New York City (NYC) was an epicenter of the coronavirus disease 2019 (COVID-19) outbreak in the United States during spring 2020 (1). During March-May 2020, approximately 203,000 laboratory-confirmed COVID-19 cases were reported to the NYC Department of Health and Mental Hygiene (DOHMH). To obtain more complete data, DOHMH used supplementary information sources and relied on direct data importation and matching of patient identifiers for data on hospitalization status, the occurrence of death, race/ethnicity, and presence of underlying medical conditions. The highest rates of cases, hospitalizations, and deaths were concentrated in communities of color, high-poverty areas, and among persons aged ≥75 years or with underlying conditions. The crude fatality rate was 9.2% overall and 32.1% among hospitalized patients. Using these data to prevent additional infections among NYC residents during subsequent waves of the pandemic, particularly among those at highest risk for hospitalization and death, is critical. Mitigating COVID-19 transmission among vulnerable groups at high risk for hospitalization and death is an urgent priority. Similar to NYC, other jurisdictions might find the use of supplementary information sources valuable in their efforts to prevent COVID-19 infections. This report describes cases of laboratory-confirmed COVID-19 among NYC residents diagnosed during February 29-June 1, 2020, that were reported to DOHMH. DOHMH began COVID-19 surveillance in January 2020 when testing capacity for SARS-CoV-2 (the virus that causes COVID-19) using real-time reverse transcription-polymerase chain reaction (RT-PCR) was limited by strict testing criteria because of limited test availability only through CDC. The NYC and New York State public health laboratories began testing hospitalized patients at the end of February and early March. DOHMH encouraged patients with mild symptoms to remain at home rather than seek health care because of shortages of personal protective equipment and laboratory tests at hospitals and clinics. Commercial laboratories began testing for SARS-CoV-2 in mid-to late March. During February 29-March 15, patients with laboratory-confirmed COVID-19 were interviewed by DOHMH, and close contacts were identified for monitoring. The rapid rise in laboratory-confirmed cases (cases) quickly made interviewing all patients, as well as contact tracing, unsustainable. Subsequent case investigations

To better understand how innate immune responses to vaccination can lead to lasting protective immunity, we used a systems approach to define immune signatures in humans over 1 wk following MRKAd5/HIV vaccination that predicted subsequent HIV-specific T-cell responses. Within 24 h, striking increases in peripheral blood mononuclear cell gene expression associated with inflammation, IFN response, and myeloid cell trafficking occurred, and lymphocyte-specific transcripts decreased. These alterations were corroborated by marked serum inflammatory cytokine elevations and egress of circulating lymphocytes. Responses of vaccinees with preexisting adenovirus serotype 5 (Ad5) neutralizing antibodies were strongly attenuated, suggesting that enhanced HIV acquisition in Ad5-seropositive subgroups in the Step Study may relate to the lack of appropriate innate activation rather than to increased systemic immune activation. Importantly, patterns of chemoattractant cytokine responses at 24 h and alterations in 209 peripheral blood mononuclear cell transcripts at 72 h were predictive of subsequent induction and magnitude of HIV-specific CD8 + T-cell responses. This systems approach provides a framework to compare innate responses induced by vectors, as shown here by contrasting the more rapid, robust response to MRKAd5/HIV with that to yellow fever vaccine. When applied iteratively, the findings may permit selection of HIV vaccine candidates eliciting innate immune response profiles more likely to drive HIV protective immunity.

Rationale: Obesity and underweight are contraindications to lung transplantation based on their associations with mortality in studies performed before implementation of the lung allocation score (LAS)-based organ allocation system in the United States Objectives: To determine the associations of body mass index (BMI) and plasma leptin levels with survival after lung transplantation.Methods: We used multivariable-adjusted regression models to examine associations between BMI and 1-year mortality in 9,073 adults who underwent lung transplantation in the United States between May 2005 and June 2011, and plasma leptin and mortality in 599 Lung Transplant Outcomes Group study participants. We measured body fat and skeletal muscle mass using whole-body dual X-ray absorptiometry in 142 adult lung transplant candidates.Measurements and Main Results: Adjusted mortality rates were similar among normal weight (BMI 18.5-24.9 kg/m 2 ), overweight , and class I obese (BMI 30-34.9) transplant recipients. Underweight (BMI , 18.5) was associated with a 35% increased rate of death (95% confidence interval, 10-66%). Class II-III obesity (BMI > 35 kg/m 2 ) was associated with a nearly twofold increase in mortality (hazard ratio, 1.9; 95% confidence interval, 1.3-2.8). Higher leptin levels were associated with increased mortality after transplant surgery performed without cardiopulmonary bypass (P for interaction = 0.03). A BMI greater than or equal to 30 kg/m 2 was 26% sensitive and 97% specific for total body fat-defined obesity.Conclusions: A BMI of 30.0-34.9 kg/m 2 is not associated with 1-year mortality after lung transplantation in the LAS era, perhaps because of its low sensitivity for obesity. The association between leptin and mortality suggests the need to validate alternative methods to measure obesity in candidates for lung transplantation. A BMI greater than or equal to 30 kg/m 2 may no longer contraindicate lung transplantation.

Objective Many transplant programs are hesitant to offer lung transplantation to patients with systemic sclerosis (SSc) due to concerns about extrapulmonary involvement that might affect survival. The aim of this study was to determine whether adults with SSc have higher 1‐year mortality rates after lung transplantation compared to those with interstitial lung disease (ILD) or pulmonary arterial hypertension (PAH) not due to SSc. Methods Using data provided by the United Network for Organ Sharing, we performed a retrospective cohort study of 229 adults with SSc, 201 with PAH, and 3,333 with ILD who underwent lung transplantation in the US between May 4, 2005 and September 14, 2012. We examined associations between diagnosis and 1‐year survival after lung transplantation using stratified Cox models adjusted for recipient, donor, and procedure factors. Results Adults with SSc undergoing lung transplantation in the US had a multivariable‐adjusted 48% relative increase in the 1‐year mortality rate compared to those with non–SSc‐related ILD (hazard ratio 1.48 [95% confidence interval 1.01–2.17]). However, we did not detect a difference in the risk of death at 1 year between those with SSc and those with non–SSc‐related PAH (hazard ratio 0.85 [95% confidence interval 0.50–1.44]). Conclusion A diagnosis of SSc may confer an increased risk of death 1 year following lung transplantation compared to a diagnosis of ILD, but this risk is similar to that of PAH, a widely accepted indication for lung transplantation. Future work should identify modifiable risk factors that can improve transplant outcomes in this population.

A large outbreak of Legionnaires' disease caused by a cooling tower occurred in a medically vulnerable community. The outbreak prompted enactment of a new city law on the operation and maintenance of cooling towers. Ongoing surveillance and evaluation of cooling tower process controls will determine if the new law reduces the incidence of Legionnaires' disease in New York City.

Lungs from older adult organ donors are often unused because of concerns for increased mortality. We examined associations between donor age and transplant outcomes among 8,860 adult lung transplant recipients using Organ Procurement and Transplantation Network and Lung Transplant Outcomes Group data. We used stratified Cox proportional hazard models and generalized linear mixed models to examine associations between donor age and both 1-year graft failure and primary graft dysfunction. The rate of 1-year graft failure was similar among recipients of lungs from donors age 18–64 years, but severely ill recipients (LAS > 47.7 or use of mechanical ventilation) of lungs from donors age 56–64 years had increased rates of 1-year graft failure (p-values for interaction = 0.04 and 0.02, respectively). Recipients of lungs from donors <18 and ≥65 years had increased rates of 1-year graft failure (adjusted hazard ratio 1.23, 95% CI 1.01–1.50 and adjusted hazard ratio 2.15, 95% CI 1.47–3.15, respectively). Donor age was not associated with the risk of primary graft dysfunction. In summary, the use of lungs from donors age 56–64 years may be safe for adult candidates without a high LAS, and the use of lungs from pediatric donors is associated with a small increase in early graft failure.

Each day, the New York City Department of Health and Mental Hygiene uses the free SaTScan software to apply prospective space–time permutation scan statistics to strengthen early outbreak detection for 35 reportable diseases. This method prompted early detection of outbreaks of community-acquired legionellosis and shigellosis.

We investigated associations of plasma lipoproteins with subclinical ILD by measuring high attenuation areas (HAA: lung voxels between −600 and −250 HU) in 6,700 adults and serum MMP-7 and SP-A in 1,216 adults age 45–84 without clinical cardiovascular disease in MESA. In cross-sectional analyses, each standard deviation (SD) decrement in HDL-C was associated with a 2.12% HAA increment (95% CI 1.44–2.79%), a 3.53% MMP-7 increment (95% CI 0.93–6.07) and a 6.37% SP-A increment (95% CI 1.35–11.13), independent of demographics, smoking, and inflammatory biomarkers. These findings support a novel hypothesis that HDL-C might influence subclinical lung injury and extracellular matrix remodeling.