Are human papillomavirus knowledge and vaccine uptake associated with HIV status and social determinants of health in young sexual minority men?

This brief report examines the relationship, if any, between human immunodeficiency virus (HIV) status, and individual-level and socio-sexual partner-level factors of social determinants of health (SDOH) that are associated with human papillomavirus (HPV) knowledge and vaccine uptake in young sexual minority men (YSMM). We used data from 126 YSMM recruited by network-based sampling during 2015-2016 in Houston, Texas. Descriptive statistics and regression analyses were conducted to test the association between HIV status, SDOH, and HPV knowledge and vaccine uptake. Those living with HIV had lower odds of knowledge of HPV-associated anal cancer (OR: 0.43, 95% CI: 0.18-0.97) and knowledge of HPV spreading via sexual contact (OR: 0.11, 95% CI: 0.01-0.64), and higher odds of HPV vaccine uptake (OR: 2.90, 95% CI: 1.11-8.02). HPV knowledge and vaccine uptake in YSMM was not associated with partner's attributes or individuals' SDOH factors in our study yet was significantly associated with HIV status. Future interventions are needed to increase HPV knowledge among individuals living with HIV and vaccine uptake particularly among YSMM living without HIV that are not engaged in healthcare.

Sex-dependent correlates of arterial stiffness in Tanzanian adults.

OBJECTIVE: Arterial stiffness is a known indicator for cardiovascular disease. However, the factors that lead to arterial stiffening have primarily been studied in participants from high-income countries. Here, we examine clinical and lifestyle metrics in relation to arterial stiffness in Tanzanian adults. METHODS: We performed pulse wave velocity (PWV), the gold standard measure of arterial stiffness, on 808 Tanzanian adults (ages 18-65) enrolled in a longitudinal cohort studying trends in blood pressure. RESULTS: As expected, PWV was strongly associated with age, blood pressure and sex. We controlled for these factors in our statistical analysis. Lifestyle metrics were compared across multiple PWV quantiles. We found that determinants of PWV varied by sex: in female participants, PWV was associated with common obesity metrics and menopause, while in male participants, PWV was associated with HIV status and duration of anti-retroviral therapy (ART). Further clinical and lifestyle factors such as marriage status and type of occupation were also significantly associated with PWV and moderated by sex. CONCLUSION: Together, our data demonstrate the importance of studying sex-specific causal pathways for arterial stiffness and of including under-represented populations in these studies.

Loss of RAD9B impairs early neural development and contributes to the risk for human spina bifida.

DNA damage response (DDR) genes orchestrating the network of DNA repair, cell cycle control, are essential for the rapid proliferation of neural progenitor cells. To date, the potential association between specific DDR genes and the risk of human neural tube defects (NTDs) has not been investigated. Using whole-genome sequencing and targeted sequencing, we identified significant enrichment of rare deleterious RAD9B variants in spina bifida cases compared to controls (8/409 vs. 0/298; p = .0241). Among the eight identified variants, the two frameshift mutants and p.Gln146Glu affected RAD9B nuclear localization. The two frameshift mutants also decreased the protein level of RAD9B. p.Ser354Gly, as well as the two frameshifts, affected the cell proliferation rate. Finally, p.Ser354Gly, p.Ser10Gly, p.Ile112Met, p.Gln146Glu, and the two frameshift variants showed a decreased ability for activating JNK phosphorylation. RAD9B knockdowns in human embryonic stem cells profoundly affected early differentiation through impairing PAX6 and OCT4 expression. RAD9B deficiency impeded in vitro formation of neural organoids, a 3D cell culture model for human neural development. Furthermore, the RNA-seq data revealed that loss of RAD9B dysregulates cell adhesion genes during organoid formation. These results represent the first demonstration of a DDR gene as an NTD risk factor in humans.