A study published in VirologyJ demonstrates that immunization with two doses of an mRNA-based rabies vaccine can achieve equal or better efficacy in mice and dogs than the inactivated vaccine.
]. Three different mRNA constructs were developed: RABV G-A, RABV G-B, and RABV G-C. The RABV G-A sequence consisted of a 5’ UTR, the ORF of RABV-G, a 3’ UTR and a 64A + 36C + histone stem loop. RABV G-B was an optimized RABV G-A sequence with a different ORF. RABV G-C was identical to RABV G-B with the exception of its poly tail. Unless specifically noted, RABV G-C was the sequence of our mRNA vaccine, named LVRNA001.
mRNAs were produced by in vitro transcription . DNA templates were linearized from plasmids containing the open reading frames flanked by 5’/ 3’UTR and Poly-A sequences. IVT reactions were performed using DNA templates, an optimized T7 RNA polymerase , NTP and Cap GAG m7GppppG . The reaction was terminated by addition of DNase I . mRNAs were purified using Oligo-dT affinity column and Tangential Flow Filtration .
For dog challenge studies, LVRNA001 or an inactivated vaccine made for human use were i.m. injected into the lateral thigh of hind limb. Blood samples were collected on days 0, 7, 9, 11, 13, 35 post first injection for antibody tests. Viruses were given to the test dogs on day 35 by i.m. injection to the biceps femoris of the hind limb at 50-fold LD.
of virulent RABV-BD06 strain in the biceps femoris of the hind limb. Six hours after challenge infection, dogs were i.m. injected with LVRNA001 or inactivated vaccine. Immunization procedures and experimental steps were the same as pre-exposure protocols shown above.Spleen lymphocytes from mice in each immunization group were collected and resuspended in RPMI 1640 medium containing 10% fetal bovine serum .
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Adverse childhood experiences and binge-eating disorder in early adolescents - Journal of Eating DisordersBackground Adverse childhood experiences (ACEs) are common and linked to negative health outcomes. Previous studies have found associations between ACEs and binge-eating disorder (BED), though they have mainly focused on adults and use cross-sectional data. The objective of this study was to examine the associations between ACEs and BED in a large, national cohort of 9–14-year-old early adolescents in the US. Methods We analyzed prospective cohort data from the Adolescent Brain Cognitive Development (ABCD) Study (N = 10,145, 2016–2020). Logistic regression analyses were used to determine the associations between self-reported ACEs and BED based on the Kiddie Schedule for Affective Disorders and Schizophrenia at two-year follow-up, adjusting for sex, race/ethnicity, baseline household income, parental education, site, and baseline binge-eating disorder. Results In the sample, (49% female, 46% racial/ethnic minority), 82.8% of adolescents reported at least one ACE and 1.2% had a diagnosis of BED at two-year follow-up. The mean number of ACEs was higher in those with a diagnosis of BED compared to those without (2.6 ± 0.14 vs 1.7 ± 0.02). The association between number of ACEs and BED in general had a dose–response relationship. One ACE (adjusted odds ratio [aOR] 3.48, 95% confidence interval [CI] 1.11–10.89), two ACEs (aOR 3.88, 95% CI 1.28–11.74), and three or more ACEs (aOR 8.94, 95% CI 3.01–26.54) were all associated with higher odds of BED at two-year follow-up. When stratified by types of ACEs, history of household mental illness (aOR 2.18, 95% 1.31–3.63), household violence (aOR 2.43, 95% CI 1.42–4.15), and criminal household member (aOR 2.14, 95% CI 1.23–3.73) were most associated with BED at two-year follow-up. Conclusions Children and adolescents who have experienced ACEs, particularly household challenges, have higher odds of developing BED. Clinicians may consider screening for ACEs and providing trauma-focused care when evaluating patients for BED.
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Neuroimmune proteins can differentiate between tauopathies - Journal of NeuroinflammationBackground Tauopathies are a group of neurodegenerative diseases where there is pathologic accumulation of hyperphosphorylated tau protein (ptau). The most common tauopathy is Alzheimer’s disease (AD), but chronic traumatic encephalopathy (CTE), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and argyrophilic grain disease (AGD) are significant health risks as well. Currently, it is unclear what specific molecular factors might drive each distinct disease and represent therapeutic targets. Additionally, there is a lack of biomarkers that can differentiate each disease in life. Recent work has suggested that neuroinflammatory changes might be specific among distinct diseases and offers a novel resource for mechanistic targets and biomarker candidates. Methods To better examine each tauopathy, a 71 immune-related protein multiplex ELISA panel was utilized to analyze anterior cingulate grey matter from 127 individuals neuropathologically diagnosed with AD, CTE, PSP, CBD, and AGD. A partial least square regression analysis was carried out to perform unbiased clustering and identify proteins that are distinctly correlated with each tauopathy correcting for age and gender. Receiver operator characteristic and binary logistic regression analyses were then used to examine the ability of each candidate protein to distinguish diseases. Validation in postmortem cerebrospinal fluid (CSF) from 15 AD and 14 CTE cases was performed to determine if candidate proteins could act as possible novel biomarkers. Results Five clusters of immune proteins were identified and compared to each tauopathy to determine if clusters were specific to distinct disease. Each cluster was found to correlate with either CTE, AD, PSP, CBD, or AGD. When examining which proteins were the strongest driver of each cluster, it was observed the most distinctive protein for CTE was CCL21, AD was FLT3L, and PSP was IL13. Individual proteins that were specific to CBD and AGD were not observ
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Fungi detected in 35 cancer types, often intracellularIn a recent article published in the journal Cell, researchers found fungal deoxyribonucleic acid (DNA) and cells at low abundances across many human cancers, with cancer type-dependent variations in fungus community composition and fungal-bacteriome interactions.
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