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On the 8th of May, 2018, an outbreak of Ebola virus disease (EVD) was declared, originating in the Bikoro region of the Democratic Republic of the Congo (DRC) near the border with neighboring Republic of the Congo (ROC). Frequent trade and migration occur between DRC and ROC-based communities residing along the Congo River. In June 2018, a field team was deployed to determine whether Zaire ebolavirus (Ebola virus (EBOV)) was contemporaneously circulating in local bats at the human-animal interface in ROC near the Bikoro EVD outbreak. Samples were collected from bats in the Cuvette and Likouala departments, ROC, bordering the Équateur Province in DRC where the Bikoro EVD outbreak was first detected. EBOV genomic material was not detected in bat-derived samples by targeted quantitative reverse transcription-polymerase chain reaction or by family-level consensus polymerase chain reaction; however, serological data suggests recent exposure to EBOV in bats in the region. We collected serum from 144 bats in the Cuvette department with 6.9% seropositivity against the EBOV glycoprotein and 14.3% seropositivity for serum collected from 27 fruit bats and one Molossinae in the Likouala department. We conclude that proactive investment in longitudinal sampling for filoviruses at the human-animal interface, coupled with ecological investigations are needed to identify EBOV wildlife reservoirs., Competing Interests: The authors have declared that no competing interests exist.

SARS-CoV-2 emerged in late 2019 and resulted in the ongoing COVID-19 pandemic. Several animal models have been rapidly developed that recapitulate the asymptomatic to moderate disease spectrum. Now, there is a direct need for additional small animal models to study the pathogenesis of severe COVID-19 and for fast-tracked medical countermeasure development. Here, we show that transgenic mice expressing the human SARS-CoV-2 receptor (angiotensin-converting enzyme 2 [hACE2]) under a cytokeratin 18 promoter (K18) are susceptible to SARS-CoV-2 and that infection resulted in a dose-dependent lethal disease course. After inoculation with either 104 TCID50 or 105 TCID50, the SARS-CoV-2 infection resulted in rapid weight loss in both groups and uniform lethality in the 105 TCID50 group. High levels of viral RNA shedding were observed from the upper and lower respiratory tract and intermittent shedding was observed from the intestinal tract. Inoculation with SARS-CoV-2 resulted in upper and lower respiratory tract infection with high infectious virus titers in nasal turbinates, trachea and lungs. The observed interstitial pneumonia and pulmonary pathology, with SARS-CoV-2 replication evident in pneumocytes, were similar to that reported in severe cases of COVID-19. SARS-CoV-2 infection resulted in macrophage and lymphocyte infiltration in the lungs and upregulation of Th1 and proinflammatory cytokines/chemokines. Extrapulmonary replication of SARS-CoV-2 was observed in the cerebral cortex and hippocampus of several animals at 7 DPI but not at 3 DPI. The rapid inflammatory response and observed pathology bears resemblance to COVID-19. Additionally, we demonstrate that a mild disease course can be simulated by low dose infection with 102 TCID50 SARS-CoV-2, resulting in minimal clinical manifestation and near uniform survival. Taken together, these data support future application of this model to studies of pathogenesis and medical countermeasure development., Competing Interests: The authors have declared that no competing interests exist.