A vibrant exchange of scientific discovery and potential strategic collaboration took place February 23–24, 2026 at the University of Virginia, as researchers from AstraZeneca met with faculty from across the School of Medicine. 

The Robert M. Berne Cardiovascular Research Center and the Beirne B. Carter Center for Immunology Research hosted the two-day event, that brought together members of AstraZeneca’s Cardiovascular, Renal and Metabolism (CVRM) team, alongside its Respiratory & Immunology (R&I) team — including representatives from the company’s Open Innovation and Corporate Affairs teams— with UVA investigators and leadership from the School of Medicine (SOM) and the Office of the Vice President for Research (VPR). 

Strong Institutional Engagement 

The meetings reflected deep engagement on both sides. More than 60 UVA faculty laboratories submitted one-page proposals outlining innovative research programs and potential areas for collaboration with AstraZeneca. Following review, 33 labs were selected to present their science and participate in focused discussions about how future collaborations could be structured to accelerate discovery and therapeutic development. 

The breadth of science represented underscored UVA’s strengths across cardiovascular, renal, metabolic, respiratory, and immunologic research. Topics ranged from inflammatory drivers of cardiometabolic disease and immune-mediated tissue injury to biomarker discovery, advanced human model systems, translational data science, and novel therapeutic targets. 

UVA School of Medicine and Office of Research leadership were in attendance throughout the program, signaling institutional commitment to fostering high-impact academic–industry partnerships and supporting pathways that move discovery from bench to bedside. 

Science at the Interface of Disciplines 

A recurring theme of the meetings was the growing intersection between immune biology and cardiometabolic disease. Investigators from across the school of medicine highlighted advances in heart failure, vascular biology, thrombosis, and metabolic regulation. Other colleagues presented cutting-edge work in immune signaling, inflammation, host defense, and tissue homeostasis. 

AstraZeneca scientists engaged deeply with presenters, exploring how UVA’s mechanistic discoveries could align with the company’s global capabilities in drug development, translational medicine, and clinical trials. The presence of AstraZeneca’s Open Innovation Team created opportunities to discuss flexible partnership models, while Corporate Strategy leaders examined long-term alignment and portfolio integration. 

From Dialogue to Discovery 

The format emphasized interaction. Following each presentation, robust scientific discussion focused not only on experimental findings but also on practical next steps — from target validation and preclinical modeling to biomarker strategy and patient stratification. 

Networking sessions and smaller breakout meetings allowed faculty and AstraZeneca representatives to explore specific collaboration concepts in greater depth. Conversations centered on building sustainable connections designed to generate new discoveries and ultimately improve outcomes for patients worldwide. 

With strong participation, engaged institutional leadership, and cross-disciplinary scientific exchange, the February gathering marked an important milestone in strengthening ties between UVA and AstraZeneca. Participants left with a shared sense of momentum — and a commitment to advancing innovative science through collaboration in service of global patient care.

Link to Article on the UVA Research Website

As Beirne Carter predicted in 1989 when he established the CIC, immunology has emerged as a pivotal discipline in the discovery of new treatments for a host of conditions such as autoimmunity, cancer, infection, neurologic, allergic, cardiometabolic, renal and lung disease.  “Today, immunologists in the CIC are discovering novel immune mechanisms and pathways with the potential to lead to new and improved therapies for patients with these immune-mediated diseases,” explains Coleen McNamara, MD (Co-Director of the CIC). Yet, translating research discoveries in immunology from the lab to the clinic can be challenging and burdensome. 

To alleviate these challenges and to make translational research more accessible for UVA researchers, HIPI will provide staff and seed funding to catalyze translating discovery to the patient. The initiative will facilitate UVA researchers’ efforts to provide customized, optimized treatments based on a patient’s unique immune “fingerprint,” ensuring the right medicines get to the right patients at the right time. Melanie Rutkowski, PhD, Associate Professor Microbiology, Immunology, and Cancer Biology and Jeff Sturek, MD, PhD, Associate Professor of Medicine in the Division of Pulmonary and Critical Care, will serve as the inaugural co-directors of HIPI. Together, they represent the clinical and fundamental research expertise that HIPI will wield to improve patient outcomes.

The CIC is grateful for the almost $13M invested by BCF in the Center since its inception. Beirne Carter and former UVA Dean Robert Carey shared the belief that immunology had the ability to transform patient care. The BCF reaffirmed this vision in 2009 with a pledge to help build the Carter-Harrison Research Building, where the CIC now resides. More recently, the BCF, now led by Carter’s daughter, Rossie Hutcheson, has supported research funding, travel and event sponsorship to enhance the CIC’s work.

With the support of the BCF, HIPI will facilitate advances in effective, targeted, and minimally invasive treatments for chronic diseases. The new Initiative will uplift the CIC and the immunology community across UVA, building on the foundations Carter and Hutcheson have provided. The CIC extends its deepest gratitude to Hutcheson and the BCF for their continued belief in the transformational power of immunological research.

“We are hoping to catalyze our discoveries into paradigm-shifting immune therapies, not only for cancer patients, but also other diseases in which the microbiome is dysregulated.”

Genome-Wide Association Studies (GWAS) compare the genetic codes of people who suffer from a particular condition and those who do not. The comparison reveals a subset of genetic variants that determine susceptibility to developing the condition. These studies do not directly identify culprit genes or reveal mechanism how these genes may function in the disease context, however. They do not pinpoint pathways, which of the patient’s cells are affected by the genetic variations, or how to target these genes for treatment. The Zhou lab aims to fill out these connections using integrative and multidisciplinary approaches. They specialize in conditions affecting the lungs—asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis. By describing all the biological steps between a mistake in someone’s DNA and the disease that arises from it, Zhou and her team turn biostatistical associations into molecular insights that can lead to new treatments for the most prevalent lung diseases.

“I’m an ambitious person,” says Zhou. “I want to see the end product of our work benefit patients.” To that end, Zhou has launched an early-stage business venture, G2Q, based on her research portfolio. She is also excited to be embedded in the collaborative research ventures at UVA, including the CIC. In fact, it was CIC member Jie Sun, PhD, who initially encouraged Zhou to explore a move to UVA. She is excited to join the CIC community and expand her research network. The Zhou lab seeks an MD-PhD student to join the team, and interested parties should contact Zhou for additional information.

Per the National Cancer Institute, ovarian cancer is the eighth most common cancer in women globally and the fifth leading cause of cancer death for women in the US. This is in part due to the cancer being difficult to detect before it has spread to other organs – nearly 80% of patients are diagnosed after the cancer has metastasized, which makes the disease much more difficult to treat. Patients will often respond well to early treatments, but their cancers very commonly recur and develop resistance to chemotherapy. Immune therapies, which harness and amplify the body’s natural defenses against cancer and disease, have transformed patient care in other cancers, but remain ineffective against ovarian cancer. The Rutkowski Lab will use this award to study how molecular signaling between bacterial flagellin and the tumor cell can smother the patient’s immune response, making immune therapies ineffective.

Rutkowski is an expert in understanding how the bacteria that live in our bodies affect cancer progression. As tumors grow, they create a microenvironment within the body. For example, some tumors actively create an acidic microenvironment, which breaks down the surrounding tissues, making it easier for the cancer to spread. These microenvironmental changes can alter the balance of bacterial species around the tumor, allowing bacteria from the mouth and gut to inhabit tissues they ordinarily could not survive in. Recently, the lab discovered that bacterial flagellin in ovarian tumors can inhibit immune therapies through TLR5 signaling, a pathway that normally activates the immune system in response to bacterial infections. Rutkowski and coworkers will use this grant award to understand this TLR5 paradox and to devise strategies that disrupt the cancer-bacterial alliance. Rutkowski and her team anticipate that this work will improve the efficacy of immune therapies for ovarian tumors, which have been largely ineffective, resulting in enhanced outcomes for women diagnosed with this disease. 

Dr. Klebanoff was hosted by Kristin Anderson, PhD. In his lecture, he described how T cell receptors allow the immune system to target proteins within the cell, rather than only those on its surface. This presents new opportunities for immune therapies against cancer, but the T cell receptors have complex structures. Dr. Klebanoff’s research described both the variations between receptors and his team’s efforts to advance their potential as immunotherapy targets. A reception followed the talk in the Braciale Courtyard of MR6.

In her lecture, “A Polyamine-mediated Posttranslational Modification That Governs Macrophage Tissue Residency,” Pearce demonstrated her expertise in immunometabolism. Her talk discussed how modifications to a protein, eukaryotic translation initiation factor 5A, regulates the future behavior of immune cells. Her work traced the downstream consequences of changes in this metabolic process into a host of organ systems. In appreciation for her excellent lecture and preeminence in immunometabolism, the CIC presented Pearce with a Jefferson Cup.

A reception followed the lecture in the Pinn Hall Conference Center atrium.

Human immunodeficiency virus (HIV) is a viral infection that destroys the body’s white blood cells. In most patients, this leads to acquired immunodeficiency syndrome (AIDS), where the immune system has been weakened to the point of incompetence. However, a small subset of HIV patients can naturally go their entire lives without developing AIDS and without need of anti-retroviral drug therapy. These ‘elite controllers’ share a distinctive genetic feature. Their NK cells express a specific inhibitory receptor, a kind of molecular sensor, that can bind HLA-B57 (an MHC class I protein) which is found on most cells in people who display extraordinary HIV protection. However, it is unknown how the inhibitory receptor and its HLA-B57 ligand together protect elite controllers from HIV & AIDS.   

Brown has long studied mouse NK cells, identifying genes used by NK cells to protect against viral infection. Years ago, his team found that the Ly49G inhibitory receptor and its MHC class I ligand known as H2-D^k in mice was linked with protection against viral infection. Getting to that point was challenging, however, and when he first reported the inhibitory receptor’s protective role, the scientific community was skeptical of his conclusions. “It was a bit of a nightmare,” recalls Brown. His resolve was strengthened by several genetic association studies in humans which reported evidence that both activating and inhibitory NK receptor genes and their MHC class I ligands were linked with protection in HIV patients.

For over a decade, Brown and his team worked to prove in a living organism that the inhibitory receptor was necessary for antiviral immunity. A common method to address this kind of question would be to delete the gene that corresponds to the receptor and observe how the NK cell behavior changes. The genes that encode the different NK receptors are very similar, however, making them difficult to specifically delete. Prior work had shown it was possible to delete multiple NK receptors instead of one, but this would not provide the specificity needed for Brown’s study. So, Brown’s team implemented state-of-the-art CRISPR technology and became the first to remove a single inhibitory receptor gene from the mouse genome. This advance was all that was needed to ultimately prove that the Ly49G inhibitory receptor is required by NK cells to protect against viral infection. Intriguingly, their same study discovered that an activating receptor known as Ly49R works together in a ‘paired fashion’ along with Ly49G to allow NK cells to find and kill virus-infected target cells.

Prior skepticism of the inhibitory receptor’s role meant Brown faced challenges securing external grant funding. In the absence of federal funds, which are critical for staff, materials, and equipment, Brown’s research productivity slowed. Interim support from the Carter Center, School of Medicine, Department of Medicine and Division of Nephrology allowed Brown to continue his work. “I was able to bring this grant in because other folks found ways to keep me here and keep me going, and for that I’m extremely grateful,” he said. This new award will reinvigorate the lab’s program. “I’ll be able to bring in staff and start training graduate students. One of the things I love most is to help young people develop and do what I’ve done in science, and this award will expand my capacity to lead in our training programs.” Extra personnel will accelerate the pace of Brown’s research which seeks to discover how paired receptor systems can enhance NK virus control and antiviral immune protection in both mouse and human studies which can lead to novel strategies to enhance immune protection in chronic viral disease settings.

The Brown Lab is looking to hire at the Research Associate level in the upcoming months. Interested parties should contact Brown via email.

Vaccines injected into muscles, like the current COVID and flu vaccines, are effective because they train the immune system to recognize viruses or viral fragments in advance of a real infection. These vaccines generate strong systemic immune responses, bringing a person’s antiviral defenses online throughout their body after infection. However, because the vaccine is delivered through the blood, the body’s response is strongest in the blood. Tang’s previous finding in the Sun Lab has shown that while people vaccinated against COVID have good immunity in their blood, the immune responses in their mucus membranes can be suboptimal. COVID infects humans through these membranes, which in part explains why the current COVID vaccine is good at preventing severe disease, but does not provide complete immunity against infection.

Tang and the Sun Lab have shown that administering a vaccine booster to the mucosal membranes provides better protection against COVID infection. There are, however, many outstanding questions for Tang to address. The behaviors of B cells, T cells, and the ability of antibody-secreting cells to produce the protective molecule Immunoglobulin A all must be studied. Tang will also study how pairing mucosal and current vaccination methods protect against COVID in children and animal models. “The work I’m going to do will show how we can most effectively stimulate our immune systems,” says Tang.

There are other challenges facing mucosal vaccine development. One of the biggest, says Tang, is delivering a mucosal vaccine to the entire respiratory tract. “A nasal spray, for example, is likely to be more effective in the upper parts of your respiratory system. You may not have the same immunity in lower areas like the windpipe and lungs.” Sun and Tang hope their research impels further research to address this problem.

Tang credits the collegial, collaborative research atmosphere at UVA for the success of his research and award application. Working with Sun and other UVA researchers, including Gerald Teague, MD, Justin Taylor, PhD, Anne Sperling, PhD, as well as Shan-Lu Liu, MD, PhD from The Ohio State University, enables Tang to access expertise in fields varying from statistics to pulmonology. “I have perfect co-mentors from every area,” says Tang. “This award is a huge milestone in my career, and they’re one of the reasons I got it.”