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Richard Ellis

Richard Ellis

· Professor of ClassicsVerified

University of California, Los Angeles · Classics

Active 1937–2026

h-index98
Citations37.8k
Papers677203 last 5y
Funding$158.4M3 active
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About

Richard Ellis is a faculty member in the Department of Classics at UCLA, having begun lecturing there in the winter quarter of 2014. He completed his undergraduate degree in Cambridge, England, and earned his doctorate at the University of Southern California. His teaching repertoire includes courses on Ancient Greek Philosophy, Greek Culture and Mythology, Ancient Tragedy, and Ancient Athletics, as well as Latin and Greek reading classes covering authors such as Homer, Hesiod, Lysias, Aeschylus, Plato, and Seneca. His research interests focus on Archaic and Classical Greek philosophy and literature. His PhD dissertation, titled ‘Heraclitus’ Children: Brains, Bodies and Culture at Play,’ explored the figure of the child in the work of the Pre-Socratic philosopher Heraclitus of Ephesus. He is working on transforming this dissertation into a book that examines the role of the child in philosophical and literary thought from ancient Greece to 20th-century Weimar Germany. His forthcoming articles will discuss Heraclitus’ ludic philosophy and his relevance to post-humanism, including dialogues with contemporary thinkers such as Eugen Fink and Gilles Deleuze. Additionally, Ellis is involved in a major project on 17th-century British philosopher John Locke, specifically his Disputations on the Law of Nature. He is co-editing a new Clarendon edition for Oxford University Press in collaboration with Dr. Hannah Dawson of the New Institute of the Humanities at the University of London.

Research topics

  • Internal medicine
  • Immunology
  • Medicine
  • Psychiatry
  • Psychology
  • Pathology
  • Neuroscience

Selected publications

  • Cannabis use by people with HIV is associated with an anti-inflammatory immunometabolic phenotype in monocyte-derived macrophages

    Journal of Neuroinflammation · 2026-04-17

    articleOpen access

    Chronic neuroinflammation is associated with comorbidities in people with HIV (PWH) on antiretroviral therapy (ART). While cannabis use is associated with reduced neuroinflammation and neurocognitive impairment (NCI) in PWH, the underlying mechanisms are unknown. To address this gap in knowledge, we analyzed monocyte-derived macrophages (MDMs) from a cohort of 50 PWH and 33 people without HIV (mean age: 61.9 years), categorized by frequency of cannabis use (naïve/low, moderate, daily). We performed immunocytochemistry, RNA sequencing, and qPCR on MDMs and quantified related biomarkers in donor plasma. In this cohort study, daily cannabis use in PWH was associated with less global neurocognitive deficits, and with an anti-inflammatory immunometabolic-phenotype in MDMs characterized by (1) a metabolic shift from glycolysis to oxidative phosphorylation, (2) higher mitochondrial numbers, (3) altered cytokine profiles (pro-inflammatory downregulation, anti-inflammatory upregulation), and (4) higher brain-derived neurotrophic factor (BDNF) expression. These cellular changes were corroborated by a plasma biomarker profile in PWH including (1) lower levels of growth differentiation factor 15 and soluble triggering receptor expressed on myeloid cells 2, and (2) higher mature BDNF/precursor BDNF ratios that correlated with better cognition. Thus, cannabis use may mitigate NCI in PWH by immunometabolically reprogramming MDM function towards an anti-inflammatory and neuroprotective state. Cannabis use by people with HIV (PWH) is associated with neuroprotective and anti-inflammatory effects, mediated in part by reprogramming the immunometabolism of monocyte-derived macrophages (MDMs). This shift involves a transition from a pro-inflammatory, glycolytic phenotype toward a more anti-inflammatory state characterized by oxidative phosphorylation and altered cytokine expression. In cannabis-Naïve/Low PWH, MDMs exhibit a pro-inflammatory profile that promotes neuroinflammation and mitochondrial damage, resulting in a reduced number of mitochondria. Chronic neuroinflammation contributes to neurodegeneration and the neurocognitive impairments (NCI) that define HIV-Associated Neurocognitive Disorders (HAND). This inflammatory and neurodegeneration profile is reflected by plasma immunometabolic biomarkers including reduced mature BDNF (mBDNF), and elevated GDF15 and soluble TREM2 (sTREM2) levels. Conversely, cannabis use in PWH induces an anti-inflammatory MDM profile that promotes reduced neuroinflammation with increased mitochondrial biogenesis. The reduced neuroinflammation leads to improved neuronal function and reduced NCI, resulting in improved memory, motor and verbal skills, and executive learning. This neuroprotective effect is corroborated by corresponding plasma biomarkers showing increased mBDNF levels, and decreased GDF15 and sTREM2 levels. Collectively, these findings suggest that cannabis use by PWH appears to mitigate neuroinflammation and NCI, with the immunometabolic reprogramming of MDMs likely playing a key mechanistic role. Graphical Methods The HIV Neurobehavioral Research Program (HNRP) donor cohort consisted of people without HIV (PWoH) and people with HIV (PWH) who were either cannabis naïve/low, moderate cannabis users, or daily cannabis users. Peripheral blood mononuclear cells (PBMCs) were isolated from donor blood samples, plated, and allowed to differentiate for two weeks into monocyte-derived macrophages (MDMs) before being tested or treated with THC and then tested. At the same time plasma samples were isolated from each donor and stored for testing. At that point specific dyes were added, and different parameters were measured such as on the CX5 CellInsight Imager or an ELISA and the data was then analyzed.

  • Linking neuroinflammation and neurodegeneration to cognitive decline in HIV

    Brain Behavior & Immunity - Health · 2026-04-14

    articleOpen access1st authorCorresponding

    Background and objectives: We investigated the relationship between cerebrospinal fluid (CSF) and plasma biomarkers of inflammation, neurodegeneration, and neurocognitive performance in people with HIV (PWH), using longitudinal samples from two previously published cohorts: ACTG A5090 (virally suppressed on antiretroviral therapy, ART) and A736 (ART-naïve or failing). Methods: We analyzed paired CSF and plasma samples, as well as 7-domain standardized neurocognitive test scores, at baseline and 24 weeks. Biomarkers included markers of inflammation (e.g., TNF-α, IL-6, IP-10) and neurodegeneration (e.g., NFL, p-Tau217, Aβ42), which were quantified via high-sensitivity immunoassays. Associations with cognition were tested using regression, mediation, and interaction models. Results: < 0.15). Exploratory mediation analysis suggested CSF TNFα, but not plasma TNFα, partially mediated the effect of CSF HIV RNA on cognition (indirect β = 0.14, 95% CI: 0.045-0.235, p = 0.006), though this finding requires replication in larger cohorts. Within-compartment biomarker correlations were stronger in CSF than plasma, and cross-compartment agreement was highest for TNFα, GFAP, and NFL. ART initiation in A736 led to significant declines in CSF IL-6, IL-10, and TNFα; no changes were observed in A5090. Exploratory interaction models suggested that astrocytic activation may amplify tau-related cognitive risk, but these effects were not statistically reliable when analyses were restricted to participants with complete data for GFAP, tau biomarkers, and cognitive scores. Discussion: These results suggest a potential role of CSF TNFα in mediating the neurocognitive effects of HIV and highlight compartment-specific inflammatory dynamics. Plasma TNFα, GFAP, and NFL may serve as peripheral indicators of CNS pathology, though with only moderate concordance. Astrocyte-tau interactions require cautious interpretation pending replication in larger cohorts.

  • Compartmentalized Biomarker Correlations in HIV: Plasma-CSF Relationships Vary by Blood-Brain/Blood-CSF Barrier Permeability and Viral Suppression

    Research Square · 2026-05-21

    preprintOpen access1st authorCorresponding
  • Community Curation of Microbial Metabolites Enables Biological Insights of Metabolomics Data

    bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-29

    articleOpen access

    Microbial metabolites play a critical role in regulating ecosystems, including the human body and its microbiota. However, understanding the physiologically relevant role of these molecules, especially through liquid chromatography tandem mass spectrometry (LC-MS/MS)-based untargeted metabolomics, poses significant challenges and often requires manual parsing of a large amount of literature, databases, and webpages. To address this gap, we established the Collaborative Microbial Metabolite Center knowledgebase (CMMC-KB), a platform that fosters collaborative efforts within the scientific community to curate knowledge about microbial metabolites. The CMMC-KB aims to collect comprehensive information about microbial molecules originating from microbial biosynthesis, drug metabolism, exposure-related molecules, food, host-derived molecules, and, whenever available, their known activities. Molecules from other sources, including host-produced, dietary, and pharmaceutical compounds, are also included. By enabling direct integration of this knowledgebase with downstream analytical tools, including molecular networking, we can deepen insights into microbiota and their metabolites, ultimately advancing our understanding of microbial ecosystems.

  • Dysregulated CSF metalloproteinases in people with HIV despite CSF and peripheral blood suppression

    SSRN Electronic Journal · 2026-01-01

    preprintOpen accessSenior author
  • No evidence of a detrimental effect of pitavastatin on neurocognitive function among people with HIV

    AIDS · 2025-06-11 · 5 citations

    articleOpen access

    OBJECTIVE: Effects of statins on neurocognitive function remain poorly understood, with some studies suggesting harm and others suggesting benefit. Limited observational data among people with HIV (PWH) is biased by indication for statin prescription. We sought to assess statin effects on neurocognitive function among PWH. DESIGN: We leveraged data from participants co-enrolled in REPRIEVE (randomized trial of pitavastatin vs. placebo among PWH with low-to-moderate cardiovascular risk) and HAILO (observational study involving repeated neurocognitive measures). METHODS: Participants with at least one measure of neurocognitive function before and after REPRIEVE randomization were included. Neurocognitive function was determined by NPZ-4, the average of the Z scores from Hopkins Verbal Learning Test Revised, Trailmaking A and B, and Digit Symbol Test every 48 weeks. Trajectories before and after randomization were analyzed with generalized estimating equation models. RESULTS: Of 181 co-enrolled participants (pitavastatin 88, placebo 93), changes over median 2.3 years on overall and individual neurocognitive scores were small, not meeting a clinically relevant threshold of more than 0.5/year, and similar between arms. Although subgroup analyses were limited by a small sample size, we observed trends toward improved Trailmaking A in participants with baseline impairment who were randomized to pitavastatin vs. placebo and towards worsened NPZ-4 in women randomized to pitavastatin vs. placebo that similarly did not reach threshold for clinical relevance. Other subgroup effects were minimal and not statistically or clinically significant. CONCLUSION: We found no evidence of a detrimental effect of pitavastatin use on a limited battery of neurocognitive assessments among PWH, even among PWH with baseline neurocognitive impairment.

  • Glycation metabolites predict incident age-related comorbidities and mortality in older people with HIV

    GeroScience · 2025-04-16 · 1 citations

    articleOpen access

    Glycation is a class of modifications arising from non-enzymatic reactions of reducing sugars with proteins, lipids, and/or DNA, generating advanced glycation end-products (AGEs). AGEs are linked to many age-related comorbidities. In response to HIV-1 infection, activated T-cells and macrophages shift their predominate metabolism from oxidative phosphorylation to glycolysis. Increased glycolytic flux enhances AGE formation, which may increase age-related comorbidities. In this prospective, multicenter cohort study of antiretroviral therapy treated people with HIV, we explored predictive associations by baseline plasma AGE concentrations and their corresponding detoxification metabolites, with incident comorbidities and mortality. AGEs included dicarbonyl sugars: 3-deoxyglucosone, glyoxal, and methylglyoxal. Methylglyoxal-derived metabolites included carboxyethyl-arginine, carboxyethyl-lysine, and methylglyoxal hydroimidazolone-1. Detoxification metabolites included reduced and oxidized glutathione, and the glyoxalase cycle products lactoyl-glutathione and lactoyl-Lysine modified proteins. Plasma was collected at study entry, in the fasting state, and assayed by liquid chromatography-mass spectroscopy. Incident clinical outcomes included diabetes, chronic kidney disease, hypertension, neurocognitive impairment, peripheral neuropathy, frailty, fractures, recurrent falls, and all-cause mortality. Among 376 participants, higher baseline plasma concentrations of methylglyoxal derived AGEs predicted increased risks of diabetes, chronic kidney disease, and recurrent falls, while higher 3-deoxyglucosone predicted an increased risk of peripheral neuropathy. By contrast, higher baseline concentrations of reduced or oxidized glutathione, lactoyl-glutathione, and/or lactoyl-Lysine modified proteins predicted lower risks of diabetes, neurocognitive impairment, frailty, fractures, recurrent falls, and all-cause mortality. These findings support growing experimental evidence of the potential to mitigate age-related declines by interventions that reduce glycation or increase glutathione.

  • <i>HV&amp;I</i> Reviewer Highlight

    Human Vaccines & Immunotherapeutics · 2025-11-18

    articleOpen access1st authorCorresponding
  • Relationship Between Estimated Drug Distribution of Antiretroviral Therapy and Immune Proteins in Cerebrospinal Fluid During Chronic HIV Suppression

    Viruses · 2025-05-23

    articleOpen access

    Antiretroviral therapy (ART) drugs vary in their distribution into cerebrospinal fluid (CSF), which can be estimated using the central nervous system (CNS) penetration effectiveness (CPE) score. Although higher CPE has been associated with lower CSF HIV RNA levels, its relationship to CSF inflammation is less clear. We investigated associations between CPE and three CSF immune biomarkers (CXCL10, TNF-α, and IL-6) in 275 virally suppressed people with HIV (PWH) on three-drug ART regimens using a training–validation design. Participants were randomized into training (TG, n = 144) and validation (VG, n = 131) groups with similar demographics, ART characteristics, and CPE scores. The CSF levels of the biomarkers were quantified by bead suspension array-based immunoassays. In both groups, higher CPE correlated with lower levels of CXCL10 (TG: r = −0.31, p &lt; 0.001; VG: r = −0.30, p &lt; 0.001) and TNF-α (TG: r = −0.19, p = 0.04; VG: r = −0.18, p = 0.03), with remarkably similar effect size. CPE did not correlate with IL-6 in either group. Multivariable models confirmed the associations between higher CPE and both lower CXCL10 (R2 = 0.16, p &lt; 0.001) and TNF-α (R2 = 0.07, p = 0.02) in CSF, and supported the relative resistance of IL-6 to ART effects. During suppressive ART, regimens that achieve higher concentrations in the CNS may better reduce some indicators of CSF inflammation (CXCL10 and TNF-α, closely related to the interferon pathway), but they may not fully normalize the neuroimmune environment (IL-6). Distinct ART regimens may produce different neuroimmune signatures, potentially contributing to heterogeneous patterns of brain injury.

  • Cannabis Use Moderates Methamphetamine- and HIV-Related Inflammation: Evidence from Human Plasma Markers

    Viruses · 2025-08-20 · 1 citations

    articleOpen access

    BACKGROUND: Methamphetamine use, which is disproportionately prevalent among people with HIV, increases risk for cardio- and neurovascular pathology through persistent immune activation and inflammation. Preclinical studies indicate that cannabinoids may reduce markers of pro-inflammatory processes, but data from people with chronic inflammatory conditions are limited. We examined potentially interacting associations of lifetime methamphetamine use disorder (MUD), recent cannabis use, and HIV with four plasma markers of immune and inflammatory functions. METHOD: = 148) provided urine and blood samples and completed neuromedical, psychiatric, and substance use assessments. Generalized linear models examined main and conditional associations of lifetime MUD, past-month cannabis use, and HIV with plasma concentrations of CXCL10/IP-10, CCL2/MCP-1, ICAM-1, and VCAM-1. RESULTS: PWH displayed higher CXCL10/IP-10 than PWoH. Past-month cannabis use was independently associated with lower CXCL10/IP-10 levels and conditionally lower CCL2/MCP-1, ICAM-1, and VCAM-1 levels among people with lifetime MUD, but only PWoH displayed cannabis-associated lower VCAM-1 levels. CONCLUSIONS: Human plasma sample evidence suggests that cannabis use is associated with lower levels of immune and inflammatory molecules in the context of MUD or HIV. Cannabinoid pathways may be worthwhile clinical targets for treating sequelae of chronic inflammatory conditions.

Recent grants

Frequent coauthors

  • Scott Letendre

    Neurobehavioral Research (United States)

    528 shared
  • Igor Grant

    University of California, San Diego

    415 shared
  • David B. Clifford

    Washington University in St. Louis

    259 shared
  • Christina M. Marra

    University of Washington

    225 shared
  • Justin C. McArthur

    Brigham and Women's Hospital

    199 shared
  • Robert K. Heaton

    University of California, San Diego

    193 shared
  • David J. Moore

    University of California, San Diego

    185 shared
  • Mariana Cherner

    Neurobehavioral Research (United States)

    176 shared

Education

  • B.A.

    Cambridge, England

  • Ph.D.

    University of Southern California

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