Background
To reduce health disparities and improve the health of Americans overall, addressing community-level social and structural factors, such as social vulnerability, may help explain the higher rates of HIV diagnoses among and between race/ethnicity groups.
Methods
Data were obtained from CDC’s National HIV Surveillance System (NHSS) and the CDC/ATSDR social vulnerability index (SVI). NHSS data for Black, Hispanic/Latino, and White adults with HIV diagnosed in 2018 were linked to SVI data. To measure the relative disparity, rate ratios (RRs) with 95% CIs were calculated to examine the relative difference comparing census tracts with the lowest SVI scores (quartile 1, Q1) to those with the highest SVI scores (quartile 4, Q4) by sex assigned at birth for age group and region of residence. Differences in the numbers of diagnoses across the quartiles were analyzed by sex assigned at birth and transmission category.
Results
There were 13,807 Black, 8747 Hispanic/Latino, and 8325 White adults who received a diagnosis of HIV infection in the United States in 2018—with the highest HIV diagnosis rates among adults who lived in census tracts with the highest vulnerability (Q4). For each race/ethnicity and both sexes, the rate of HIV diagnoses increased as social vulnerability increased. The highest disparities in HIV diagnosis rates by SVI were among persons who inject drugs, and the highest within-group RRs were typically observed among older persons and persons residing in the Northeast.
Conclusion
To reach the goals of several national HIV initiatives, efforts are needed to address the social vulnerability factors that contribute to racial and ethnic disparities in acquiring HIV and receiving care and treatment.
Host genetic background is a significant driver of the variability in neurological responses to viral infection. Here, we leverage the genetically diverse Collaborative Cross (CC) mouse resource to better understand how chronic infection by Theiler’s Murine Encephalomyelitis Virus (TMEV) elicits diverse clinical and morphologic changes in the central nervous system (CNS). We characterized the TMEV-induced clinical phenotype responses, and associated lesion distributions in the CNS, in six CC mouse strains over a 90 day infection period. We observed varying degrees of motor impairment in these strains, as measured by delayed righting reflex, paresis, paralysis, seizures, limb clasping, ruffling, and encephalitis phenotypes. All strains developed neuroparenchymal necrosis and mineralization in the brain, primarily localized to the hippocampal regions. Two of the six strains presented with axonal degeneration with myelin loss of the nerve roots in the lumbar spinal cord. Moreover, we statistically correlated lesion distribution with overall frequencies of clinical phenotypes and phenotype progression to better understand how and where TMEV targets the CNS, based on genetic background. Specifically, we assessed lesion distribution in relation to the clinical progression of these phenotypes from early to late TMEV disease, finding significant relationships between progression and lesion distribution. Finally, we identified quantitative trait loci associated with frequency of lesions in a particular brain region, revealing several loci of interest for future study: lysosomal trafficking regulator (Lyst) and nidogen 1 (Nid1). Together, these results indicate that the genetic background influences the type and severity of clinical phenotypes, phenotypic resilience to TMEV, and the lesion distribution across strains.
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