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This document is a correction notice for an article titled "Phospholipid scramblase 1 interacts with influenza A virus NP, impairing its nuclear import and thereby suppressing virus replication." The correction addresses errors in the figures of the original article, including the reuse of data and incorrect images. The corrected figures are provided in the notice, and the original unadjusted images are available as supplementary material. The authors apologize for the errors and provide an updated Data Availability statement. [Extracted from the article]

Racial/ethnic disparities are among the top-selective underlying determinants associated with the disproportional impact of the COVID-19 pandemic on human mobility and health outcomes. This study jointly examined county-level racial/ethnic differences in compliance with stay-at-home orders and COVID-19 health outcomes during 2020, leveraging two-year geo-tracking data of mobile devices across ~4.4 million point-of-interests (POIs) in the contiguous United States. Through a set of structural equation modeling, this study quantified how racial/ethnic differences in following stay-at-home orders could mediate COVID-19 health outcomes, controlling for state effects, socioeconomics, demographics, occupation, and partisanship. Results showed that counties with higher Asian populations decreased most in their travel, both in terms of reducing their overall POIs' visiting and increasing their staying home percentage. Moreover, counties with higher White populations experienced the lowest infection rate, while counties with higher African American populations presented the highest case-fatality ratio. Additionally, control variables, particularly partisanship, median household income, percentage of elders, and urbanization, significantly accounted for the county differences in human mobility and COVID-19 health outcomes. Mediation analyses further revealed that human mobility only statistically influenced infection rate but not case-fatality ratio, and such mediation effects varied substantially among racial/ethnic compositions. Last, robustness check of racial gradient at census block group level documented consistent associations but greater magnitude. Taken together, these findings suggest that US residents' responses to COVID-19 are subject to an entrenched and consequential racial/ethnic divide. [ABSTRACT FROM AUTHOR]

During the outbreak of the COVID-19 pandemic, Non-Pharmaceutical and Pharmaceutical treatments were alternative strategies for governments to intervene. Though many of these intervention methods proved to be effective to stop the spread of COVID-19, i.e., lockdown and curfew, they also posed risk to the economy; in such a scenario, an analysis on how to strike a balance becomes urgent. Our research leverages the mobility big data from the University of Maryland COVID-19 Impact Analysis Platform and employs the Generalized Additive Model (GAM), to understand how the social demographic variables, NPTs (Non-Pharmaceutical Treatments) and PTs (Pharmaceutical Treatments) affect the New Death Rate (NDR) at county-level. We also portray the mutual and interactive effects of NPTs and PTs on NDR. Our results show that there exists a specific usage rate of PTs where its marginal effect starts to suppress the NDR growth, and this specific rate can be reduced through implementing the NPTs. [ABSTRACT FROM AUTHOR]

Transcription and replication of the influenza A virus (IAV) genome occur in the nucleus of infected cells and are carried out by the viral ribonucleoprotein complex (vRNP). As a major component of the vRNP complex, the viral nucleoprotein (NP) mediates the nuclear import of the vRNP complex via its nuclear localization signals (NLSs). Clearly, an effective way for the host to antagonize IAV infection would be by targeting vRNP nuclear import. Here, we identified phospholipid scramblase 1 (PLSCR1) as a binding partner of NP by using a yeast two-hybrid (Y2H) screen. The interaction between NP and PLSCR1 in mammalian cells was demonstrated by using co-immunoprecipitation and pull-down assays. We found that the stable overexpression of PLSCR1 suppressed the nuclear import of NP, hindered the virus life cycle, and significantly inhibited the replication of various influenza subtypes. In contrast, siRNA knockdown or CRISPR/Cas9 knockout of PLSCR1 increased virus propagation. Further analysis indicated that the inhibitory effect of PLSCR1 on the nuclear import of NP was not caused by affecting the phosphorylation status of NP or by stimulating the interferon (IFN) pathways. Instead, PLSCR1 was found to form a trimeric complex with NP and members of the importin α family, which inhibited the incorporation of importin β, a key mediator of the classical nuclear import pathway, into the complex, thus impairing the nuclear import of NP and suppressing virus replication. Our results demonstrate that PLSCR1 negatively regulates virus replication by interacting with NP in the cytoplasm and preventing its nuclear import. [ABSTRACT FROM AUTHOR]