Background Improving patient retention in HIV care is crucial to improving the HIV care continuum. We instituted and evaluated a relinkage program that uses clinical data to identify potentially out-of-care patients, matches those data to public health surveillance, and employs a linkage specialist (LS) to coordinate care relinkage. Methods The intervention began November 1, 2012 in the largest HIV clinic in Washington State. We evaluated program outcomes and compared patient outcomes in the year following initiation of the intervention to a historical control cohort of patients. Cox proportional hazard ratios were used to compare time to relinkage to care between cohorts, and regression models using generalized estimated equations were preformed to examine secondary outcomes of relinkage to care, engagement in care, and viral suppression. Results 753 patients were identified as “out of care” on 11/1/12. Matching with surveillance data and initial LS investigations found that 596 (79%) of these patients had moved, transferred care or were incarcerated. Of the 157 remaining patients: 40 (25%) relinked to care before LS contact, and the LS successfully contacted 38 (24%). A total of 116 (15%) patients in the intervention cohort relinked to care and 24 (20%) were contacted by the LS. Compared to the historical cohort, the time to relinkage was shorter among patients in the intervention cohort [adjusted HR=1.7 (1.2-2.3)] and a greater proportion relinked [15% vs. 10%]. Conclusions This clinic-based, surveillance-informed relinkage intervention showed statistically significant but modest effectiveness in returning out-of-care patients to HIV care compared to historical controls.

Individuals with 16p11.2 copy number variant (CNV) show considerable phenotypic heterogeneity. Although autism spectrum disorder (ASD) is reported in approximately 20–23% of individuals with 16p11.2 CNVs, ASD‐associated symptoms are observed in those without a clinical ASD diagnosis. Previous work has shown that genetic variation and prenatal and perinatal birth complications influence ASD risk and symptom severity. This study examined the impact of genetic and environmental risk factors on phenotypic heterogeneity among 16p11.2 CNV carriers. Participants included individuals with a 16p11.2 deletion (N = 96) or duplication (N = 77) with exome sequencing from the Simons VIP study. The presence of prenatal factors, perinatal events, additional genetic events, and gender was studied. Regression analyses examined the contribution of each risk factor on ASD symptomatology, cognitive functioning, and adaptive abilities. For deletion carriers, perinatal and additional genetic events were associated with increased ASD symptomatology and decrements in cognitive and adaptive functioning. For duplication carriers, secondary genetic events were associated with greater cognitive impairments. Being female sex was a protective factor for both deletion and duplication carriers. Our findings suggest that ASD‐associated risk factors contribute to the variability in symptom presentation in individuals with 16p11.2 CNVs. Lay Summary There are a wide range of autism spectrum disorder (ASD) symptoms and abilities observed for individuals with genetic changes of the 16p11.2 region. Here, we found perinatal complications contributed to more severe ASD symptoms (deletion carriers) and additional genetic mutations contributed to decreased cognitive abilities (deletion and duplication carriers). A potential protective factor was also observed for females with 16p11.2 variations. Autism Res 2020, 13: 1300–1310. © 2020 International Society for Autism Research, Wiley Periodicals, Inc.

Background HIV care continuum estimates derived from laboratory surveillance typically assume that persons without recently reported CD4 count or viral load results are out of care. Methods We conducted a multi-state project (Alaska, Idaho, Montana, Oregon, Washington and Wyoming) to ascertain the status of HIV cases that appeared to be out of care during a 12 month period. We used laboratory surveillance to identify cases in all states but Idaho, where viral load reporting is not mandatory, requiring us to rely on clinic records. After complete investigation, we assigned each case one of the following dispositions: moved out of state, died, in HIV care, no evidence of HIV care, or data error. Results We identified 3,866 cases with no CD4 count or viral load result in a ≥12 month period during 2012-14, most (85%) of which were in Washington or Oregon. A median of 43% (range: 20%-67%) of cases investigated in each state had moved, 9% (0%-16%) had died, and 11% (8%-33%) were in care during the 12 month surveillance period. Only 28% of investigated cases in the region and a median of 30% (10%-57%) of investigated cases in each state had no evidence of care, migration, or death after investigation. Conclusions Most persons living with HIV in the Northwest US who appear to be out of care based on laboratory surveillance are not truly out of care. Our findings highlight the importance of improving state surveillance systems to ensure accurate care continuum estimates and guide Data to Care efforts.

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