COVID-19 Contact Tracing Conundrums: Insights From the Front Lines.

COVID-19 contact tracing is an induction social network intervention in which the structure of the social network is leveraged to deploy proven COVID-19 interventions such as testing and social distancing. The Howard Brown Health organization has rapidly expanded to include COVID-19 testing, contact tracing, and linkage to resources since the first cases were identified in Chicago, Illinois. COVID-19 is penetrating the most vulnerable networks in the United States; existing inequities are widening as community resources and organizations have had to place services on hold.Here we address several questions that arise as organizations build capacity for contact tracing, including questions involving the potential impact of contact tracing, stakeholders who could be involved, the timing of contact tracing deployment, and the impact potential for digital technology.Contact tracing is critical at later stages of epidemic decline given the potential for isolated outbreaks as larger events, schools, stadiums, and festivals reopen. Local contact tracing efforts can have other indirect benefits with respect to limiting transmission, such as increasing testing rates and addressing structural barriers through provision of life-saving resources and access to crucial social support.

HIV-1 Tat increases oxidant burden in the lungs of transgenic mice.

Chronic human immunodeficiency virus infection is associated with higher incidence of pulmonary complications including hypertension, vasculopathy, lymphocytic alveolitis, and interstitial pneumonitis not attributed to either opportunistic infections or presence of the virus. The Tat (transactivator of transcription) protein, a required transactivator for expression of full-length viral genes, is pleiotropic and influences expression of cellular inflammatory genes. Tat-dependent transactivation of cellular genes requires specific mediators, including NF-κB, widely recognized as sensitive to changes in cellular oxidant burden. We hypothesized that overproduction of Tat leads to increased oxidant burden and to alterations in basal inflammatory status as measured by NF-κB activation. We engineered transgenic mouse lines that express Tat (86-amino-acid isoform) in the lung under the control of the surfactant protein C promoter. Tat-transgenic mice exhibit increased pulmonary cellular infiltration, increased nitrotyrosine and carbonyl protein modifications, and increased levels of NF-κB, MnSOD, and thioredoxin-interacting protein. These data indicate that Tat increases oxidant burden and resets the threshold for inflammation, which may increase susceptibility to secondary injuries.