About

Allison M Andrews is an Associate Professor in the Department of Pathology, Immunology and Laboratory Medicine at the University of Florida College of Medicine. Her research focuses on neuroimmune interactions, particularly the effects of substances such as nicotine, fentanyl, cocaine, and cannabinoids on the blood-brain barrier, HIV replication, and neuroHIV. She investigates the mechanisms underlying blood-brain barrier dysfunction, HIV reservoirs in the central nervous system, and the impact of substance abuse on neuroimmune health. Her work involves developing innovative in-situ imaging techniques to visualize HIV reservoirs in the CNS and studying how drugs influence blood-brain barrier integrity and hematopoietic stem cell differentiation. She serves as the principal investigator on multiple projects funded by the National Institute of Health (NIH), exploring the neuroimmune and cognitive consequences of substance use and its implications for anti-retroviral therapies. Dr. Andrews contributes to the academic community through teaching courses such as GMS5905 – Special Topics in Biomedical Sciences, and she is actively involved in advancing understanding of neuroimmune mechanisms related to HIV and substance abuse.

Research topics

• Biology
• Cell biology
• Neuroscience
• Anatomy
• Chemistry

Selected publications

• The 30 ^th Scientific Conference of the Society on NeuroImmune Pharmacology in Annapolis, Maryland, May 3 ^rd – 6 ^th , 2026

  NeuroImmune Pharmacology and Therapeutics · 2026-03-01

  articleOpen access

  Abstract The 30 th Annual Society on Neuroimmune Pharmacology (SNIP) conference will be held on May 3-6 th at the Graduate Hotel by Hilton in Annapolis, Maryland. This 4-day conference will present preclinical, translational, and clinical research in the intersecting fields of neuro-HIV and substance use disorders, as well as related neurodegenerative conditions. The speakers and poster presenters will share cutting-edge research funded by the National Institutes of Health. On the first day, we will have two concurrent preconference symposia. The first is “Single Cell HIV and SUD Effects on the Brain: SCORCH Consortium Progress”, with an overview and 7 presentations by investigators, highlighting the outstanding work in the Single Cell Opioid Response in the Context of HIV (SCORCH). The second concurrent symposium is “Catalyzing Interdisciplinary Research on HIV-Associated Co-occurring Conditions.” In the evening, we will have our first Poster Session with 52 abstracts by early-stage-career investigators (ECIs), including those that received the ECI travel awards. On days 2-4, in addition to a plenary talk and two memorial lectures, we will have 11 symposia, with 62 speakers (including 12 who are early-stage career investigator travel awardees), and 65 additional poster presentations. In total, the 30 th SNIP conference received 185 abstracts for the 70 oral presentations and 115 posters. Topics covered by these symposia and poster presentations include mechanistic and observational studies that evaluate neuronal injury and neuroinflammation associated with HIV brain infection, and how drugs of abuse, including stimulants, opioids, and cannabis, may exacerbate or mitigate neuropathogenesis. In addition, with the aging population of people with HIV and many with substance use disorders, recent work also evaluated how aging and various neurodegenerative disorders could further impact brain health. At the plenary lecture, Dr. Nora Volkow will highlight the priorities of HIV research at the National Institute on Drug Abuse (NIDA), while our banquet speaker, Dr. Avindra Nath will elucidate how viruses, particularly retroviruses, may invade the brain, infect brain cells, and adapt to the local environment for decades or mutate and possibly lead to neurodegenerative disorders. This will be an exciting conference that will continue SNIP’s emphasis on the career development of early-stage investigators.

  PublisherOA PDFDOI

• Abstract 4087: Senescent cancer cells facilitate metastasis by adhesion-mediated clustering and immune modulation

  Cancer Research · 2026-04-03

  article

  Abstract Therapy-induced senescence (TIS) occurs following cytotoxic stress and has previously shown to promote tumor metastasis through senescence-associated secretory phenotype (SASP) of stromal cells in the tumor microenvironment, however, whether senescent cancer cells directly participate in metastatic dissemination remains unclear. Here, we report that therapy-induced senescent breast cancer cells actively promote metastatic seeding by physically adhering to parental breast cancer cells and forming circulating senescent-parental cell clusters. Senescence was induced in MDA-MB-231 cells with doxorubicin (39 nM, 7 days) or in 4T1 cells via irradiation (50 Gy, 7 days) and confirmed by X-gal staining, NIR-BG2 senescence probe activity, and increased p16 and SASP expression. RNA-seq revealed upregulation of migration, motility, and adhesion pathways of senescence cells with specific increases in ICAM1, JUP, CLDN1, and CLDN7. Functionally, senescent cells were able to migrate independently, but the presence of both senescent and parental cells in co-culture significantly enhanced migration of both cell types in trans-well and wound healing assays. Hanging-drop aggregation produced large mixed clusters in co-culture, whereas parental cells alone formed scattered microcolonies. Direct adhesion assays showed parental tumor cells preferentially attached to senescent cells versus the substrate, with individual senescent cells binding multiple parental cells. In vivo, orthotopic co-injection of senescent and parental MDA-MB-231 cells in NSG mice resulted in significantly increased lung metastasis. Early tail-vain tracking revealed greater initial lung seeding when co-injected parental cancer cells with senescent MDA-MB-231 in NSG mice and 4T1 cells in NSG and BALB/c mice models, respectively. Interestingly, in immune competent BALB/c mice, metastatic progression sustained over time. These findings reveal a previously unrecognized mechanism in which senescent cancer cells cooperate with parental cancer cells through cell-cell adhesion mediated clustering to facilitate early metastatic colonization. Ongoing studies examine the functional role of ICAM1 and JUP, and the involvement of the immune system as a second phase of metastasis following dissemination, where senescent cells may reshape the microenvironment to promote tumor cells survival. These results suggest that targeting senescent cell adhesion and immune programs may suppress early dissemination and metastatic relapse following cancer therapy. Citation Format: Seyedehalaleh Anvar, Chandra Maharjan, Zixin Chen, Johnathan D Somers, Zeng Jin, Heather R Kates, Servio H. Ramirez, Allison M. Andrews, Breanna M. Runyon, Madison Elizabeth Carelock, Yuzhao Zhang, Jun Liu, Weizhou Zhang, Lina Cui. Senescent cancer cells facilitate metastasis by adhesion-mediated clustering and immune modulation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 4087.

  PublisherDOI

• Extracellular Microvesicles Released From Brain Endothelial Cells are Detected in Animal Models Of HIV-1 Signifying Unresolved Inflammation

  UNC Libraries · 2025-05-16

  articleOpen accessSenior author
  PublisherDOI

• Cannabis use is associated with a lower likelihood of presence of HIV drug resistance mutations in a retrospective cohort of adults with HIV

  NeuroImmune Pharmacology and Therapeutics · 2025-02-07

  articleOpen accessSenior author

  Objectives: 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. Methods: 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. Results: 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). Conclusions: 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.

  PublisherOA PDFDOI

• Review for "The influence of blood brain barrier permeability on CSF-to-serum ratios of neurobiomarkers in people with HIV"

  2025-12-17

  peer-review1st authorCorresponding
  PublisherDOI

• Correction to: Extracellular Microvesicles Released From Brain Endothelial Cells are Detected in Animal Models Of HIV‑1 Signifying Unresolved Inflammation

  UNC Libraries · 2025-05-16

  articleOpen access
  PublisherDOI

• The 29th Scientific Conference of the Society on NeuroImmune Pharmacology in Omaha, NE, June 8–12, 2025

  NeuroImmune Pharmacology and Therapeutics · 2025-03-01

  articleOpen access1st authorCorresponding

  , 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 Swarts, the Robert Eisenberg Family, Howard Kooper, the Gendelman Family Research Endowment, Fisher Scientific, Amy Sather, and the research community for sponsoring this meeting and its exchanges.

  PublisherOA PDFDOI

• In pursuit of an HIV cure: from stem cell transplants to gene therapies

  Frontiers in Genome Editing · 2025-09-05 · 2 citations

  reviewOpen accessSenior author

  Since 2009, seven people living with human immunodeficiency virus (PLHIV) have been declared cured of HIV after receiving allogeneic hematopoietic stem cell transplants (alloHSCTs) to treat hematologic malignancies. In this sense, cure signifies the absence of viral DNA/RNA and undetectable viral loads without the use of antiretroviral therapy (ART). Five of these transplants utilized mutated C-C motif chemokine receptor type 5 (CCR5 Δ32/Δ32 ) stem cells. Much has been learned from these and past cases, and although effective, bone marrow transplants cannot be easily or safely translated to cure the millions of PLHIV across the globe. A successful eradicating cure includes both the prevention of HIV from entering new cells and the elimination of tissue reservoirs. Protecting hematopoietic stem and progenitor cells (HSPCs) from infection is a key consideration since there is evidence that HSPCs themselves, not only their descendants, are susceptible to infection. Gene therapy approaches have the potential to bring about an eradicating HIV cure that could be highly effective, broadly applicable, less expensive, and practical to implement. Current strategies are tackling this problem by removing the integrated proviral DNA from infected cells and/or eliminating the co-receptor(s) necessary for HIV viral entry into target cells. Both approaches hold promise, but they require overcoming key challenges (i.e., vector toxicity, transduction efficacy, elimination of reservoir cells, etc.). This review summarizes and examines the lessons learned about curing HIV through bone marrow transplants, the current gene therapy methodologies, pitfalls of eradication strategies as well as future directions of the field.

  PublisherOA PDFDOI

• Engineered Dual Antioxidant Enzyme Complexes Targeting ICAM-1 on Brain Endothelium Reduce Brain Injury-Associated Neuroinflammation

  Bioengineering · 2024-02-21 · 6 citations

  articleOpen access

  The neuroinflammatory cascade triggered by traumatic brain injury (TBI) represents a clinically important point for therapeutic intervention. Neuroinflammation generates oxidative stress in the form of high-energy reactive oxygen and nitrogen species, which are key mediators of TBI pathology. The role of the blood-brain barrier (BBB) is essential for proper neuronal function and is vulnerable to oxidative stress. Results herein explore the notion that attenuating oxidative stress at the vasculature after TBI may result in improved BBB integrity and neuroprotection. Utilizing amino-chemistry, a biological construct (designated "dual conjugate" for short) was generated by covalently binding two antioxidant enzymes (superoxide dismutase 1 (SOD-1) and catalase (CAT)) to antibodies specific for ICAM-1. Bioengineering of the conjugate preserved its targeting and enzymatic functions, as evaluated by real-time bioenergetic measurements (via the Seahorse-XF platform), in brain endothelial cells exposed to increasing concentrations of hydrogen peroxide or a superoxide anion donor. Results showed that the dual conjugate effectively mitigated the mitochondrial stress due to oxidative damage. Furthermore, dual conjugate administration also improved BBB and endothelial protection under oxidative insult in an in vitro model of TBI utilizing a software-controlled stretching device that induces a 20% in mechanical strain on the endothelial cells. Additionally, the dual conjugate was also effective in reducing indices of neuroinflammation in a controlled cortical impact (CCI)-TBI animal model. Thus, these studies provide proof of concept that targeted dual antioxidant biologicals may offer a means to regulate oxidative stress-associated cellular damage during neurotrauma.

  PublisherOA PDFDOI

• Effects of Drag-Reducing Polymers on Hemodynamics and Whole Blood–Endothelial Interactions in 3D-Printed Vascular Topologies

  ACS Applied Materials & Interfaces · 2024-03-15 · 4 citations

  articleOpen access

  Most in vitro models use culture medium to apply fluid shear stress to endothelial cells, which does not capture the interaction between blood and endothelial cells. Here, we describe a new system to characterize whole blood flow through a 3D-printed, endothelialized vascular topology that induces flow separation at a bifurcation. Drag-reducing polymers, which have been previously studied as a potential therapy to reduce the pressure drop across the vascular bed, are evaluated for their effect on mitigating the disturbed flow. Polymer concentrations of 1000 ppm prevented recirculation and disturbed flow at the wall. Proteomic analysis of plasma collected from whole blood recirculated through the vascularized channel with and without drag-reducing polymers provides insight into the effects of flow regimes on levels of proteins indicative of the endothelial-blood interaction. The results indicate that blood flow alters proteins associated with coagulation, inflammation, and other processes. Overall, these proof-of-concept experiments demonstrate the importance of using whole blood flow to study the endothelial response to perfusion.

  PublisherOA PDFDOI

Frequent coauthors

• Bruce G. Calman

  University of Florida

  35 shared

• W. Clay Smith

  University of Florida

  22 shared

• B.‐A. Battelle

  University of Florida

  22 shared

• Barbara‐Anne Battelle

  University of Florida

  18 shared

• Michael A. Malone

  University of St. Augustine for Health Sciences

  9 shared

• M. B. Mleziva

  University of Florida

  9 shared

• Robert M. Greenberg

  University of Pennsylvania

  9 shared

• Chelsi Cacciatore

  Whitney Museum of American Art

  9 shared

Labs

• Genomic LaboratoriesPI

Education

• Ph.D., Biomedical Engineering

  Drexel University

  2012

• B.S., Agricultural & Biological Engineering

  University of Florida

  2006