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Background: Research has demonstrated that common chronic conditions, especially those related to cardiovascular health, are important risk factors for severe COVID-19 symptoms or hospitalization. Population prevalence rates of such conditions have not previously been examined in relation to COVID-19 case fatality rates in the Central Appalachian region. Purpose: This study examined prevalence rates of selected chronic conditions and COVID-19 case fatality rates to determine whether the relationship between them is consistent across Appalachian and non-Appalachian regions of Kentucky. Methods: Data from Kentucky’s Behavioral Risk Factor Survey (KyBRFS) were used to calculate prevalence rates of asthma, diabetes, influenza vaccination, hypertension, obesity, having a personal doctor, physical inactivity, and cigarette smoking. Publicly available COVID-19 case and death counts by county were used to calculate incidence and case fatality rates. Units of analysis were 41 single- and multi-county areas developed to visualize KyBRFS prevalence rates. Analysis included t-tests to compare Appalachian and non-Appalachian regions, and correlations characterizing associations between COVID-19 case fatality and rates of chronic conditions and behaviors. Results: Incidence and case fatality rates for COVID-19 were slightly lower in the Appalachian region, but not significantly. Significant correlations between COVID-19 case fatality and the prevalence of chronic conditions and behaviors were more common in the non-Appalachian region. Implications: Case fatality rates in Appalachia appear lower than expected, given the high prevalence of important chronic conditions and behaviors known to be associated with poor COVID-19 outcomes. This phenomenon merits further research and should be considered by public health researchers when examining COVID-19 outcomes in Kentucky and neighboring states., Copyright © 2021 W. Jay Christian

Loss of T cell immunogenicity due to mutations in virally encoded epitopes is a well-described adaptation strategy to limit host anti-viral immunity. Another described, but less understood, adaptation strategy involves the selection of mutations within epitopes that retain immune recognition, suggesting a benefit for the virus despite continued immune pressure (termed non-classical adaptation). To understand this adaptation strategy, we utilized a single cell transcriptomic approach to identify features of the HIV-specific CD8+ T cell responses targeting non-adapted (NAE) and adapted (AE) forms of epitopes containing a non-classical adaptation. T cell receptor (TCR) repertoire and transcriptome were obtained from antigen-specific CD8+ T cells of chronic (n=7) and acute (n=4) HIV-infected subjects identified by either HLA class I tetramers or upregulation of activation markers following peptide stimulation. CD8+ T cells were predominantly dual tetramer+, confirming a large proportion of cross-reactive TCR clonotypes capable of recognizing the NAE and AE form. However, single-reactive CD8+ T cells were identified in acute HIV-infected subjects only, providing the potential for the selection of T cell clones over time. The transcriptomic profile of CD8+ T cells was dependent on the autologous virus: subjects whose virus encoded the NAE form of the epitope (and who transitioned to the AE form at a later timepoint) exhibited an ‘effective’ immune response, as indicated by expression of transcripts associated with polyfunctionality, cytotoxicity and apoptosis (largely driven by the genes GZMB, IFNɣ, CCL3, CCL4 and CCL5). These data suggest that viral adaptation at a single amino acid residue can provide an alternative strategy for viral survival by modulating the transcriptome of CD8+ T cells and potentially selecting for less effective T cell clones from the acute to chronic phase.

Extrapulmonary TB (EPTB) occurs with increased frequency in persons with underlying immunodeficiency. Even after recovery from acute illness, differences in immune phenotype and activation persist. Studies defining characteristics of immune responses after recovery from extrapulmonary TB may provide insights into factors that increase TB risk. We performed two case-control studies (in the United States and Brazil) among HIV-seronegative adults with previous EPTB (n = 9; 25), previous pulmonary TB (n = 7; 25), latent M. tuberculosis (Mtb) infection (n = 11; 25), and uninfected TB contacts (n = 10; 25). We assessed the frequency of dual CD4+ interferon-γ and tumor necrosis factor-α responses after stimulation with overlapping Mtb peptides from ESAT-6 or CFP-10, or gamma-irradiated Mtb H37Rv, proliferative responses to Mtb antigens, T-regulatory cell (Treg) frequency and phenotype. In both study populations, individuals with prior EPTB had the highest frequency of intracellular cytokine-producing cells in response to Mtb antigens (p < 0.05; p

Supplemental material, Appendix_1_-_Interview_Guide for Lifetime Smoking Patterns and Preferences for Smoking Cessation Among Women Veterans Receiving Veterans Health Administration Care by Sarah M. Wilson, Alyssa M. Medenblik, Julia M. Neal, Jennifer L. Strauss, J. Murray McNiel, Warren E. Christian, Jean C. Beckham and Patrick S. Calhoun in Qualitative Health Research

For much of the twentieth century, the United States led the world in both the production of lead products AND the study of lead’s risks. Having brought its own exposures to its lowest levels in a century, America has not taken the lead in continuing that environmental cleansing to the rest of the world. This talk surveys the history of lead and lead poisoning in America and Europe from the late 19th century to the early 21st , focusing on the changing nature of exposures, the creation of knowledge about the health effects of lead, and the regulatory efforts to minimize those health consequences. A century ago, the United States overtook other nations in the production and consumption of lead, but it lagged far behind Europe in keeping its workers safe. The unique dangers of tetraethyl lead, introduced in the mid-1920s, forced America to take a leadership role in the industrial toxicology, and eventually the public health epidemiology of lead. The decades since the 1960s saw a revolution in the definition...

This paper examines a pivotal moment in the history of the built environment in America. At the beginning of the twentieth century, factions within the American paint industry fought in state and federal legislatures over the definition of paint: What was pure paint? Were new paint formulations to be encouraged, or labeled “adulterated”? Was the known toxicity of lead to be a consideration? Despite some opponents' recourse to a rhetoric of toxicity and public health, all sides agreed that the best paints contained a significant quantity of lead, and that government should stay out of setting industry standards. This accord all but assured that Americans would apply tons of lead paint on the walls of their homes.

Environmental historians, especially those working at the intersection of environment and health, talk about ‘human interactions with the built environment’; this is, strictly speaking, redundant, since, by and large, what has defined the species homo sapiens since its appearance 30,000 years ago is our steadfast manipulation of the environment, cleverly exploiting resources and altering surroundings to counteract deficiencies in brawn, speed or other innate physical abilities.1 Every technology we have adopted, from fire to stone tools, to agriculture and medicine, has enhanced our odds against the lions, tigers and bears. But we grew more dependent upon those technologies and came to rely less and less upon our bodies, our instincts and our knowledge of the natural world. The pace of this transformation has accelerated in the last two centuries, so that by the mid-twentieth century, careful observers worried that technological innovation was outstripping biological evolution in determining the nature of human existence, risking physical, social and psychic alienation from the natural order.2