With the human life expectancy doubling in only the last 100 years, science has opened us up to this new found idea of longevity and healthy aging. Congruently, people living with HIV have longer life expectancies and can expect to live as long as those who do not have HIV. Healthy aging strategies to navigate living with HIV have only recently developed. The purpose of this study is to explore the associations between physical activity and cardiorespiratory fitness (VO2 peak) in older adults living with HIV. We will conduct a secondary analysis of cross-sectional baseline data of older adults living with HIV, who are participating in the HEALTH randomized clinical trial (ClinicalTrials.gov NCT04550676). This secondary analysis focuses on data involving waist-worn actigraph GT3X/1 monitors, home based actigraphy, and graded exercise tests involving VO2 max that are collected from the ongoing HEALTH clinical trial. We will analyze VO2 max and accelerometry data at baseline between decades of people in their 50, 60, and 70s. This sample is approximately 50 older adults with HIV. We will use descriptive analysis, Pearson correlation coefficient, and Chi-squared test. VO2 max is a valid measure of cardiovascular fitness and aerobic endurance based on the maximal oxygen consumption of individuals during an exercise protocol. This project cultivates an awareness around healthy aging strategies and bio behavioral interventions with a population that has low cardiorespiratory fitness. Both cardiorespiratory fitness and physical activity have been poorly measured using self-report methods in older adults. This secondary analysis uses gold standard objective measures (VO2 Max) to show data points with relation to variability in exercise. This data empowers people living with HIV to engage in strategies to improve their physical function and suggests the need for more bio behavioral interventions to be defined in order to facilitate healthy aging.

Schools across the country struggle with the issue of meal debt and lunch shaming practices used to discourage the accumulation of negative meal balances. These practices include dumping students’ trays in the trash upon non-payment, requiring students to work off their debt, or publicly shaming them. Although lunch shaming was banned in Washington State in 2018, the impacts of this policy shift have not been studied. High-poverty schools shifted to government-subsidized universal school meal programs (USMP) to address students’ food insecurity. Studies show USMP significantly increase the meal participation of students who were already enrolled in free lunch programs. While scholars speculate stigma might explain this phenomenon, it has not been studied directly. This study explores the role of stigma in school meal participation by studying two populations; students who are considered non-poor with meal debt and students who are enrolled in free and reduced priced meal programs. This study considers the role of stigma as a barrier to school meal participation by studying meal debt and students at the eligibility margins in free lunch programs. This study addresses existing gaps in the literature through a combination of in-depth interviews and observations of schools ineligible for government-subsidized USMP. In-depth interviews with school administrators expand understandings of school-level cultures, mealtime procedures, and experiences with meal debt. Observations at a single school over a 2-month period reveal how students experience mealtime, how kitchen workers execute meal debt policies, and the dynamics between students, their peers, and authority figures in the lunchline. Findings show that stigma is reproduced in the lunch line and act as a barrier to student meal participation. 

Merkel cell carcinoma (MCC) is a rare and aggressive skin cancer with a mortality rate of ~30%. In ~80% of cases, MCC development is attributed to the integration of Merkel cell polyomavirus (MCPyV) DNA into the host’s genome, leading to the expression of viral oncoproteins and tumorigenesis. Developing treatments that sustain immunity against MCC is imperative to address recurrent and/or progressive disease. In many cancers, tumor-infiltrating B cells have been associated with better prognosis and response to immunotherapies. However, the mechanisms by which B cells contribute to tumor immunity in humans have been difficult to resolve in part due to the inter-patient heterogeneity of tumor-specific antigens. The shared nature of MCPyV tumor antigens in MCC allows for MCC-specific B cell responses to be studied across patients. Using DNA-barcoded and fluorescently labeled viral oncoprotein tetramers, we analyzed the transcriptome, proteome, and receptor repertoire of MCC tumor-infiltrating B cells in 12 patient samples at single-cell resolution. From paired heavy and light chain sequences, we cloned 8 antibodies from B cells specific for the MCPyV oncoproteins to confirm binding to MCC-specific antigens. Transcriptomic and proteomic analyses of MCPyV-specific B cells revealed heterogeneity of intra-tumoral B cell responses. Interestingly, we found that the absence of MCC-specific germinal center (GC) B cells in MCC tumors associates with disease progression: ~80% of patients with no detectable GC B cells had MCC progression within a year post-surgery, whereas patients with detectable GC B cells remained progression-free a year after surgery (n=12, p=0.0043). These results suggest strong synergy between B cells and T cells may regulate tumor growth, as B cells rely on signals presented by T cells to differentiate into GC cells. Our long-term objective is to identify B cell phenotypes associated with anti-MCC responses to develop therapeutics that boost cancer-specific immunity.