Background People with HIV (PWH) may have numerous risk factors for acquiring Coronavirus disease-19 (COVID-19) and developing severe outcomes, but current data are conflicting. Methods Healthcare providers enrolled consecutively by non-random sampling PWH with lab-confirmed COVID-19, diagnosed at their facilities between April 1st and July 1st, 2020. De-identified data were entered into an electronic Research Electronic Data Capture (REDCap). The primary endpoint was severe outcome, defined as a composite endpoint of intensive care unit (ICU) admission, mechanical ventilation, or death. The secondary outcome was the need for hospitalization. Results 286 patients were included; the mean age was 51.4 years (SD, 14.4), 25.9% were female, and 75.4% were African-American or Hispanic. Most patients (94.3%) were on antiretroviral therapy (ART), 88.7% had HIV virologic suppression, and 80.8% had comorbidities. Within 30 days of positive SARS-CoV-2 testing, 164 (57.3%) patients were hospitalized, and 47 (16.5%) required ICU admission. Mortality rates were 9.4% (27/286) overall, 16.5% (27/164) among those hospitalized, and 51.5% (24/47) among those admitted to an ICU. The primary composite endpoint occurred in 17.5% (50/286) of all patients and 30.5% (50/164) of hospitalized patients. Older age, chronic lung disease, and hypertension were associated with severe outcomes. A lower CD4 count (<200 cells/mm³) was associated with the primary and secondary endpoints. There was no association between the antiretroviral regimen or lack of viral suppression and predefined outcomes. Conclusion Severe clinical outcomes occurred commonly in PWH and COVID-19. The risk for poor outcomes was higher in those with comorbidities and lower CD4 cell counts, despite HIV viral suppression.

Background Combination antiretroviral therapy suppresses but does not eradicate human immunodeficiency virus type 1 (HIV-1) in infected persons, and low-level viremia can be detected despite years of suppressive antiretroviral therapy. Short (28d) course antiretroviral intensification of standard combination therapy is a useful approach to determine whether complete rounds of HIV-1 replication in rapidly cycling cells contribute to persistent viremia. We investigated whether intensification with the integrase inhibitor raltegravir decreases plasma viremia in patients on suppressive antiretroviral therapy. Methods Subjects (N=10) with long term HIV-1 suppression on combination antiretroviral regimens were intensified for 4 weeks with raltegravir. Plasma viremia was determined prior to, during, and following the 4-week intensification period using a sensitive HIV-1 RNA assay (limit of detection of 0.2 copies HIV-1 RNA/ml plasma). A four week intensification course was chosen to investigate potential HIV-1 replication in cells with relatively short (c. 1-14 d) half-lives. Results There was no evidence in any subject of decline in HIV-1 RNA levels during the period of raltegravir intensification or rebound after discontinuation. Median levels of HIV-1 RNA prior to (0.17 log10 copies/ml), during (0.04 log10 copies/ml), and following (0.04 log10 copies/ml) raltegravir intensification (p >0.1 for all comparisons in parametric analyses). HPLC/mass spectroscopy studies confirmed that therapeutic levels of raltegravir were achieved in plasma during intensification. Conclusions Intensification of antiretroviral therapy with a potent HIV-1 integrase inhibitor did not decrease persistent viremia in subjects on suppressive regimens, indicating that rapidly cycling cells infected with HIV-1 were not present. Eradication of HIV-1 from infected persons will require new therapeutic approaches.

OBJECTIVE. We sought to evaluate the impact of intense influenza media coverage during the 2003–2004 influenza season on the influenza vaccination status of children 6 to 59 months of age. METHODS. Children 6 to 59 months of age who presented to a large, academic pediatric continuity clinic or affiliated acute care clinic in the summer of 2004 were enrolled. A parental survey ascertained the influenza vaccination status of the child and family members during the 2003–2004 influenza season and factors that influenced their vaccination status. For children vaccinated in the clinic or health department, influenza vaccination dates were confirmed in a computerized medical chart or state immunization registry. RESULTS. Of 256 enrolled children, 98 (38%) parents reported that their child had received the 2003–2004 influenza vaccine, and 64 (65%) had confirmed influenza vaccination dates. Unlike the previous influenza season in which confirmed influenza vaccination dates from a similar study population were distributed more evenly from October through December, most children (75%) with confirmed vaccination dates received the vaccine after the media coverage in mid-November. Influenza vaccinations per week increased dramatically after the media coverage began (2.4 vs 8.6 per week; t test: P < .001). In late November and December 2003, the influenza-related media coverage, which focused primarily on an early, severe influenza season, increased dramatically and explained 85% of the variation in influenza vaccinations. Multivariate analysis showed that recalling a physician recommendation (odds ratio [OR]: 6.8; 95% confidence interval [CI]: 2.3–19.7), having a family member who had received the influenza vaccine (OR: 9.5; 95% CI: 4.3–21.3), having a continuity clinic visit between October and January (OR: 4.5; 95% CI: 2.0–10.1), and having a high-risk medical condition (OR: 2.9; 95% CI: 1.1–7.8) strongly predicted the influenza vaccination status in the children. CONCLUSION. Media coverage in conjunction with explicit physician recommendation for children and their contacts are key factors that are associated with influenza vaccination rates in children.

Significance In persons living with HIV-1 who start antiretroviral therapy, virus in the blood decreases rapidly to below the detection limit. The decrease occurs in two phases: a rapid initial decrease in the first weeks, followed by a second, slower phase occurring over the next few months. These decay processes are important because infected cells that remain may become part of the stable latent reservoir that prevents cure. The decay in virus levels in blood presumably reflects the loss of infected cells, but the relationship between the decay of free virus and of infected cells has been unclear. Here, we have analyzed this question using an assay that distinguishes between cells with intact and defective forms of the viral genome.