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Human T-lymphotropic virus 1 (HTLV-1) integrates into host DNA, resulting in life-long infection that underlies malignancy, inflammatory disease, and early all-cause mortality. HTLV-1 subtype-C endures as an endemic infection in Central Australia, and is associated with pulmonary disease. The cellular and viral features driving HTLV-1c pathogenesis remain poorly understood. We recruited a cohort of 41 First Nations participants from Alice Springs Hospital in Central Australia. We analysed plasma biomarker sVCAM1, and three circulating CD4+ T-cell phenotypes by flow cytometry: Lung-homing (TLH, CCR4+CC49d+Integrinβ7-), regulatory T-cells (TREG, CCR4+CD49d-CD127-) and CCR4- (TCCR4-). We determined the proviral load by ddPCR. Haplotype resolved proviruses were assembled from 6 donors using single provirus amplification and long-read sequencing (SPA-ONT-seq). Analysis of CD4+ T-cell phenotypes and the proviral landscape was also performed in a humanised mouse model of HTLV-1c infection. All HTLV-1c+ participants showed expansion of chronically activated TLH cells. These cells were highly infected with HTLV-1c provirus and enriched in the lung tissue of humanised mice, confirming pulmonary trafficking. Despite extensive structural diversity in the proviral landscape, defective proviruses in participants with pulmonary disease preferentially retain virulence factor hbz. Defective proviruses were detected in the sputum of HTLV-1c+ participants. We discovered chimeric HTLV-1c:human proviruses containing internalised host DNA segments, and implicated them in modulating host gene expression. HTLV-1c likely contributes to pulmonary disease through lung-homing of chronically activated CD4+ T-cells harbouring defective proviruses that retain hbz. CD49d and hbz could represent potential therapeutic targets. Single-provirus sequencing revealed previously unrecognised structural complexity, including functional viral-host chimeras, with implications for HTLV-1 pathogenesis. This work was supported by NHMRC, Mater Foundation, ACH4, and Miller Foundation PhD Scholarship.
Failure of epilepsy pharmacotherapy is common, justifying efforts to identify optimal cell targets for advanced therapies. Genetic manipulations of the inhibitory system in principle offer a finely tuned intervention that cannot be achieved with a broad reduction of pyramidal neuron excitability. In this context, neuron-derived neurotrophic factor-expressing (NDNF+) interneurons evoke long-lasting GABAA and GABAB receptor-mediated inhibition. However, their contribution to restraining hyperexcitability during epileptiform activity remains unexplored. To address this, we employed calcium imaging, optogenetics, and chemogenetics in an NDNF-Cre mouse line to investigate how NDNF+ interneurons influence cortical and hippocampal hyperactivity and spontaneous seizures. We show that NDNF+ interneurons are actively recruited during interictal spikes and focal seizures, although more slowly than parvalbumin-positive interneurons (mean difference: 2.8 s, p = 0.023). Optogenetic hyperpolarisation of NDNF+ interneurons exacerbates epileptic discharges (normalised seizure-duration mean difference: 0.23, p = 0.0474), whereas their depolarisation suppresses focal seizures, even when the optogenetic stimulus is delayed by several seconds from seizure onset (normalized seizure-duration mean difference: -0.27, p = 0.03). This effect is largely mediated by GABAB receptors. Additionally, chemogenetic depolarisation of NDNF+ interneurons has an important anti-seizure effect in the hippocampus both ex vivo (normalised seizure-duration mean difference: -0.92, p < 0.001) and in vivo. Collectively, these findings establish NDNF+ neurons as key regulators of both cortical and hippocampal excitability even during epileptic activity, and identify them as promising cellular targets for the development of anti-seizure therapies. Epilepsy Research UK, Wellcome, the Medical Research Council, the Gatsby Charitable Foundation, and The Rosetrees Trust.
Despite effective suppression of HIV-1 replication by antiretroviral therapy (ART), persistent viral reservoirs prevent cure and necessitate lifelong treatment. While short-term dynamics of HIV-1 rebound following treatment interruption have been extensively studied, the longer-term consequences of immune perturbation and transient viraemia for reservoir quality and immune architecture remain incompletely understood. We leveraged a rare historical human cohort that experienced prolonged viral rebound during a dendritic cell-based therapeutic vaccine study as a "perturbation model" to explore HIV-1 reservoir characteristics and immune remodelling more than a decade after ART resumption. We combined functional inducible HIV-1 reservoir measurements with high-dimensional immune phenotyping and included comparator analyses using a separate cohort of eight individuals with sustained ART-mediated suppression. We observed higher inducible HIV-1 reservoir activity in nine participants from the Dendritic Cell-Tat, Rev, and Nef (DC-TRN) trial who previously experienced viral rebound and subsequently achieved viral re-suppression on long-term ART (p = 0.01). This increase in inducible HIV-1 reservoir activity occurred in the absence of major changes in total or intact proviral DNA (p = 0.99, and p = 0.35, respectively). Immune profiling suggested persistent differences in memory T cell phenotypes, after long-term re-suppression on ART, including enrichment of CXCR3-expressing central memory CD4+ T cells that positively correlated with inducible tat/rev msRNA expression (r2 = 0.54, p = 0.03). Together, these findings suggest that immune perturbation and viral rebound may be associated with persistent changes in HIV-1 reservoir inducibility and immune architecture after viral re-suppression. Our study highlights a possible increase in inducible HIV-1 reservoir activity associated with a CXCR3+ memory T cell phenotype, supporting further evaluation of reservoir quality endpoints, candidate immunophenotypic correlates, and long-term monitoring strategies in contemporary remission trials. This research was supported by grants from Aidsfonds (P-60602, P-263, P-53302, P-53601, P-60804), MRACE (EMC2020-083); Horizon Europe (681032); Health Holland (LSHM19100-SGF and EMCLSH19023), and NWO (ZonMW-40-44600-98-333).
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The re-emergence of orthopoxviruses, most notably mpox virus (MPXV), poses a growing global public health threat. Well-characterised murine anti-orthopoxvirus antibodies are clinically limited by anti-mouse antibody responses, while traditional sequence-based humanisation often impairs antigen-binding activity. We developed an experimentally validated structure-guided computational humanisation framework prioritising 3D architectural congruence over sequence identity, integrating Foldseek-based structural alignment and interface-residue constraints. We applied this framework to humanise two murine anti-orthopoxvirus antibodies (7D11, A27D7), with comprehensive in vitro and in vivo validation. Structural superimposition confirmed high conformational conservation between the humanised variants (POX1.1 and POX2.1) and their parental mAbs, with root mean square deviation (RMSD) values below 0.6 Å for all variable domains. Both humanised variants retained full epitope specificity with natural humanness profiles. POX1.1 showed enhanced neutralisation potency against vaccinia virus (VACV) and MPXV, compared with the parental 7D11. POX2.1 preserved the broad cross-reactive binding and the extracellular enveloped virion neutralising activity of the parental A27D7. In the lethal VACV mouse model, both monotherapies conferred significant prophylactic and therapeutic protection, reducing pulmonary viral loads and improving survival. The dual-targeting combination of POX1.1 and POX2.1 achieved markedly improved in vivo efficacy compared with individual antibodies, delivering 100% survival even when administered 2 days post-challenge. In the MPXV CAST/EiJ mouse model, the combination significantly reduced splenomegaly and MPXV DNA loads in plasma, spleen and lung tissues, effectively suppressing systemic viral dissemination. These findings establish that the structure-centric workflow enables efficient humanisation of well-characterised murine anti-orthopoxvirus antibodies, providing a validated framework to support the development of countermeasures for orthopoxvirus pandemic. This work was supported by the National Natural Science Foundation of China, the Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences, the Scientific Research Innovation Capability Support Project for Young Faculty and the National Science and Technology Major Project.
Extracellular adenosine triphosphate (ATP) signalling via purinergic receptors plays a key role in cochlear adaptation to loud sound. Traditionally, ATP activation of purinergic receptor P2X receptors has been proposed to induce a cation shunt, reducing the endolymphatic potential and the driving force for sound transduction. However, direct evidence for this protective mechanism remains limited. Here, we provide direct experimental evidence identifying a distinct, compartment-specific ATP signalling pathway that modulates cochlear function. In mature Dunkin-Hartley guinea pigs of either sex, we combined time-resolved confocal microscopy, electrophysiology, live-cell imaging, and fluorescence spectroscopy to characterise how compartmentalised extracellular ATP regulates cochlear function during moderate loud sound exposure. ATP delivered to the perilymphatic space where P2X2 receptors localised in Reissner's membrane epithelial cells, supporting cells, and hair cells significantly reduced sound-evoked electrical potentials from 486 μV to 315 μV, outer hair cell stereocilia motion from 135 nm to 99 nm and Hensen's cell motion from 128 nm to 101 nm at 80 dB SPL. These effects were reversible upon ATP removal and accompanied by decreased intracellular calcium. In contrast, ATP applied to the endolymph produced no comparable changes. These findings demonstrate that extracellular ATP in the perilymph protects the cochlea from high-intensity sound through a mechanism distinct from the classical cation shunt model. These findings reveal a previously unrecognised perilymph-driven ATP signalling pathway that extend beyond the traditional P2X-mediated cation shunt, demonstrating that extracellular ATP plays a critical role in protecting the cochlea mainly from loud sound-induced hearing loss. Swedish Research Council 2017-06092 and 2022-00548.
Psychotropic medications remain foundational in psychiatric care, yet the neurophysiological mechanisms through which they exert therapeutic and adverse effects are still poorly characterised, limiting the field's ability to optimise treatment selection and monitoring. Electroencephalography (EEG) offers a non-invasive, real-time window into brain function that could support more precise, mechanism-informed prescribing; however, progress has been constrained by the absence of sufficiently large and systematically analysed pharmaco-EEG datasets. In this cross-sectional observational study, we analysed over 24,000 clinical EEG recordings (∼6000 h of data) obtained across a wide range of psychiatric diagnoses and medication regimens. We compared more than 75,000 spectral, connectivity, and nonlinear EEG features across major drug classes, including benzodiazepines, SSRIs, antipsychotics, and anticonvulsants. Dimensionality-reduced analyses revealed robust, class-specific neurophysiological signatures that can be linked to psychotropic drugs' mechanisms of action: benzodiazepines increased beta and decreased theta-alpha power; SSRIs enhanced gamma-band coherence; and antipsychotics and anticonvulsants produced marked slow-wave amplification and reductions in signal complexity. All results are made publicly accessible through an interactive resource (BrainwavesRX), enabling clinicians and researchers to explore medication-specific EEG effects at multiple levels of granularity. By establishing a population-level reference atlas of psychotropic medication effects on human neural dynamics, this study provides an important foundation for future studies leveraging EEG to predict treatment response, detect insufficient or excessive pharmacological effects, and ultimately advance the development of individualised, data-driven psychiatric care. The publication was prepared as part of Foundation of Polish Science's Proof of Concept (FENG.02.01-IP.05-0010/24) and BRAINCITY IRAP (FENG.02.07-IP.05-0179/23) projects.
Circadian disruption affects multiple aspects of human health, but the genetic architecture of individual susceptibility remains unclear. We examined the genetics of the Circadian Imbalance Index (CII), an additive 0-5 score combining evening chronotype, short/long sleep, high neuroticism, atypical caffeinated coffee intake, and low vitamin D. We ran a genome-wide association study (GWAS) of CII in 312,935 European-ancestry UK Biobank participants, compared signals with component-specific and leave-one-component-out (LOCO) GWASs, and tested sex and shift work interactions. CII polygenic score (PRS) PheWAS analyses were evaluated in Mass General Brigham Biobank (N = 50,908) and All of US (N = 98,182), with component-weighted PRS sensitivity analyses. Replication was assessed in Nurses' Health Study II women (N = 11,344). We estimated genetic correlations and performed bidirectional two-sample Mendelian randomisation (MR) with MR-Egger, weighted median and LOCO sensitivity analyses. We identified 27 loci mapping to 72 genes, including genes with reported links to circadian regulation or circadian-related pathways, such as CALCA, DHCR7, KDM5A, HAL, and CRX. Five genes (EPHB1, SERPING1, C12orf74, PLEKHG7, and EEA1) were observed in the CII analysis but not in component-specific analyses. LOCO analyses indicated that the CII genetic signal was not reducible to any single component. The CII PRS was associated with metabolic and psychiatric phenotypes. CII was genetically correlated with insomnia, mood swings, body mass index, type 2 diabetes, coronary artery disease, and myocardial infarction. MR analyses provided suggestive directional evidence, strongest for reverse associations of mood swings and coronary artery disease with CII. The CII captures a polygenic composite susceptibility signal associated with cardiometabolic and mood outcomes, with suggestive evidence of directional relationships. European Research Council Advanced Grant CLOCKrisk (101053225).
Patients with eosinophilic asthma are responsive to treatment with corticosteroids and biologics. Eosinophilia is usually identified based on blood eosinophil counts, but there is discordance between blood and sputum in some cases. A subset of patients may have sputum eosinophilia despite low blood eosinophil levels. The clinical implications of this so-called isolated sputum eosinophilia are unknown. The aim of this study is to investigate the clinical expression of asthma in patients with isolated sputum eosinophilia. In this post-hoc ATLANTIS analysis we included patients with available blood and/or sputum data from ATLANTIS. Patients were classified according to blood eosinophils (< or ≥300 cells/μL). Patients with isolated sputum eosinophilia were compared with those with low eosinophils in both compartments. Of the 487 patients with low blood eosinophils counts, sputum samples were available in 146. Among these, 25 (17%) had isolated sputum eosinophilia. Compared with patients with low eosinophils in both compartments (n = 121), patients with isolated sputum eosinophilia had more airflow obstruction (FEV1/FVC ratios (68.8% vs. 75.4%, p <0.01)) and small airways dysfunction (Scond0.05 vs. 0.03 1/L, p = 0.02) and more frequently reported exacerbations in the year prior to inclusion (28% vs. 9%, p = 0.01). Clinical characteristics were broadly comparable to those observed in patients with blood eosinophilia. Isolated sputum eosinophilia occurs in a subgroup of patients with asthma, in association with worse clinical outcomes. These findings suggest that airway eosinophilia may not always be captured by conventional blood biomarkers and warrant further investigation into the clinical implications of this phenotype to determine whether these patients may benefit from treatment strategies targeting type 2 inflammation, such as intensified steroids or biologics. Chiesi Farmaceutici sponsored the ATLANTIS study.
Urinary proteomic profiling (UPP) provides insights in disease mechanisms and origin of symptoms. Using UPP, this study aimed at deepening insight in the biology of exercise tolerance. In the HOMAGE trial, 268 patients at risk of heart failure underwent the incremental shuttle walk test (SWT) and UPP by capillary electrophoresis coupled with mass spectrometry at baseline (discovery) and the 9-month final visit (replication). Sequencing of 1498 urinary peptides identified 170 non-collagen and 40 collagen-derived proteins. Ten exercise-related variables, including heart rate and blood pressure responses, symptoms and walking distance were summarised into a single factor, higher values indicating exercise intolerance. In exploratory analyses, exercise intolerance was related to the UPP, first in linear and logistic regression models, considering one peptide at a time, and next by elastic net regression considering the peptides retained in the previous step. Replicated proteins were subjected to pathway analysis. Twenty-nine non-collagen and 31 collagen-derived peptides were associated with reduced exercise capacity with correction for multiple testing. In elastic net regression, exercise intolerance was in >50% of 1000 bootstrap runs associated with the non-collagen proteins FXYD2, GAPDH, HBB, KCNB1, MB, MYOCD, SECTM1, SNX9, TACC3, TMSB4X, and TTN and with collagens COL5A1, COL6A1, COL11A2, and COL28A1. Enriched pathways involved oxygen homoeostasis, oxidative stress regulation, metabolic and developmental processes, and muscle biology. In HOMAGE patients, UPP identified parent proteins regulating exercise endurance, which are involved in oxygenation, vascular and muscle structure and function, maintenance of the circulating volume, and protection against oxidative stress. European Union.
The determinants of the species barrier preventing human infections with avian influenza A viruses (IAV) are incompletely understood. We previously identified loss-of-function variants of the interferon-regulated antiviral factor MxA as a genetic factor for increased susceptibility to infections with the H7N9 subtype. Given the central role of type I IFNs (IFN-I) in antiviral defence, we hypothesised that IFN-I-neutralising autoantibodies may similarly predispose to zoonotic H7N9 infection. In this observational case-control study, serum samples collected between 2013 and 2017 from 199 Chinese patients with laboratory-confirmed H7N9 infection and 531 healthy, uninfected controls (269 poultry workers, 262 close contacts) were screened for IgG autoantibodies binding IFNα2, IFNβ1b, or IFNω using a multiplex bead-based assay. Positive samples were tested for IFN-neutralising activity in a luciferase-based reporter assay. To confirm their ability to block IFNα2-mediated antiviral activity, selected samples (n = 19) were analysed in IAV infection experiments. Associations between age, sex, H7N9 case status, case fatality, and the presence of neutralising autoantibodies were evaluated by logistic regression. Available whole-genome sequencing data from 26 individuals with neutralising autoantibodies were screened for variants in genes linked to IFN-I autoimmunity. Neutralising autoantibodies against at least one IFN-I were detected in 19.1% (38/199) of patients but in only 1.1% (6/531) of controls, consistent with published general population data. Most patient sera targeted IFNα2 and/or IFNω (35/199), and 18.1% (36/199) neutralised even high IFN-I concentrations of 1-10 ng/ml. The presence of neutralising autoantibodies was associated with 8.2- to 25.3-fold higher odds of H7N9 infection (p < 0.0001), depending on antibody specificity and reference group. Autoantibody prevalence increased significantly with age in patients (44.8% ≥70 years; OR = 1.05; 95% CI 1.02-1.07; p = 0.0001), but was not associated with sex (OR for males vs. females = 0.52; 95% CI 0.23-1.14; p = 0.106). All selected sera containing neutralising autoantibodies blocked IFNα2-induced antiviral activity in cell culture. No known genetic predisposition for IFN-I autoimmunity was identified. Our findings suggest that IFN-I-targeting autoimmunity is associated with susceptibility to zoonotic IAV infection with the H7N9 subtype, and possibly also other subtypes, including panzootic H5N1. Given the ease of implementation, screening for anti-IFN-I autoantibodies could be readily integrated into surveillance or targeted testing. This could be relevant in environments with increased exposure to zoonotic IAVs. Shenzhen Medical Research Fund, National Natural Science Foundation of China, Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences, Guangdong Provincial Science and Technology Program, Program for Youzuzhikeyan of Shenzhen University, German Research Foundation, Swiss National Science Foundation.
This randomised crossover trial (ClinicalTrials.gov: NCT05768958) examined how high-intensity interval exercise (HIIE) vs. rest and time of day affect ad libitum energy intake, subjective appetite, and metabolic markers, and whether responses differ by type 2 diabetes (T2D) status. Fifty-eight adults with overweight/obesity (with and without T2D) completed four laboratory visits (HIIE or rest in the morning or late afternoon). Participants were randomised using a balanced incomplete block design; blinding was not feasible. The primary outcome was ad libitum energy intake; secondary outcomes included 24-h post-visit energy intake, subjective appetite, satiety quotient and metabolic markers (including glucose, insulin, ghrelin, Glucagon-Like Peptide-1, Fibroblast Growth Factor 21 (FGF21), and Growth Differentiation Factor 15 (GDF15)). Energy intake was lower after HIIE than rest (-361 kJ (95% CI: -520: -202), p < 0.001) with no compensation over the next 24 h. Appetite ratings were lower after HIIE, accompanied by reduced ghrelin and increased FGF21 and GDF15. Time of day did not affect outcomes; however, only participants without T2D consumed less after morning than late afternoon HIIE. FGF21 and GDF15 increased after exercise compared to rest independent of time of day. GDF15 showed a significantly greater response and higher concentrations in participants with T2D. In participants with T2D, morning HIIE elicited higher FGF21 concentrations than late afternoon HIIE. Other time-of-day effects were minimal. No serious adverse events occurred. In conclusion, acute HIIE suppresses energy intake and elevates GDF15 and FGF21 in people with overweight/obesity, with modest timing effects that differ by diabetes status. Novo Nordisk A/S.
Testosterone therapy (TT) is increasingly initiated outside classical hypogonadism, but long-term cardiovascular safety in this context remains uncertain. We assessed whether TT initiation without evidence of hypogonadism is associated with higher long-term cardiovascular risk than TT initiation with evidence of hypogonadism. In this global retrospective real-world cohort study, men aged 30-75 years initiating TT were identified from secondary, de-identified structured EHR data from 123 healthcare organisations. A prespecified 3-year pre-index washout excluded prior TT and major cardiovascular/thromboembolic events. Men initiating TT without evidence of hypogonadism were compared with those with evidence of hypogonadism using 1:1 propensity-score matching. The primary outcome was major adverse cardiovascular events (MACE); secondary outcomes included separately all-cause mortality, myocardial infarction, ischaemic stroke, cardiac arrest, and heart failure. Acute appendicitis served as a negative-control outcome. Among 358,957 TT initiators, 127,152 (35.4%) had no evidence of hypogonadism. After matching, 113,554 pairs were followed for up to 10 years. TT without evidence of hypogonadism was associated with higher risk of MACE (16.53% vs 11.83%; HR 1.51, 1.45-1.56) and all-cause mortality (HR 1.90, 1.79-2.00), with higher risks of ischaemic stroke (HR 1.23, 1.14-1.33), cardiac arrest (HR 1.41, 1.23-1.61), and heart failure (HR 1.32, 1.26-1.39). Race-stratified estimates were directionally consistent but varied in magnitude. The cardiovascular safety of TT appears context-dependent and less favourable when treatment is initiated without evidence of hypogonadism, with clinically relevant heterogeneity across race/ethnicity, supporting biologically informed prescribing and cardiovascular risk surveillance. Deutsche Forschungsgemeinschaft, Schleswig-Holstein Excellence-Chair Program, and Region Stockholm.
Polycystic ovary syndrome (PCOS), recently renamed polyendocrine metabolic ovarian syndrome (PMOS), is characterised by neuroendocrine dysfunction with accelerated gonadotrophin-releasing hormone (GnRH)/luteinising hormone (LH) pulsatility driving hyperandrogenism and anovulatory infertility. We used the prenatal anti-Müllerian hormone (AMH)-exposed PMOS-like mouse model (PAMH) and a phase I clinical trial in women with PMOS without obesity. PAMH and control mice received acute or intermittent low-dose Ganirelix, and oestrous cyclicity, ovulation, gonadotrophins, and steroids were assessed. In women, two subtherapeutic Ganirelix doses (0.025 mg, n = 8; 0.0625 mg, n = 10) were administered once in early follicular phase, with 10-min blood sampling over 8 h to quantify LH pulsatility and reproductive hormones. In PMOS-like mice, a single Ganirelix injection normalised exaggerated LH pulsatility, and six-week intermittent treatment restored oestrous cyclicity, ovulation, and testosterone levels without affecting controls. In women with PMOS both Ganirelix doses reduced LH pulse frequency, basal, mean and total LH, and decreased the LH/FSH ratio. D4-androstenedione fell by 25-30% at both doses, AMH declined modestly at 0.0625 mg, while oestradiol remained unchanged. Low-dose GnRH-receptor antagonism with Ganirelix can recalibrate, rather than suppress, GnRH/LH signalling, attenuating hyperandrogenism and, in mice, restoring ovulatory function. These data identify partial GnRHR blockade as a promising neuroendocrine-centred strategy in PMOS and provide a rationale for phase II trials evaluating repeated low-dose regimens, ovulatory restoration, and fertility outcomes. This work was supported by the European Research Council (ERC) Horizon-ERC-POC grant (ERC-2022-POC2, n° 101111874) and the French National Research Agency (ANR-24-CHBS-0002, France 2030).
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Vaccination is a vital tool in preventing acute COVID-19 and may confer additional protection against Long COVID, although it is unclear whether this protection wanes over time. We assessed electronic health record (EHR) data from a national, retrospective cohort of patients, comparing the 12-month cumulative incidence of Long COVID (ICD-10 code U09.9) among (A) patients who were vaccinated versus unvaccinated (two or more versus zero doses) and (B) patients diagnosed with acute COVID-19 1-3 months, 3-5 months, or 5-7 months after vaccination. In our binary cohort (n = 519,980), we found that patients who were vaccinated had a lower risk of Long COVID (adjusted risk ratio 0.84 (0.81, 0.88)) or mortality (adjusted risk ratio 0.83 (0.81, 0.86)) than patients who were unvaccinated. In our longitudinal cohort (n = 1,085,291), we did not find significant heterogeneity in Long COVID risk during the seven months following vaccination. We found that COVID-19 vaccination was protective against Long COVID, and we did not observe a significant waning of this protection within seven months after vaccination. This research was financially supported by the National Institute of Allergy and Infectious Diseases (1K01AI182501 to Zachary Butzin-Dozier) and a Global Development grant (OPP1165144) from the Bill & Melinda Gates Foundation to the University of California, Berkeley, CA, USA. Individual authors were supported by the following funding sources: NIMHR01131542 (PI Rena C. Patel), Jerrod Anzalone is supported by the National Institute of General Medical Sciences, U54 GM115458, which funds the Great Plains IDeA-CTR Network. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
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