We report on prime-boost vaccine regimens with two simian adenovirus (Ad) vectors (SAdV) or two human serotype Ad vectors (HAdV) expressing Gag and gp160 of simian immunodeficiency virus (SIV)mac239 tested in HAdV-seropositive rhesus macaques (RMs) repeatedly challenged rectally with low doses of SIVmac251. Both vaccine regimens reduced set point and peak viral loads (PVL) and accelerated viral clearance. In SAdV-vaccinated controller genotype RMs resistance against infection correlated with levels of envelope (Env)-specific antibody (Ab) titers. In both vaccine groups CD8+T cells controlled viral loads (VL) upon infection. Circulating CD4+ and CD8+ T cells showed significant changes in their transcriptome over time following vaccination, which differed between the vaccine groups. T cells from SIV-resistant RMs had unique transcriptional profiles indicating that both follicular T helper (TFH) cell responses and highly activated CD8+ T cells may play a role in protection.
Background: The modulation of brain circuits of emotion is a promising pathway to treat Borderline Personality Disorder (BPD). Precise and scalable approaches have yet to be established. Two studies investigating the Amygdala Electrical Fingerprint (Amyg-EFP) in BPD are presented: One study addressing the deep-brain correlates of Amyg-EFP, and a second study investigating neurofeedback (NF) as a means to improve brain self-regulation. Methods: Study 1 combined EEG and simultaneous fMRI to investigate the replicability of Amyg-EFP-related brain activation found in the reference dataset (N=24 healthy subjects, 8 female; re-analysis of published data) in the replication dataset (N=16 female individuals with BPD). In the replication dataset, we additionally explored how the Amyg-EFP would map to neural circuits defined by the Research Domain Criteria. Study 2 investigated a 10-session Amyg-EFP NF training in parallel to a 12-weeks residential Dialectical Behavior Therapy (DBT) program. N=15 patients with BPD completed the training, N=15 matched patients served as DBT-only controls. Results: Study 1 replicated previous findings and showed significant amygdala BOLD-activation in a whole-brain regression analysis with the Amyg-EFP. Neurocircuitry activation (negative affect, salience, and cognitive control) was correlated with the Amyg-EFP signal. Study 2 showed significant learning of Amyg-EFP modulation with NF training. No clinical benefits of NF beyond DBT-only were observed. Conclusions: Recorded via scalp EEG, the Amyg-EFP picks up brain activation of high relevance for emotion. Administering Amyg-EFP NF in addition to standardized BPD treatment was shown to be feasible. Clinical utility remains to be investigated.
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