The quantitative viral outgrowth assay (QVOA) provides a precise minimal estimate of the reservoir of resting CD4 + T-cell infection (resting cell infection [RCI]). However, the variability of RCI over time during antiretroviral therapy (ART), relevant to assess potential effects of latency-reversing agents or other interventions, has not been fully described. We performed QVOA on resting CD4 + T cells obtained via leukapheresis from 37 human immunodeficiency virus (HIV)-infected patients receiving stable suppressive ART for a period of 6 years. Patients who started ART during acute (n = 17) or chronic (n = 20) HIV infection were studied once HIV RNA levels were <50 copies/mL for ≥6 months. Using random effects analysis of 160 RCI measurements, we found that RCI declined significantly over time (P < .001), with an estimated mean half-life of 3.6 years (95% confidence interval, 2.3-8.1 years), remarkably consistent with findings of prior studies. There was no evidence of more rapid decay in acute versus chronic HIV infection (P = .99) for patients suppressed ≥6 months. RCI was reliably estimated with longitudinal measurements generally showing <2-fold variation from the previous measure. When QVOA is performed in this format, RCI decreases of >6-fold were rare. We suggest that a 6-fold decline is a relevant threshold to reliably identify effects of antilatency interventions on RCI.

COVID-19-associated deaths were reported in the United States (1). Understanding the demographic and clinical characteristics of decedents could inform medical and public health interventions focused on preventing COVID-19-associated mortality. This report describes decedents with laboratory-confirmed infection with SARS-CoV-2, the virus that causes COVID-19, using data from 1) the standardized CDC case-report form (case-based surveillance) (https://www.cdc.gov/coronavirus/2019-ncov/php/ reporting-pui.html) and 2) supplementary data (supplemental surveillance), such as underlying medical conditions and location of death, obtained through collaboration between CDC and 16 public health jurisdictions (15 states and New York City). Case-based surveillanceDemographic and clinical data about COVID-19 cases are reported to CDC from 50 states, the District of Columbia, New York City, and U.S. territories using a standardized case-report form (case-based surveillance) or in aggregate. Data on 52,166 deaths from 47 jurisdictions among persons with laboratoryconfirmed COVID-19 were reported individually to CDC via case-based surveillance during February 12-May 18, 2020. Among the 52,166 decedents, 55.4% were male, 79.6% were aged ≥65 years, 13.8% were Hispanic/Latino (Hispanic), 21.0% were black, 40.3% were white, 3.9% were Asian, 0.3% were American Indian/Alaska Native (AI/AN), 0.1% were Native Hawaiian or other Pacific Islander (NHPI), 2.6% were multiracial or other race, and race/ethnicity was unknown for 18.0%. (Table 1). Median decedent age was 78 years (interquartile range (IQR) = 67-87 years). Because information about underlying medical conditions was missing for the majority of these decedents (30,725; 58.9%), data regarding medical conditions were not analyzed further using the case-based surveillance data set. Because most decedents reported to the supplementary data program were also reported to case-based surveillance, no statistical comparisons of the decedent characteristics between the data sets were made. * Underlying medical conditions include cardiovascular disease (congenital heart disease, coronary artery disease, congestive heart failure, hypertension, cerebrovascular accident/stroke, valvular heart disease, conduction disorders or dysrhythmias, other cardiovascular disease); diabetes mellitus; chronic lung disease (chronic obstructive pulmonary disease/emphysema, asthma, tuberculosis, other chronic lung diseases); immunosuppression (cancer, human immunodeficiency virus (HIV) infection, identified as being immunosuppressed); chronic kidney disease (chronic kidney disease, end-stage renal disease, other kidney diseases); neurologic conditions (dementia, seizure disorder, other neurologic conditions); chronic liver disease (cirrhosis, alcoholic hepatitis, chronic liver disease, end-stage liver disease, hepatitis B, hepatitis C, nonalcoholic steatohepatitis, other chronic liver diseases); obesity (body mass index ≥30 kg/m 2 ). Information was collected from decedent medical records or death certificates. ...

Preventing transmission of SARS-CoV-2, the virus that causes coronavirus disease 2019 , in institutes of higher education presents a unique set of challenges because of the presence of congregate living settings and difficulty limiting socialization and group gatherings. Before August 2020, minimal data were available regarding COVID-19 outbreaks in these settings. On August 3, 2020, university A in North Carolina broadly opened campus for the first time since transitioning to primarily remote learning in March. Consistent with CDC guidance at that time (1,2), steps were taken to prevent the spread of SARS-CoV-2 on campus. During August 3-25, 670 laboratory-confirmed cases of COVID-19 were identified; 96% were among patients aged <22 years. Eighteen clusters of five or more epidemiologically linked cases within 14 days of one another were reported; 30% of cases were linked to a cluster. Student gatherings and congregate living settings, both on and off campus, likely contributed to the rapid spread of COVID-19 within the university community. On August 19, all university A classes transitioned to online, and additional mitigation efforts were implemented. At this point, 334 university A-associated COVID-19 cases had been reported to the local health department. The rapid increase in cases within 2 weeks of opening campus suggests that robust measures are needed to reduce transmission at institutes of higher education, including efforts to increase consistent use of masks, reduce the density of on-campus housing, increase testing for SARS-CoV-2, and discourage student gatherings.University A students returned to residence halls during August 3-9, 2020, and in-person classes began on August 10. Mitigation steps taken to prevent the spread of SARS-CoV-2 on campus included scheduling move-in appointments across a 1-week period, decreasing classroom density to facilitate physical distancing, and reducing maximum dining hall capacity and increasing takeout options. Students were required to sign an acknowledgment of community standards and university guidelines recommending daily symptom checks, * These authors contributed equally.

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AGS-004 consists of matured autologous dendritic cells co-electroporated with in vitro transcribed RNA encoding autologous HIV antigens. In an open-label, single arm sub-study of AGS-004-003, AGS-004 was administered monthly to suppressed participants who started antiretroviral therapy (ART) during acute HIV infection. HIV-1 specific T cell responses were measured by multicolor flow cytometry after 3-4 doses. The frequency of resting CD4+ T-cell infection (RCI) was measured by quantitative viral outgrowth assay. Participants demonstrating increased immune response postvaccination were eligible for analytic treatment interruption (ATI). AGS-004 induced a positive immune response defined as ‡2-fold increase from baseline in the number of multifunctional HIV-1 specific CD28+ /CD45RA -CD8 + effector/memory cytoxic T-lymphocytes (CTLs) in all six participants. All participants underwent ATI with rebound viremia at a median of 29 days. Immune correlates between time to viral rebound and the induction of effector CTLs were determined. Baseline RCI was low in most participants (0.043-0.767 IUPM). One participant had a >2-fold decrease (0.179-0.067 infectious units per million [IUPM]) in RCI at week 10. One participant with the lowest RCI had the longest ATI. AGS-004 dendritic cell administration increased multifunctional HIV-specific CD28 + /CD45RA -CD8 + memory T cell responses in all participants, but did not permit sustained ART interruption. However, greater expansion of CD28 -/CCR7 -/CD45RA -CD8 + effector T cell responses correlated with a longer time to viral rebound. AGS-004 may be a useful tool to augment immune responses in the setting of latency reversal and eradication strategies.