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Abstract The Enriquillo–Plantain Garden fault (EPGF), the southern branch of the northern Caribbean left-lateral transpressional plate boundary, has ruptured in two devastating earthquakes along the Haiti southern peninsula: the Mw 7.0, 2010 Haiti and the Mw 7.2, 2021 Nippes earthquakes. In Jamaica, the 1692 Port Royal and 1907 Great Kingston earthquakes caused widespread damage and loss of life. No large earthquakes are known from the 200-km-long Jamaica Passage segment of this plate boundary. To address these hazards, a National Science Foundation Rapid Response survey was conducted to map the EPGF in the Jamaica Passage south of Kingston, Jamaica, and east of the island of Jamaica. From the R/V Pelican we collected >50 high-resolution seismic profiles and 47 gravity cores. Event deposits (EDs) were identified from lithology, physical properties, and geochemistry and were dated in 13 cores. A robust 14C chronology was obtained for the Holocene. A Bayesian age model using OxCal 4.4 calibration was applied. Out of 58 EDs that were recognized, 50 have ages that overlap within their 95% confidence ranges. This allowed for their grouping in multiple basins located as much as 150 km apart. The significant age overlap suggests that EDs along the Enriquillo–Plantain Garden plate boundary resulted from large and potentially dangerous earthquakes. Most of these earthquakes may derive from the EPGF but also from thrust faulting at this strain-partitioned transpressional boundary. The recent increase in Coulomb stress on the EPGF from the Mw 7.2 Nippes earthquake in southwestern Haiti and the discoveries reported here enhance the significance for hazard in the Jamaica Passage. 

Abstract Patients with chronic lung disease (CLD) have an increased risk for severe coronavirus disease-19 (COVID-19) and poor outcomes. Here, we analyze the transcriptomes of 611,398 single cells isolated from healthy and CLD lungs to identify molecular characteristics of lung cells that may account for worse COVID-19 outcomes in patients with chronic lung diseases. We observe a similar cellular distribution and relative expression of SARS-CoV-2 entry factors in control and CLD lungs. CLD AT2 cells express higher levels of genes linked directly to the efficiency of viral replication and the innate immune response. Additionally, we identify basal differences in inflammatory gene expression programs that highlight how CLD alters the inflammatory microenvironment encountered upon viral exposure to the peripheral lung. Our study indicates that CLD is accompanied by changes in cell-type-specific gene expression programs that prime the lung epithelium for and influence the innate and adaptive immune responses to SARS-CoV-2 infection.