Future studies with improved serological tests for WNV surveillance in Latin America are needed to enhance our understanding of the epidemiology and transmission of WNV in the Western Hemisphere.'}, {'@Label': 'IMPORTANCE', '@NlmCategory': 'OBJECTIVE', '#text': 'Since its arrival to North America in 1999, West Nile virus (WNV) has caused multiple outbreaks in birds and humans, with thousands of human cases in the USA and Canada, whereas in Latin America, WNV has mainly been detected in birds and horses with few human cases. Due to cross-reactivity of anti-envelope antibodies among different flaviviruses, detection of WNV infection by serology to explore its epidemiology in Latin America remains a challenge. Previously, we reported that anti-premembrane antibodies can discriminate four flavivirus infections using Western blot analysis. Based on anti-WNV premembrane antibodies and confirmation by neutralization test, we report three Nicaraguan children with WNV infection, corresponding to a seropositive rate of 7.5%. Our findings underscore the transmission of WNV in humans in Central America and the application of improved seroepidemiological tools to address the knowledge gaps on the prevalence and distribution of WNV in Latin America and the Western Hemisphere.'}]
Johnson MM, Kaushik A, Kline OA, Smith EM, Zhou X, Pat Y, Buergi L, Aguilera J, Alkotob S, Simonin EM, Favaro A, Couto M, Bennett O, Chinthrajah RS, Parsons E, Shamji M, Burke M, Bondy M, Akdis M, Akdis CA, Nadeau KC
Nature medicine
2025-06-26
PMID: 40571754
HIPC 3 (2022)
Stanford
Abstract:
Exposure to fire smoke has become a global health concern and is associated with increased morbidity and mortality. There is a lack of understanding of the specific immune mechanisms involved in smoke exposure, with preventive and targeted interventions needed. After exposure to fire smoke, which includes PM2.5, toxic metals and perfluoroalkyl and polyfluoroalkyl substances, epidemiology-based studies have demonstrated increases in respiratory (for example, asthma exacerbation), cardiac (for example, myocardial infarction, arrhythmias), neurological (for example, stroke) and pregnancy-related (for example, low birthweight, premature birth) outcomes. However, mechanistic studies exploring how smoke exposure disrupts cellular homeostasis are lacking. Therefore, we collected blood from smoke-exposed individuals (n = 31) and age-matched and sex-matched non-smoke-exposed controls (n = 29), and investigated these complex interactions using a single-cell exposomic approach based on both methylation and mass cytometry. Overall, our data demonstrated a strong association between smoke exposure and methylation at 133 disease-relevant gene loci, while immunophenotyping showed increased homing and activation biomarkers. We developed an application of mass cytometry to analyze single-cell/metal binding and found, for example, increased levels of mercury in dead cells and cadmium in the live and dead cell populations. Moreover, mercury levels were associated with years of smoke exposure. Several epigenetic sites across multiple chromosomes were associated with individual toxic metal isotopes in single immune cells. Our methods for detecting the effect of smoke exposure at the single-cell level and the study results may help to determine the timing of exposure and identify specific molecular targets that could be modified to prevent and manage exposure to smoke.
Ratnasiri K, Mach SN, Blish CA, Khatri P
bioRxiv : the preprint server for biology
2025-06-08
PMID: 40501846
HIPC 3 (2022)
Stanford
Abstract:
Traditional differential gene expression methods are limited for analysis of single cell RNA-sequencing (scRNA-seq) studies that use paired repeated measures and matched cohort designs. Many existing approaches consider cells as independent samples, leading to high false positive rates while ignoring inherent sampling structures. Although pseudobulk methods address this, they ignore intra-sample expression variability and have higher false negatives rates. We propose a novel meta-analysis approach that accounts for biological replicates and cell variability in paired scRNA-seq data. Using both real and synthetic datasets, we show that our method, single-cell MetaIntegrator (https://github.com/Khatri-Lab/scMetaIntegrator), provides robust effect size estimates and reproducible p-values.
Jasset OJ, Lopez Zapana PA, Bahadir Z, Shook L, Dennis M, Gilbert E, Liu ZA, Yinger RV, Bald C, Bradford CG, Silfen AH, Klein SL, Pekosz A, Permar S, Konnikova L, Yonker LM, Lauffenburger D, Nelson A, Elovitz MA, Edlow AG
American journal of obstetrics and gynecology
2025-06-01
PMID: 39515450
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Immport Dataset Available
SDY2917
Adult
Antibodies, Viral
Female
Fetal Blood
Gestational Age
HIPC 3 (2022)
Humans
Immunity, Maternally-Acquired
Infant
Infant, Newborn
Male
Massachusetts Institute of technology
Maternal-Fetal Exchange
Placenta
Pregnancy
Pregnancy Complications, Infectious
Prospective Studies
Respiratory Syncytial Virus Infections
Respiratory Syncytial Virus, Human
Respiratory Syncytial Virus Vaccines
Time Factors
Vaccination
Abstract:
[{'@Label': 'BACKGROUND', '@NlmCategory': 'BACKGROUND', '#text': 'Respiratory syncytial virus is associated with significant neonatal and infant morbidity and mortality. Maternal bivalent respiratory syncytial virus prefusion F respiratory syncytial virus vaccination to protect neonates and infants was approved in September 2023 for administration between 32+0 and 36+6 weeks to protect neonates and infants. This approved timeframe is narrower than the 24 to 36 week window evaluated in the clinical trial, due to the possible association between preterm birth and vaccine administration. Currently, data are lacking on how maternal vaccine timing within the approved window affects the transfer of antibodies from mother to fetus, critical information that could influence clinical practice.'}, {'@Label': 'OBJECTIVE', '@NlmCategory': 'OBJECTIVE', '#text': 'We sought to examine how gestational age at vaccination and time elapsed from maternal respiratory syncytial virus vaccination to delivery impacted transfer of maternal antibodies measured in the umbilical cord at delivery and in peripheral blood of 2-month infants. We also examined differences in maternal and cord respiratory syncytial virus antibody levels achieved by vaccination vs natural RSV infection.'}, {'@Label': 'STUDY DESIGN', '@NlmCategory': 'METHODS', '#text': 'A prospective cohort study was conducted at 2 academic medical centers between September 20, 2023 and March 21, 2024, enrolling 124 individuals who received the respiratory syncytial virus vaccine during pregnancy. Infant capillary blood was collected at 2 months of age from 29 of the infants. Maternal and cord immunoglobulin G levels achieved by respiratory syncytial virus vaccination were compared to those associated with maternal natural respiratory syncytial virus infection, using banked blood from 20 maternal:cord dyads collected prior to the availability of the maternal respiratory syncytial virus vaccine. Levels of immunoglobulin G against respiratory syncytial virus strain A2 and B fusion (F) and attachment (G) proteins and against pertussis toxin (as a comparator antigen from a vaccine routinely administered earlier in pregnancy) were measured using a Binding Antibody Multiplex Assay. Differences in titers between vaccination and natural infection were examined using Wilcoxon rank-sum test. Differences in cord:maternal transfer ratios and 2-month infant antibody levels by timing of maternal vaccination were evaluated by Kruskal-Wallis testing.'}, {'@Label': 'RESULTS', '@NlmCategory': 'RESULTS', '#text': 'Maternal respiratory syncytial virus vaccination resulted in significantly higher maternal and cord antirespiratory syncytial virus F antibody levels than natural infection (5.72 vs 4.82 log10 mean fluorescence intensity, P<.0001 maternal; 5.81 vs 5.03 log10 mean fluorescence intensity, P<.0001 cord). Maternal vaccination 2 to 3 weeks and 3 to 4 weeks prior to delivery was associated with significantly lower cord:maternal transfer ratios than were observed when vaccination occurred >5 weeks prior to delivery (P=.03 for 2-3 weeks, P=.007 for 3-4 weeks), and significantly lower transfer ratios than observed for pertussis vaccination administered prior to 30 weeks of gestation (P=.008 for 2-3 weeks, P=.03 for 3-4 weeks, similar at >4 weeks).'}, {'@Label': 'CONCLUSION', '@NlmCategory': 'CONCLUSIONS', '#text': 'Vaccine administration earlier in the approved 32 to 36 week window (at least 5 weeks prior to delivery) results in the highest transplacental transfer of maternal antibodies to the neonate. These results should inform the counseling of pregnant individuals on optimal vaccination timing.'}]
Jones DC, Elz AE, Hadadianpour A, Ryu H, Glass DR, Newell EW
Nature methods
2025-06-01
PMID: 40404994
Algorithms
Carcinoma, Renal Cell
CD8-Positive T-Lymphocytes
Chemokine CXCL13
Computational Biology
Computer Simulation
Gene Expression Profiling
HIPC 2 (2015)
HIPC 3 (2022)
Humans
Kidney Neoplasms
Lymphocytes, Tumor-Infiltrating
Neutrophils
Seattle Children's Research Institute
Single-Cell Analysis
Transcriptome
Tumor Microenvironment
Abstract:
Single-cell spatial transcriptomics promises a highly detailed view of a cell's transcriptional state and microenvironment, yet inaccurate cell segmentation can render these data murky by misattributing large numbers of transcripts to nearby cells or conjuring nonexistent cells. We adopt methods from ab initio cell simulation, in a method called Proseg (probabilistic segmentation), to rapidly infer morphologically plausible cell boundaries. Benchmarking applied to datasets generated by three commercial platforms shows superior performance and computational efficiency of Proseg when compared to existing methods. We show that improved accuracy in cell segmentation aids greatly in detection of difficult-to-segment tumor-infiltrating immune cells such as neutrophils and T cells. Last, through improvements in our ability to delineate subsets of tumor-infiltrating T cells, we show that CXCL13-expressing CD8+ T cells tend to be more closely associated with tumor cells than their CXCL13-negative counterparts in data generated from samples from patients with renal cell carcinoma.
Doni Jayavelu N, Qi JJ, Fourati S, Kheradmand F, Langelier CR, Ehrlich LIR, Diray-Arce J, Hoch A, Kraft M, Becker PM, Altman MC, Montgomery RR
American journal of respiratory cell and molecular biology
2025-06-01
PMID: 40444914
HIPC 1 (2010)
HIPC 2 (2015)
HIPC 3 (2022)
Yale University
Abstract:
None
Yin X, Pu Y, Yuan S, Pache L, Churas C, Weston S, Riva L, Simons LM, Cisneros WJ, Clausen T, Biddle G, Doss-Gollin S, Deming M, De Jesus PD, Kim HN, Fuentes D, Whitelock JM, Esko JD, Lord MS, Mena I, García-Sastre A, Hultquist JF, Frieman MB, Ideker T, Pratt D, ...
PLoS biology
2025-06-01
PMID: 40504864
Animals
COVID-19
HIPC 2 (2015)
Host-Pathogen Interactions
Humans
Proteomics
RNA, Small Interfering
SARS-CoV-2
Virus Replication
Abstract:
Defining the subset of cellular factors governing SARS-CoV-2 replication can provide critical insights into viral pathogenesis and identify targets for host-directed antiviral therapies. While a number of genetic screens have previously reported SARS-CoV-2 host dependency factors, most of these approaches relied on utilizing pooled genome-scale CRISPR libraries, which are biased toward the discovery of host proteins impacting early stages of viral replication. To identify host factors involved throughout the SARS-CoV-2 infectious cycle, we conducted an arrayed genome-scale siRNA screen. Resulting data were integrated with published functional screens and proteomics data to reveal (i) common pathways that were identified in all OMICs datasets-including regulation of Wnt signaling and gap junctions, (ii) pathways uniquely identified in this screen-including NADH oxidation, or (iii) pathways supported by this screen and proteomics data but not published functional screens-including arachionate production and MAPK signaling. The identified proviral host factors were mapped into the SARS-CoV-2 infectious cycle, including 32 proteins that were determined to impact viral replication and 27 impacting late stages of infection, respectively. Additionally, a subset of proteins was tested across other coronaviruses revealing a subset of proviral factors that were conserved across pandemic SARS-CoV-2, epidemic SARS-CoV-1 and MERS-CoV, and the seasonal coronavirus OC43-CoV. Further studies illuminated a role for the heparan sulfate proteoglycan perlecan in SARS-CoV-2 viral entry and found that inhibition of the non-canonical NF-kB pathway through targeting of BIRC2 restricts SARS-CoV-2 replication both in vitro and in vivo. These studies provide critical insight into the landscape of virus-host interactions driving SARS-CoV-2 replication as well as valuable targets for host-directed antivirals.
Ritacco DA, Shahnawaz H, Oduguwa A, Hawk J, Vizcaino B, Farber D, Gaudet RG
bioRxiv : the preprint server for biology
2025-05-19
PMID: 40475483
Columbia University
HIPC 2 (2015)
HIPC 3 (2022)
Abstract:
Lysosomal damage is an endogenous danger signal to the cell, but its significance for innate immunity and how specific signaling pathways are engaged by this stressor remain unclear. Here, we uncover an immune-inducible pathway that connects lysosomal damage to mitochondrial DNA (mtDNA) efflux and type I IFN production. Lysosomal damage elicits mitochondrial outer membrane permeabilization (MOMP) via BAK/BAX macropores; however, the inner mitochondrial membrane (IMM) prevents wholesale mtDNA release in resting cells. Priming with type II IFN (IFN-γ) induced the antibacterial effector apolipoprotein L-3 (APOL3), which upon transient lysosomal damage, targets mitochondria undergoing MOMP and selectively permeabilizes the IMM to enhance mtDNA release and activate cGAS/STING signaling. Biochemical and cellular reconstitution revealed that analogous to its bactericidal detergent-like mechanism, APOL3 solubilizes cardiolipin to permeabilize the IMM. Our findings illustrate how cells use an antibacterial protein to expedite the breakdown of endosymbiosis and facilitate a heightened response to injury and infection.
Narendra R, Lydon EC, Van Phan H, Spottiswoode N, Neyton LP, Diray-Arce J, Becker PM, Kim-Schulze S, Hoch A, Pickering H, van Zalm P, Cairns CB, Altman MC, Augustine AD, Bosinger S, Eckalbar W, Guan L, Jayavelu ND, Kleinstein SH, Krammer F, Maecker HT, Ozonoff A, ...
medRxiv : the preprint server for health sciences
2025-05-19
PMID: 40475132
HIPC 1 (2010)
HIPC 2 (2015)
HIPC 3 (2022)
Yale University
Abstract:
[{'@Label': 'BACKGROUND', '@NlmCategory': 'UNASSIGNED', '#text': 'Predicting mortality risk in patients with COVID-19 remains challenging, and accurate prognostic assays represent a persistent unmet clinical need. We aimed to identify and validate parsimonious transcriptomic signatures that accurately predict fatal outcomes within 48 hours of hospitalization.'}, {'@Label': 'METHODS', '@NlmCategory': 'UNASSIGNED', '#text': 'We studied 894 patients hospitalized for COVID-19 across 20 US hospitals and enrolled in the prospective Immunophenotyping Assessment in a COVID-19 Cohort (IMPACC) with peripheral blood mononuclear cells (PBMC) and nasal swabs collected within 48 hours of admission. Host gene expression was assessed by RNA sequencing, nasal SARS-CoV-2 viral load was measured by RT-qPCR, and mortality was assessed at 28 days. We first defined transcriptional signatures and biological features of fatal COVID-19, which we compared against mortality signatures from an independent cohort of patients with non-COVID-19 sepsis (n=122). Using least absolute shrinkage and selection operator (LASSO) regression in 70% of the COVID-19 cohort, we trained parsimonious prognostic classifiers incorporating host gene expression, age, and viral load. The performance of single and three-gene classifiers was then determined in the remaining 30% of the cohort and subsequently externally validated in an independent, contemporary COVID-19 cohort (n=137) with vaccinated patients.'}, {'@Label': 'RESULTS', '@NlmCategory': 'UNASSIGNED', '#text': 'Fatal COVID-19 was characterized by 4189 differentially expressed genes in the peripheral blood, representing marked upregulation of neutrophil degranulation, erythrocyte gas exchange, and heme biosynthesis pathways, juxtaposed against downregulation of adaptive immune pathways. Only 7.6% of mortality-associated genes overlapped between COVID-19 and sepsis due to other causes. A COVID-specific three-gene peripheral blood classifier (CD83, ATP1B2, DAAM2) combined with age and SARS-CoV-2 viral load achieved an area under the receiver operating characteristic curve (AUC) of 0.88 (95% CI 0.82-0.94). A three-gene nasal classifier (SLC5A5, CD200R1, FCER1A), in comparison, yielded an AUC of 0.74 (95% CI 0.64-0.83). Notably the expression of OLAH alone, a gene recently implicated in severe viral infection pathogenesis, yielded an AUC of 0.86 (0.79-0.93). Both peripheral blood classifiers demonstrated comparable performance in vaccinated patients from an independent external validation cohort (AUCs 0.74-0.80).'}, {'@Label': 'CONCLUSIONS', '@NlmCategory': 'UNASSIGNED', '#text': 'A three-gene peripheral blood signature, as well as OLAH alone, accurately predict COVID-19 mortality early in hospitalization, including in vaccinated patients. These parsimonious blood- and nasal-based classifiers merit further study as accessible prognostic tools to guide triage, resource allocation, and early therapeutic interventions in COVID-19.'}]
Davis-Porada J, Tozlu C, Aiello C, Apostolidis SA, Bar-Or A, Bove R, Espinoza DA, Ferreira Brito S, Jacobs D, Kakara M, Onomichi K, Ricci A, Sabatino JJ, Walker E, Wherry EJ, Zhang L, Zhu W, Xia Z, De Jager P, Wesley SF, Straus Farber R, Farber DL
NPJ vaccines
2025-05-17
PMID: 40382362
Columbia University
HIPC 2 (2015)
HIPC 3 (2022)
Abstract:
Immune-mediated protection generated to COVID-19 mRNA vaccines is associated with anti-Spike (S) protein neutralizing antibodies. However, humoral immunity is compromised in B cell depleting (BCD) therapies, used to treat autoimmune diseases such as Multiple Sclerosis (MS). To study the effect of BCD on the durability and protective efficacy of vaccine-induced immunity, we evaluated S-reactive antibodies and T cell responses 1-70 weeks post-vaccination in MS cohorts treated with BCD compared to non-BCD therapies from four centers. BCD-treated participants had significantly reduced antibody levels and enhanced frequencies of S-reactive CD4+ and CD8+ memory T cells to COVID-19 vaccination compared to the non-BCD group, with some variations among different BCD formulations. T cell memory responses persisted up to 14 months post-vaccination in both BCD and non-BCD cohorts, who experienced similar clinical protection from COVID-19. Together, our results establish a critical role for T cell-mediated immunity in anti-viral protection independent of humoral immunity.
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