NeuroImmune pharmacology and therapeutics最新文献

{"title":"Sex-dependent modulation of behavioral allocation via ventral tegmental area-nucleus accumbens shell circuitry.","authors":"Kristen A McLaurin, Jessica M Illenberger, Hailong Li, Rosemarie M Booze, Charles F Mactutus","doi":"10.1515/nipt-2025-0002","DOIUrl":"10.1515/nipt-2025-0002","url":null,"abstract":"<p><p>Diagnostic criteria for substance use disorder, cocaine type (i.e., cocaine use disorder), outlined in the 5th edition of the <i>Diagnostic and Statistical Manual of Mental Disorders</i>, imply that the disorder arises, at least in part, from the maladaptive allocation of behavior to drug use. To date, however, the neural circuits involved in the allocation of behavior have not been systematically evaluated. Herein, a chemogenetics approach (i.e., designer receptors exclusively activated by designer drugs (DREADDs)) was utilized in combination with a concurrent choice self-administration experimental paradigm to evaluate the role of the mesolimbic neurocircuit in the allocation of behavior. Pharmacological activation of hM3D(G_q) DREADDs in neurons projecting from the ventral tegmental area (VTA) to the nucleus accumbens (AcbSh) induced a sex-dependent shift in the allocation of behavior in rodents transduced with DREADDs. Specifically, male DREADDs animals exhibited a robust increase in responding for a natural (i.e., sucrose) reward following pharmacological activation of the VTA-AcbSh circuit; female DREADDs rodents, in sharp contrast, displayed a prominent decrease in drug-reinforced (i.e., cocaine) responding. The sequential activation of hM3D(G_q) and KORD DREADDs within the same neuronal population validated the role of the VTA-AcbSh circuit in reinforced responding for concurrently available natural and drug rewards. Collectively, the VTA-AcbSh circuit is fundamentally involved in behavioral allocation affording a key target for the development of novel pharmacotherapies.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 2","pages":"237-252"},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12304879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adaptive immunity in the pathogenesis and treatments of Parkinson's disease.","authors":"Xiaoqing Du, Samia Akter, Davina B Oludipe, Susmita Sil, Chen Zhang, Howard E Gendelman, R Lee Mosley","doi":"10.1515/nipt-2025-0008","DOIUrl":"10.1515/nipt-2025-0008","url":null,"abstract":"<p><p>Neuroimmunity drives the pathophysiology of Parkinson's disease (PD). This disease affects both the central and peripheral nervous systems. The immune system is engaged through the progressive accumulation of alpha-synuclein (α-syn), a driver of immunity and a pathological hallmark of PD. Consequent α-syn-induced immune activation leads to neuronal damage. This leads not only to the activation of microglia within the central nervous system, but also to the recruitment and activation of peripheral immune cells that infiltrate the brain and contribute to a widespread immune response. Moreover, PD-associated genes and risk factors have been increasingly recognized as essential regulators of immune functions. This review summarizes the current understanding of adaptive immunity in PD and explores emerging immunomodulatory strategies that may inform future therapeutic development.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 2","pages":"273-284"},"PeriodicalIF":0.0,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12304880/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pannexin-1 channels, extracellular ATP, and purinergic receptors are essential for CCR5/CXCR4 clustering and HIV entry.","authors":"David Ajasin, Stephani Velasquez, Joy Gibson, Eliana Scemes, Antonio Cibelli, David Spray, Eliseo A Eugenin","doi":"10.1515/nipt-2025-0005","DOIUrl":"10.1515/nipt-2025-0005","url":null,"abstract":"<p><strong>Objective: </strong>The Human Immunodeficiency Virus-1 (HIV) cell entry has been well characterized with the identification of CD4 as the main receptor and CXCR4 and CCR5 as co-receptors for the virus. However, how the virus uses the cell machinery for entry and infection is still a work-in-progress. Previously, we identified that the Pannexin-1 (Panx-1) channel, extracellular ATP, and purinergic receptors axis are essential for HIV entry and replication in macrophages, but the mechanisms were not fully explored.</p><p><strong>Methods: </strong>Electrophysiology, ATP quantifications, confocal, HIV entry and replication experiments were used to determine the role of Panx-1 channels in HIV entry.</p><p><strong>Results: </strong>Here, we identified that HIV or gp120 induces Panx-1 channel opening in association with ATP secretion, purinergic activation, and CCR5/CXCR4/actin clustering to enable HIV entry. Blocking Panx-1 channel opening, ATP secretion, or purinergic signaling prevented co-receptor clustering, HIV entry, and subsequent replication in multiple cell types.</p><p><strong>Conclusion: </strong>We conclude that gp120 binding to the cell induces Panx-1 opening to promote the clustering of CCR5 or CXCR4 to the site of CD4-gp120 contact to aid viral entry.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 2","pages":"217-236"},"PeriodicalIF":0.0,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12304881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Co-exposure of antiretroviral therapy and nicotine induces brain metabolic impairments in a mouse model.","authors":"Gabriel C Gauthier, Emma G Foster, Mariano G Uberti, Balasrinivasa R Sajja, Aditya N Bade, Yutong Liu","doi":"10.1515/nipt-2025-0006","DOIUrl":"10.1515/nipt-2025-0006","url":null,"abstract":"<p><strong>Objectives: </strong>Anti-retroviral therapy (ART) drastically improves human immunodeficiency virus type 1 (HIV-1) outcomes, but may induce adverse neurochemical changes. Interactive effects of ART with recreational drugs are unknown. Notably, people living with HIV-1 (PLWH) smoke at twice the rate of the general population and are more prone to tobacco-linked illness. Thus, chemical exchange saturation transfer (CEST) magnetic resonance imaging (MRI) was employed to investigate potential ART-nicotine co-morbid neuro-metabolomic influence.</p><p><strong>Methods: </strong>16 healthy, male, C57BL/6 mice were divided into four groups: vehicle-treatment, ART-treatment, nicotine-treatment, and ART-nicotine co-treatment. CEST-MRI was performed at day 12 following daily treatments to determine effects on neurometabolic profiles. Magnetic resonance spectroscopy (MRS) was used to contextualize metabolic outcomes.</p><p><strong>Results: </strong>CEST-MRI detected significantly lower 3 ppm contrast in ART, nicotine, and co-treatment groups, suggesting ART- and nicotine-linked glutamate alteration. Co-treatment induced significantly higher hippocampal nuclear Overhauser effects (NOE) compared to ART-treatment, whereas individual treatments lacked effect on NOE, indicating adverse effect on membrane lipids. MRS confirmed CEST findings of membrane turnover, detecting significantly lower hippocampal total choline across all groups compared to controls.</p><p><strong>Conclusions: </strong>CEST-MRI detects adverse neuro-metabolomic alterations induced by ART- and nicotine-exposure. This warrants investigation with HIV-1-infection to assess potential influences of co-exposure on PLWH cognition.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 2","pages":"265-271"},"PeriodicalIF":0.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The 29th Scientific Conference of the Society on NeuroImmune Pharmacology in Omaha, NE, June 8-12, 2025.","authors":"Allison M Andrews, Linda Chang, Rosemarie Booze, Sabita Roy, Santhi Gorantla, IIker K Sariyer, Jerel Fields, Eliseo Eugenin, Howard E Gendelman","doi":"10.1515/nipt-2025-0004","DOIUrl":"10.1515/nipt-2025-0004","url":null,"abstract":"<p><p>The 29^th Scientific Conference of the Society on Neuroimmune Pharmacology (SNIP) in Omaha, NE, will occur from June 8^th to 11^th, 2025. This four-day conference showcases world-renowned biomedical research, providing insights into the latest advancements in the intersecting fields of neuroscience, immunology, pharmacology, and virology. Presentation abstracts are organized into sections that include early career development investigators, mouse models, neurodegenerative diseases, therapeutics, substance use disorders, counseling, drug targeting, disease pathobiology, Blood-Brain Barrier integrity, educational opportunities, young investigator talks, and translational medicine. SNIP remains the sole global meeting dedicated to neuroimmune pharmacology. The focus of research centers on how the neuroimmune axis connects drug abuse, inflammation, and brain functional integrity. The conference features several plenary speakers who have made unique and significant contributions to their fields alongside renowned physician-scientists and luminaries. Symposia will include the SNIP Presidential Symposium on Pathobiology and Novel Therapies for Neurodegenerative Diseases, Ultra Long-Acting Medicines, Development and Delivery of Diagnostic and Therapeutic Biomarkers to disease regions, overcoming barriers to treating neurological disorders, neuroinflammation, and reward pathways for addiction, as well as neuron-glia interaction. All presentations are framed within the context of microbial infections, drugs of abuse, and therapeutics. Therapeutics include nanopharmacology and advances in informatics analysis of multi-omics data to decipher the complex cell and molecular interactions that underpin the function of the nervous system. SNIP member symposia and a local series of presentations will highlight outstanding talent from the University of Nebraska. Additional events include lunch with NIH program officials and a NeuroImmune Pharmacology and Therapeutics Journal dinner. The goal is to unite investigators from diverse basic, clinical, and translational fields to discuss and advance our understanding of the multifactorial impact of substance abuse, inflammation, and infections critical to human health. We aim to engage and mentor young investigators in neuroimmune pharmacology and disseminate information presented at the conference to the scientific community, the general public, and healthcare providers. Cultivating the next generation of scientists is vital to our mission. The agenda encompasses early-career investigator presentations, poster sessions, meet-the-mentors luncheons, and a special panel of junior faculty. The conference also provides an enriching environment for scientists and clinicians to share ideas, foster the next generation of scientists, and promote current disease pathobiology and therapeutics trends. Opportunities to visit the Omaha zoo will be available with guest passes. We thank Dr. Carol Swa","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 1","pages":"131-192"},"PeriodicalIF":0.0,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12041845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144038094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Socioeconomic status and economic hardship attenuated the associations between early tobacco or nicotine use and brain outcomes in preadolescent children.","authors":"Pedro J Rodriguez Rivera, Miriam S Menken, William Chan, Amal Isaiah, Meghann C Ryan, Christine C Cloak, Thomas Ernst, Linda Chang","doi":"10.1515/nipt-2024-0022","DOIUrl":"10.1515/nipt-2024-0022","url":null,"abstract":"<p><strong>Objectives: </strong>Early tobacco use (before age 11) is linked to poorer cognition and reduced cortical surface area and volume in young adolescents. This study examined how socioeconomic status (SES) factors - parental education, household income, and economic hardships - influenced these associations.</p><p><strong>Methods: </strong>Using baseline (N=11,876) and year 3 (N=10,414) datasets from the Adolescent Brain Cognitive Development study, we assessed the impact of baseline tobacco/nicotine use initiation on cognitive scores, cortical volume, thickness, and surface area across the entire cohort and in propensity-matched subgroups. Linear mixed effects models controlled for SES and other covariates, with multiple comparison correction. Analyses were cross-sectional at baseline and longitudinal with both timepoints.</p><p><strong>Results: </strong>Compared to non-users (N=11,240), early users (N=110) had more advanced pubertal development (p=0.003) and economic hardships (p<0.001), but fewer girls (p=0.04), Hispanics (p=0.02), parents with graduate degrees (p<0.001) and high-income families >$100 K (p=p<0.001). Relative to non-users, early users had poorer cognitive scores (Cohen's <i>d</i>: -0.69 to -0.24), smaller surface areas (Cohen's <i>d</i>: -2.28 to -0.22), similar cortical thickness at both timepoints, and by year 3, smaller cortical volumes (Cohen's <i>d</i>: -1.06 to -1.24). However, SES-adjustments eliminated cognitive scores and volumes differences and reduced cortical surface area effects at both timepoints (Cohen's <i>d</i>: -1.92 to -0.51). After propensity score matching, early users and non-users showed no cognitive or brain differences, regardless of SES adjustments.</p><p><strong>Conclusions: </strong>Adjusting for SES eliminated the negative impact of early tobacco/nicotine use on cognition and reduced its effect on brain surface area, underscoring the importance of SES in morphometry studies.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 2","pages":"193-207"},"PeriodicalIF":0.0,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12304878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct circulating monocyte profiles in chronic cannabis users compared to cocaine users without changes in plasma levels of proinflammatory cytokines and LPS.","authors":"Douglas Johnson, Zhenwu Luo, Sylvia Fitting, Zizhang Sheng, Wei Jiang","doi":"10.1515/nipt-2025-0003","DOIUrl":"10.1515/nipt-2025-0003","url":null,"abstract":"<p><strong>Objectives: </strong>Chronic cannabis use is linked to anti-inflammatory effects, and cocaine exhibits context-dependent immunomodulation; their distinct impacts on monocyte subsets and systemic inflammation are not fully understood. Systemic microbial translocation contributes to monocyte differentiation, but the levels in chronic cocaine and cannabis users in humans <i>in vivo</i> are lacking.</p><p><strong>Methods: </strong>Peripheral blood mononuclear cells (PBMCs) and plasma samples were collected from chronic cocaine users, cannabis users, and non-drug users. The route of drug administration was via smoking or snorting. Monocyte subsets were analyzed using flow cytometry; plasma levels of cytokines (IL-2, IL-4, IL-6, IL-10, TNF-α, and IFN-γ) and lipopolysaccharide (LPS, a marker of microbial translocation) were measured using a Meso Scale immunoassay and Limulus amoebocyte lysate assay, respectively.</p><p><strong>Results: </strong>Cannabis use was associated with increased total monocyte counts, increased percentages of a classical subset (CD14++CD16-), and decreased percentages of a non-classical subset (CD14+CD16++) in CD14+ monocytes compared to cocaine users and/or healthy controls. Similar levels were observed in the percentages of intermediate monocytes (CD14++CD16+) and plasma levels of six cytokines and LPS among the three study groups. Cocaine users exhibited similar frequencies of monocyte subsets, cytokine levels, and LPS levels compared to controls.</p><p><strong>Conclusions: </strong>Chronic use of cannabis, but not cocaine, is associated with shifts in non-activated monocyte subset distribution, characterized by increased classical and decreased non-classical monocyte subsets, without concurrent systemic cytokine dysregulation or LPS translocation. These findings highlight substance-specific immune effects, potentially affecting long-term immune function.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 2","pages":"209-216"},"PeriodicalIF":0.0,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455578/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HIV-1 infection facilitates Alzheimer's disease pathology in humanized APP knock-in immunodeficient mice.","authors":"Shaurav Bhattarai, Rana Kadry, Pravin Yeapuri, Yaman Lu, Emma G Foster, Chen Zhang, Prasanta Dash, Larisa Y Poluektova, Santhi Gorantla, R Lee Mosley, Howard E Gendelman","doi":"10.1515/nipt-2024-0018","DOIUrl":"https://doi.org/10.1515/nipt-2024-0018","url":null,"abstract":"<p><strong>Objectives: </strong>Amyloid-β (Aβ) plaque deposition in the brain is a principal pathological feature of both Alzheimer's disease (AD) and progressive human immunodeficiency virus type one (HIV-1) infection. Both enable Aβ assembly and Aβ protein aggregation. The potential link between HIV-1 and AD remains uncertain, supporting the need for a reliable animal model. HIV-1 is tropic and pathogenic for humans. It does not replicate in mice. The restricted species tropism has slowed progress in basic research activities. The current study seeks to correct animal model limitations.</p><p><strong>Methods: </strong>We created an AD mouse to address the need to develop an small animal model that allows studies of viral infection by making a knock-in (KI) with the human amyloid precursor protein (APP)^KM670,671NL Swedish mutation to the mouse genome. The resulting founder mice were crossed with immunodeficient NOG (NOD. Cg-<i>Prkdc</i> ^<i>scid</i> <i>Il2rg</i> ^{<i>tm1Sug</i>} Tg(CMV<i>-IL-34</i>)<i>1</i>/Jic) to generate NOG/APP^KM670,671NL/IL-34 (NAIL) mice. The mice were reconstituted with human hematopoietic stem cells to generate NAIL mice with functional adaptive and innate human immune systems. Four-month-old, humanized NAIL mice were infected with HIV-1_ADA, a macrophage-tropic viral strain then evaluated for viral infection and AD pathology.</p><p><strong>Results: </strong>Productive HIV-1 infection was confirmed by plasma HIV-1 RNA levels in infected NAIL mice. The viral load increased by tenfold between day 10 and day 25 post-infection. By day 25, viral DNA confirmed the establishment of HIV-1 reservoirs in CD45+ cells from the immune tissues of infected NAIL mice. Additionally, p24 measurements in lymphoid and brain tissues of NAIL mice validated productive HIV-1 infection. Amyloid burden from infected NAIL mice was increased. Immunofluorescence staining revealed co-localization of Aβ fibrils and HLA-DR⁺ microglia in infected NAIL mice.</p><p><strong>Conclusions: </strong>These results highlight the AD-HIV model's unique pathobiological and infectious features where the viral and immune responses can now be measured.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 1","pages":"27-38"},"PeriodicalIF":0.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12041850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurovirulent and non-neurovirulent strains of HIV-1 and their Tat proteins induce differential cytokine-chemokine profiles.","authors":"Vasudev R Rao, Milka Rodriguez, Siddappa N Byrareddy, Udaykumar Ranga, Vinayaka R Prasad","doi":"10.1515/nipt-2024-0020","DOIUrl":"10.1515/nipt-2024-0020","url":null,"abstract":"<p><strong>Objectives: </strong>HIV-1 enters the central nervous system (CNS) early in infection, and a significant proportion of people with HIV experience CNS complications despite anti-retroviral therapy. Chronic immune dysfunction, inflammatory cytokines and chemokines, and viral proteins like Tat and gp120 released by HIV-1-infected immune cells are implicated in the pathogenesis of HIV-1-associated neurocognitive disorders (HAND).</p><p><strong>Methods: </strong>To elucidate the contribution of non-viral factors to CNS complications in people with HIV-1, a comparative analysis of neurovirulent subtype B (HIV-1_ADA) and non-neurovirulent subtype C (HIV-1_Indie-C1) isolates was performed. Culture supernatants from HIV-1-infected PBMCs, either with or without immunodepletion of Tat and gp120, were used to treat SH-SY5Y neuroblastoma cells.</p><p><strong>Results: </strong>HIV-1_ADA-infected PBMC media showed significantly higher neurotoxicity than HIV-1_IndieC1-infected PBMC media, notwithstanding the depletion of Tat and gp120, highlighting the role of non-viral factors (e.g., cytokines) contributing to neurotoxicity. A comparison of inflammatory profiles revealed that HIV-1_ADA media contained elevated levels of cytokines (IL-1α, IL-1β, IL-6 and TNFα) and chemokines (CCL2, CCL3, CCL4 and IP-10). Given the involvement of Tat in upregulating immune mediators, we tested the role of purified Tat proteins from HIV-1 subtypes B and C in inducing an inflammatory phenotype in PBMCs. PBMCs from healthy subjects were treated with recombinant purified Tat from subtype B or C. Subtype B Tat induced a stronger inflammatory response than subtype C Tat.</p><p><strong>Conclusions: </strong>These results confirm that both viral and non-viral immune factors mediate neuronal damage in people with HIV.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 1","pages":"39-47"},"PeriodicalIF":0.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12041847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cannabis use is associated with a lower likelihood of presence of HIV drug resistance mutations in a retrospective cohort of adults with HIV.","authors":"Jonathan F Hale, Shellynea Reynolds, Heather R Kates, Roberto D Palella, Mohammed M Benmassaoud, Kelly A Smith, Daohai Yu, Servio H Ramirez, Allison M Andrews","doi":"10.1515/nipt-2024-0010","DOIUrl":"10.1515/nipt-2024-0010","url":null,"abstract":"<p><strong>Objectives: </strong>A significant clinical concern in the era of Pre-Exposure Prophylaxis (PrEP) is the increased incidence of HIV Anti-Retroviral Drug Resistance Mutations (ARV-DRM). Previous research has indicated that there is an association between substance use and failed viral suppression, which can lead to ARV-DRM. The goal of this retrospective study was to investigate whether substance use as determined by at least one positive urinalysis screen is associated with increased/decreased odds of having a ARV-DRM.</p><p><strong>Methods: </strong>This study used firth logistic regression analyses of data retrieved from the National NeuroAIDS Tissue Consortium Data Coordinating Center to examine the relationship between substance use and ARV-DRM. The dataset analyzed 614 participants with the following criteria: HIV+ status, at least one paired plasma and cerebrospinal fluid (CSF) viral load measurement, at least one urinalysis of substance use, at least 18 years of age, and analysis of DRM in CSF/Plasma.</p><p><strong>Results: </strong>Cannabis use was a significant predictor of ARV-DRM and was associated with a lower odds of having ARV-DRM (odds ratio=0.189), after accounting for demographic variables and the interaction between polysubstance use and cannabis use. A significant negative relationship was observed between a cannabis positive test and high viremia (>1,000 copies/mL) but not between a cannabis positive test and CSF Escape (viral load CSF>viral load plasma).</p><p><strong>Conclusions: </strong>The above results may suggest an immunomodulatory role for cannabis that impacts the propensity for ARV-DRM. These findings could incentivize future research to further investigate effects of cannabis use on the development of HIV ARV-DRM.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 1","pages":"49-57"},"PeriodicalIF":0.0,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12041849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}