The ARTAS linkage case management intervention provides a model that health departments and CBOs can use to ensure that recently diagnosed HIV-infected persons attend an initial HIV care encounter.

Abstract. Semliki Forest virus (SFV) infects cells by anacid-dependent membrane fusion reaction catalyzed by the virus spike protein, a complex containing E1 and E2 transmembrane subunits. E1 carries the putative virus fusion peptide, and mutations in this domain of the spike protein were previously shown to shift the pH threshold of cell-cell fusion (G91A), or block cell-cell fusion (G91D). We have used an SFV infectious clone to characterize virus particles containing these mutations. In keeping with the previous spike protein resuits, G91A virus showed limited secondary infection and an acid-shifted fusion threshold, while G91D virus was noninfectious and inactive in both cell-cell and virus-liposome fusion assays. During the low pHinduced SFV fusion reaction, the E1 subunit exposes new epitopes for monoclonal antibody (mAb) binding and forms an SDS-resistant homotrimer, the virus associates hydrophobically with the target membrane, and fusion of the virus and target membranes occurs. After low pH treatment, G91A spike proteins were shown to bind conformation-specific mAbs, associate with target liposome membranes, and form the E1 homotrimer. However, both G91A membrane association and homotrimer formation had an acid-shifted pH threshold and reduced efficiency compared to wt virus. In contrast, studies of the fusion-defective G91D mutant showed that the virus efficiently reacted with low pH as assayed by mAb binding and liposome association, but was essentially inactive in homotrimer formation. These results suggest that the G91D mutant is noninfectious due to a block in a late step in membrane fusion, separate from the initial reaction to low pH and interaction with the target membrane, and involving the lack of efficient formation of the E1 homotrimer.

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Current literature on retention in HIV care fails to account for patients who continually/simultaneously access different providers. This statewide study examined retention in early HIV medical care and its impact on viro-immunological improvement and survival outcomes. It was a retrospective study of South Carolina residents ≥13 years old who were diagnosed with HIV infection in 2004-2007 and initially entered in care. CD4 count/percent and viral load (VL) tests that must be reported to the South Carolina HIV surveillance database were used as a proxy for a clinical visit. Retention was defined as at least one visit in each of four 6-month periods over 2 years postlinkage. Retention rates were categorized as "optimal" (visits in four intervals), "suboptimal" (visits in three intervals), sporadic (visits in two or one intervals), and "dropout" (no visits). Logistic regression and Cox proportional analyses were used to examine retention. Of the 2197 persons, about 50% failed to maintain optimal retention in care postlinkage. Male gender, nonwhite race/ethnicity, younger age, delayed linkage, and HIV-only status were significant predictors of lower rate of retention. Mean decrease in baseline log(10) VL was greater among those with optimal compared to suboptimal (-1.81 vs. -1.42; p < 0.001) and sporadic retention (-1.81 vs. -0.70; p < 0.001). Mean increase in baseline CD4 count was greater in optimal retention compared to suboptimal (169.70 vs. 107.5; p < 0.001) and sporadic retention (169.70 vs. 2.43; p < 0.001). Increased risk of mortality was associated with sporadic retention (aHR 2.91; 95% CI 1.54-5.50) and "dropout" (aHR 4.00; 95% CI 1.50-10.65). Rate of poor retention in early HIV medical care was relatively higher than reported in clinic-based data. Increasing the rate of retention in early HIV care could substantially improve viro-immunological parameters and survival outcomes.