Research spotlight: Medicare spending on clinical care for people aging with HIV projected to rise steeply over next decade
As more Americans with HIV live into older age, Medicare spending on their care is projected to rise dramatically from $10.9 billion in 2026 to $27.3 billion in 2035, with HIV medications accounting for nearly two-thirds of total costs.
Brigham and Women's Hospital
Emily P. Hyle, MD, and Kenneth A. Freedberg, MD, of the Medical Practice Evaluation Center within the Department of Medicine at Mass General Brigham, are the lead and senior authors of a paper published in JAMA Network Open, “Ten-Year Cost Projections for Medicare Beneficiaries 65 Years or Older With HIV.”
Q: What challenges or unmet needs make this study important?
Survival among people with HIV in the United States continues to improve due to highly effective antiretroviral therapy (ART), a lifelong treatment. As a result, costs to Medicare are expected to rise substantially as more adults with HIV live long enough to age into the program. However, it’s been largely unknown just how extensive the increase in Medicare beneficiaries may be over the next decade and how much the program’s spending could rise.
Q: What central question(s) were you investigating?
Our team used simulation modeling to answer these three main questions:
- Over the next decade, how many people with HIV (who are receiving HIV care) over the age of 65 are likely to be enrolled in Medicare?
- How much is Medicare estimated to spend on this population over this time period?
- How might policies or strategies to reduce the cost of ART impact these projections?
Q: What methods or approach did you use?
We developed and populated a new model called CHARMED with projections from the previously validated CEPAC model, Medicare claims data, and publicly available data. Our aim was to simulate a population of Medicare beneficiaries with HIV, aged 65+ and being treated with ART, and their associated costs.
To address uncertainty in model estimates and trends, we examined scenarios where the size and associated costs of this group varied—for example, by assessing the potential impact of policies to reduce the cost of ART. Such policies included the Inflation Reduction Act (IRA), which allows Medicare to negotiate the cost of Biktarvy, the most prescribed ART regimen in the United States, with lower prices to take effect in 2028. Additionally, generic dolutegravir is expected to become available in 2031, thereby enabling a highly effective, well-tolerated, fully generic ART regimen.
Q: What did you find?
Our projections show that nearly 122,000 older adults receiving HIV care may be enrolled in Medicare by the end of 2026—a number that may increase to about 193,600 by the end of 2035. We also estimated that annual Medicare spending for this population may increase from $10.9 billion at the end of 2026 to $27.3 billion at the end of 2035.
Cumulative 10-year costs may reach $187.2 billion, with 63% attributable to ART costs alone. If ART costs were reduced by 60%, Medicare could potentially save $70.3 billion over the next decade. Moreover, if current prescribing patterns remain unchanged, policies such as the IRA and the availability of generic HIV medications could save Medicare approximately $19 billion between 2026 and 2035.
Q: What are the real-world implications, particularly for patients?
Our findings demonstrate that the number of older adults living with HIV is likely to increase substantially over the next decade, driving up Medicare enrollment. Clinicians and healthcare systems must be prepared to address the medical needs of this growing population through comprehensive, person-centered care—especially given these individuals’ increased risk of comorbidities and polypharmacy (taking several medications regularly).
We also conclude that policymakers for Medicare and other public programs will likely seek out ways to reduce the cost of HIV care. While recent proposals have included higher Medicare premiums, drug coverage reductions, and stricter eligibility for drug assistance programs, our paper points to other promising strategies to reduce ART costs without increasing patient costs or limiting access.
Authorship: In addition to Hyle and Freedberg, Mass General Brigham authors include Luke Ang, Grace Luu, Florence Ebem, Satoshi Koiso, Paul E. Sax, John Giardina, E. John Orav, Anne M. Neilan, and Jose F. Figueroa. Additional authors include Parastu Kasaie, Dannie Dai, Jessica Phelan, Ciara Duggan, Elizabeth Humes, Dori Molozanov, Lucas Gerace, Tim Horn, Ankur Pandya, and Keri N. Althoff.
Paper cited: Hyle, EP., et al. “Ten-Year Cost Projections for Medicare Beneficiaries 65 Years or Older with HIV.” JAMA Network Open. DOI: 10.1001/jamanetworkopen.2026.21966
Funding: This research was funded by the National Institutes of Health (R01 AG069575, R01 AI042006, R01 AG081151, U01 AI069918, R01 AG053100, R01 AI179776) and the Massachusetts General Hospital Jerome and Celia Reich HIV Scholar Award.
Disclosures: Hyle, Humes, Giardina, Neilan, Figueroa, Althoff and Freedberg reported receiving grants from the National Institute of Health (NIH).
Journal
JAMA Network Open
Method of Research
Data/statistical analysis
Subject of Research
People
Article Title
Ten-Year Cost Projections for Medicare Beneficiaries 65 Years or Older with HIV
Article Publication Date
7-Jul-2026
COI Statement
Hyle, Humes, Giardina, Neilan, Figueroa, Althoff and Freedberg reported receiving grants from the National Institute of Health (NIH).
Tumor-like tissue environments could hold clues to curing HIV
Viral reservoirs in a proxy animal model of HIV share features with immune-suppressive tumors
Northwestern University
- Rather than study specific cells, study zoomed out to examine broader microenvironment in animal models with SIV, a proxy of HIV
- First systematic comparisons between virus microenvironment and tumor microenvironment in gut tissue
- Scientists used novel molecular imaging, spatial transcriptomics and machine-learning techniques
CHICAGO — The tissue microenvironments surrounding HIV-infected immune cells look a lot like those surrounding cancerous tumors, reports a new Northwestern University study.
The findings help explain why HIV has been so difficult to cure. Scientists found that viral reservoirs exist within tissue microenvironments that resemble immune-suppressive tumor microenvironments, suggesting that future HIV cure strategies may benefit from approaches traditionally used in cancer therapy.
The study was published Aug. 4 in the journal Frontiers in Immunology.
By integrating molecular imaging, spatial transcriptomics and machine learning, the scientists created a detailed map of the viral microenvironment in animal models with Simian Immunodeficiency Virus (SIV), which is commonly studied to better understand HIV. In doing so, they identified shared biological programs between viral persistence and tumor immune evasion.
“We are interested in the similarities with cancer because to cure any type of cancer, you need to deal with a series of factors, not just one thing,” said corresponding author Ramon Lorenzo-Redondo, assistant professor of medicine in the division of infectious diseases at Northwestern University Feinberg School of Medicine. “We are now trying to understand the chain of events that leads to that environment to then target all the components of this multi-component, multi-systemic problem.”
Viral reservoirs create a ‘sanctuary’ for HIV to thrive
The resemblance to cancer emerged from the scientists’ effort to better understand viral reservoirs, the small pockets of virus that remain hidden in the body after treatment. These can reignite infection if therapy is stopped, making a functional cure difficult to achieve.
“We think the virus promotes a whole sanctuary-type environment that allows it to survive, but also, because it's immune exclusive, it stops the cells that are supposed to kill the virus,” Lorenzo-Redondo said. “As soon as you remove treatment, because these populations are ready to go and cannot be cleared, they again trigger a chain of events that will infect other cells.”
Study zooms out to see the entire HIV microenvironment
To understand why these reservoirs persist for decades, the researchers looked beyond the infected cells themselves.
Previous studies focused on identifying the cells that harbor HIV. This study instead examined the broader tissue microenvironment, revealing how the surrounding “neighborhood” helps the virus persist and rebound when treatment stops.
“Imagine the infected cell is a beautiful house, set near the beach with a stunning mountain view,” Lorenzo-Redondo said. “If you change the neighborhood — build a highway through it, remove what makes it desirable — you make it much harder for anyone to stay. Our goal is to understand how to reshape that neighborhood so the immune system can move in, break down these reservoirs and finally do its job.”
The findings lay critical groundwork for future HIV cure strategies aimed not only at eliminating infected cells, but also at disrupting the environments that protect them and make viral persistence possible.
Studying gut tissues — not just blood — revealed tumor environment similarities
The tumor-like characteristics became apparent only when the scientists examined SIV reservoirs within gut tissue, where most persistent virus survives during therapy. This was novel compared to previous research that focused only on blood samples.
Two Northwestern labs approached the problem in complementary ways, allowing them to see the same phenomenon from multiple perspectives. Co-corresponding author Thomas J. Hope, professor of cell and developmental biology and obstetrics and gynecology at Feinberg, likened the collaboration to reconstructing events at a party. His lab's imaging methods provided snapshots of what is happening in tissues at a given moment, while Lorenzo-Redondo’s computational analyses revealed the relationships and interactions occurring behind the scenes.
“With imaging, we're taking snapshots of the party,” Hope said. “We can see who's there, where they are and what's happening in that moment. But Ramon can use these large-scale sequencing datasets to figure out who was talking to whom, what groups formed and how the interactions changed over time.”
Using a novel imaging and spatial transcriptomics platform that combines immunoPET/CT-guided tissue mapping with high-resolution genomic analysis, the scientists, led by Eliana Crentsil, a graduate student in Hope’s and Lorenzo-Redondo’s labs, located and analyzed rare sites of viral persistence within tissues in the guts of non-human primate animal models.
The team noticed the collection of cells, signals and tissues that surround viral reservoirs, called the viral microenvironment (VME), may share important features with so-called “cold” tumor microenvironments (TME), which are known to suppress immune responses and resist clearance by the body’s defenses.
“When two completely different approaches keep pointing to the same conclusion, it gives you a lot of confidence that you've uncovered something real,” Hope said. “In our case, both approaches pointed to HIV reservoirs existing within tissue environments that resemble those seen in difficult-to-treat cancers.”
The reservoirs that shared features with the “cold” tumors showed increased activity in biological pathways linked to tissue remodeling and immune suppression. In contrast, short-lived reservoirs more closely resembled “hot” tumors, which attract stronger immune responses and showed higher levels of immune cells capable of killing infected cells. The scientists also found that regulatory T cells, which help control immune activity, played a central role in the cell-to-cell communication networks around viral reservoirs.
Using machine learning, the team identified several human genes, including KRT8, EPCAM and RRM2, as important contributors to the tumor-like features seen in persistent viral reservoirs.
Together, the findings suggest HIV persistence depends not only on infected cells, but also on the tissue environments that shield them. By disrupting those protective environments, researchers may eventually make viral reservoirs more vulnerable to immune attack, much as cancer therapies seek to overcome immune-suppressive tumor microenvironments.
The study is titled, “A tissue microenvironment analogous to certain tumor microenvironments facilitates HIV persistence.” Natalie Stegman is a Northwestern co-author on the study.
Journal
Frontiers in Immunology
Article Title
A tissue microenvironment analogous to certain tumor microenvironments facilitates HIV persistence
Article Publication Date
4-Aug-2026
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