Investigating Barriers to Vaccination Among Durham County's Vulnerable Populations.

BACKGROUND: As antivaccination movements increase in the United States, underlying structural barriers to vaccination are often ignored. This study examines barriers to vaccination in an adult population to uncover factors leading to vaccination rates in underserved populations. METHODS: This study was approved by the Duke University Campus Institutional Review Board. Fifty-four patients at the Adult Immunizations Clinic of the Durham County Department of Public Health were interviewed throughout June and July 2019. Subjects were enrolled on a voluntary basis followed by oral consent. Eligible subjects included English-speaking adults receiving vaccines aged 19 or older. Anonymous and confidential interviews were conducted verbally. RESULTS: This study found that a large proportion of study participants were referred by their provider to receive vaccines at the health department. It was also found that having a provider appeared to lead to a decrease in vaccine hesitancy. Enhanced patient understanding of vaccines was not necessarily contributing to the apparent decrease in vaccine hesitancy. Patients who understood the importance of public health had the same rate of vaccine hesitancy as those who had no reason for receiving vaccines. LIMITATIONS: External validity is limited due to small sample size. CONCLUSIONS: Health care providers may play an essential role in reducing vaccine hesitancy. However, increases in vaccine uptake due to provider-level interventions may not necessarily be due to an enhanced understanding of vaccines or their importance to public health.

Striatal Projection Neurons Require Huntingtin for Synaptic Connectivity and Survival.

Huntington's disease (HD) is caused by an autosomal dominant polyglutamine expansion mutation of Huntingtin (HTT). HD patients suffer from progressive motor, cognitive, and psychiatric impairments, along with significant degeneration of the striatal projection neurons (SPNs) of the striatum. HD is widely accepted to be caused by a toxic gain-of-function of mutant HTT. However, whether loss of HTT function, because of dominant-negative effects of the mutant protein, plays a role in HD and whether HTT is required for SPN health and function are not known. Here, we delete Htt from specific subpopulations of SPNs using the Cre-Lox system and find that SPNs require HTT for motor regulation, synaptic development, cell health, and survival during aging. Our results suggest that loss of HTT function in SPNs could play a critical role in HD pathogenesis.