Virtual Reality to Assess Resident Recognition of Impending Respiratory Failure During COVID-19.

OBJECTIVES: To assess the performance of pediatric residents in recognizing a decompensating patient with impending respiratory failure and appropriately escalating care using a virtual reality (VR) simulated case of an infant with bronchiolitis after an extended period of decreased clinical volumes during the coronavirus disease 2019 (COVID-19) pandemic. METHODS: Sixty-two pediatric residents at a single academic pediatric referral center engaged in a 30-minute VR simulation on respiratory failure in a 3-month-old admitted to the pediatric hospital medicine service with bronchiolitis. This occurred in a socially distant manner across the Zoom platform during the COVID-19 pandemic (January-April 2021). Residents were assessed on their ability to (1) recognize altered mental status (AMS), (2) designate clinical status as "(impending) respiratory failure," and (3) escalate care. Statistical differences between and across postgraduate year (PGY) levels were examined using χ2 or Fisher's exact test, followed by pairwise comparison and posthoc multiple testing using the Hochberg test. RESULTS: Among all residents, 53% successfully recognized AMS, 16% identified respiratory failure, and 23% escalated care. No significant differences were seen across PGY levels for recognizing AMS or identifying respiratory failure. PGY3+ residents were more likely to escalate care than PGY2 residents (P = .05). CONCLUSIONS: In the setting of an extended period with decreased clinical volumes during the COVID-19 pandemic, pediatric residents across all PGY levels demonstrated challenges with identifying (impending) respiratory failure and appropriately escalating care during VR simulations. Though limited, VR simulation may serve as a safe adjunct for clinical training and assessment during times of decreased clinical exposure.

Inhibition of HIV-1 replication in alveolar macrophages by adenovirus gene transfer vectors.

To assess the hypothesis that infection of alveolar macrophages (AM) with adenovirus (Ad) gene transfer vectors might prevent subsequent human immunodeficiency virus (HIV)-1 replication in AM, AM isolated from normal volunteers were infected with increasing doses of first generation (E1(-)) Ad vectors, followed 72 h later by infection with HIV-1(JRFL), an R5/M-tropic strain that preferentially uses the CCR5 coreceptor. As a measure of HIV-1 replication, p24 Ag was quantified by enzyme-linked imunosorbent assay in supernatants on Days 4 to 14 after HIV-1infection. Pretreatment of the AM with an Ad vector resulted in a dose- and time-dependent suppression of subsequent HIV-1 replication. The Ad vector inhibition of HIV-1 replication was independent of the transgene in the Ad vector expression cassette and E4 genes in the Ad backbone. Moreover, it did not appear to be secondary to a soluble factor released by the AM, nor was it overridden by the concomitant transfer of the CCR5 or CXCR4 receptors to the AM before HIV-1 infection. These observations have implications regarding pulmonary host responses associated with HIV-1 infection, as well as possibly uncovering new therapeutic strategies against HIV-1 infection.