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Long-term severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) shedding was observed from the upper respiratory tract of a female immunocompromised individual with chronic lymphocytic leukemia and acquired hypogammaglobulinemia. Shedding of infectious SARS-CoV-2 was observed up to 70 days, and of genomic and subgenomic RNA up to 105 days, after initial diagnosis. The infection was not cleared after the first treatment with convalescent plasma, suggesting a limited effect on SARS-CoV-2 in the upper respiratory tract of this individual. Several weeks after a second convalescent plasma transfusion, SARS-CoV-2 RNA was no longer detected. We observed marked within-host genomic evolution of SARS-CoV-2 with continuous turnover of dominant viral variants. However, replication kinetics in Vero E6 cells and primary human alveolar epithelial tissues were not affected. Our data indicate that certain immunocompromised individuals may shed infectious virus longer than previously recognized. Detection of subgenomic RNA is recommended in persistently SARS-CoV-2-positive individuals as a proxy for shedding of infectious virus., Graphical Abstract, Highlights • Persistent SARS-CoV-2 infection and shedding in immunocompromised individual • Infectious SARS-CoV-2 isolated up to 70 days after diagnosis • Observed within-host genetic variation with continuous turnover of viral variants • SARS-CoV-2 isolates from the individual do not display altered replication, This case study describes a female immunocompromised individual with chronic lymphocytic leukemia and acquired hypogammaglobulinemia who became persistently infected with SARS-CoV-2. Although asymptomatic throughout the course of infection, she demonstrated prolonged shedding of infectious SARS-CoV-2 virus and RNA. This study demonstrates that certain individuals may remain infectious for prolonged periods of time and highlights the need for further studies to understand risk factors for prolonged infectious SARS-CoV-2 shedding.

The coronavirus pandemic has created worldwide shortages of N95 respirators. We analyzed 4 decontamination methods for effectiveness in deactivating severe acute respiratory syndrome coronavirus 2 virus and effect on respirator function. Our results indicate that N95 respirators can be decontaminated and reused, but the integrity of respirator fit and seal must be maintained.

Long-term SARS-CoV-2 shedding was observed from the upper respiratory tract of an immunocompromised patient with chronic lymphocytic leukemia and acquired hypogammaglobulinemia. Shedding of SARS-CoV-2 genomic and subgenomic RNA was observed up to 105 days, and infectious virus up to 70 days past the initial diagnosis. The infection was not cleared after a first treatment with convalescent plasma, suggesting limited impact on SARS-CoV-2 in the upper respiratory tract. SARS-CoV-2 RNA was no longer detected several weeks after a second transfusion of convalescent plasma. There was marked within-host genomic evolution of SARS-CoV-2, with continuous turnover of dominant viral variants. However, replication kinetics in VeroE6 cells and primary human alveolar epithelial tissues were not affected. Our data indicate that certain immunocompromised patients may shed infectious virus for longer durations than previously recognized. Detection of of subgenomic RNA is recommended in persistently SARS-CoV-2 positive individuals as a proxy for shedding of infectious virus. Funding: This work was supported by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases (NIAID). T.A.B. is supported by the Medical Research Council UK (MR/S007555/1). The Wellcome Centre for Human Genetics is supported by Wellcome Centre grant 203141/Z/16Z. Conflict of Interest: The authors declare no competing interests.

Recent nosocomial transmission events of emerging and re-emerging viruses, including Ebola virus, Middle East respiratory syndrome coronavirus, Nipah virus, and Crimean–Congo hemorrhagic fever orthonairovirus, have highlighted the risk of nosocomial transmission of emerging viruses in health-care settings. In particular, concerns and precautions have increased regarding the use of aerosol-generating medical procedures when treating patients with such viral infections. In spite of increasing associations between aerosol-generating medical procedures and the nosocomial transmission of viruses, we still have a poor understanding of the risks of specific procedures and viruses. In order to identify which aerosol-generating medical procedures and emerging viruses pose a high risk to health-care workers, we explore the mechanisms of aerosol-generating medical procedures, as well as the transmission pathways and characteristics of highly pathogenic viruses associated with nosocomial transmission. We then propose how research, both in clinical and experimental settings, could advance current infection control guidelines.

Rapid sequencing of RNA/DNA from pathogen samples obtained during disease outbreaks provides critical scientific and public health information. However, challenges exist for exporting samples to laboratories or establishing conventional sequencers in remote outbreak regions. We successfully used a novel, pocket-sized nanopore sequencer at a field diagnostic laboratory in Liberia during the current Ebola virus outbreak.

Background During the pandemic of coronavirus disease 2019 (COVID-19), many questions arose regarding risks for hospital-acquired or nosocomial transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Aerosol generating medical procedures (AGMPs), techniques that can generate infectious, virus-laden aerosols, could potentially amplify transmission among healthcare workers (HCWs). Thus, it was widely recommended that HCWs use airborne precautions when performing AGMPs. However, in clinical settings it is often unclear what procedures constitute AGMPs and how the risk varies by procedure or pathogen. We set out to further define AGMPs and assess the risk for nosocomial transmission of SARS-CoV-2 and other high-risk viruses via AGMPs. Methods We identified potential AGMPs and emerging viruses that were high-risk for nosocomial transmission through reviewing experimental and clinical data. Potential AGMPs were those associated with previous virus transmission or mechanically capable of transmission. High-risk viruses were defined as those that cause severe disease in humans for which limited therapies or interventions exist, are infectious via aerosols in humans or non-human primates (NHPs), found in the respiratory tract of infected humans or NHPs, and had previous evidence of nosocomial transmission. Results We identified multiple potential AGMPs, which could be divided into those that generate aerosols or induce a patient to form aerosols, as well as eight families of high-risk viruses. All of the viruses were emerging zoonotic RNA viruses. In the family Coronaviridae, we identified potential evidence for SARS-CoV-1, MERS-CoV, and SARS-CoV-2 transmission via AGMPs. SARS-CoV-1 and SARS-CoV-2 were also found to be similarly stable when aerosolized. Conclusion Multiple emerging zoonotic viruses pose a high risk for nosocomial transmission through a variety of AGMPs. Given the similar stability of SARS-CoV-2 with SARS-CoV-1 when aerosolized and prior nosocomial transmission of SARS-CoV-1 via AGMPs, we suspect that certain AGMPs pose an increased risk for SARS-CoV-2 transmission. Additional experimental studies and on-site clinical sampling during AGMPs are necessary to further risk stratify AGMPs. Disclosures All Authors: No reported disclosures

We evaluated the stability of Ebola virus on surfaces and in fluids under simulated environmental conditions for the climate of West Africa and for climate-controlled hospitals. This virus remains viable for a longer duration on surfaces in hospital conditions than in African conditions and in liquid than in dried blood.

The ongoing Ebola virus outbreak in West Africa has highlighted questions regarding stability of the virus and detection of RNA from corpses. We used Ebola virus–infected macaques to model humans who died of Ebola virus disease. Viable virus was isolated

An unprecedented number of Ebola virus infections among healthcare workers and patients have raised questions about our understanding of Ebola virus transmission. Here, we explore different routes of Ebola virus transmission between people, summarizing the known epidemiological and experimental data. From this data, we expose important gaps in Ebola virus research pertinent to outbreak situations. We further propose experiments and methods of data collection that will enable scientists to fill these voids in our knowledge about the transmission of Ebola virus.

On March 20, 2015, a case of Ebola virus disease was identified in Liberia that most likely was transmitted through sexual contact. We assessed the efficiency of detecting Ebola virus in semen samples by molecular diagnostics and the stability of Ebola virus in ex vivo semen under simulated tropical conditions.

Ebola virus disease afflicts both human and animal populations and is caused by four ebolaviruses. These different ebolaviruses may have distinct reservoir hosts and ecological contexts that determine how, where, and when different ebolavirus spillover events occur. Understanding these virus-specific relationships is important for preventing transmission of ebolaviruses from wildlife to humans. We examine the ecological contexts surrounding 34 human index case infections of ebolaviruses from 1976–2014. Determining possible sources of spillover from wildlife, characterizing the environment of each event, and creating ecological niche models to estimate habitats suitable for spillover, we find that index case infections of two ebolaviruses, Ebola virus and Sudan virus, have occurred under different ecological contexts. The index cases of Ebola virus infection are more associated with tropical evergreen broadleaf forests and consuming bushmeat than the cases of Sudan virus. Given these differences, we emphasize caution when generalizing across different ebolaviruses and that location and virus-specific ecological knowledge will be essential to unravelling how human and animal behavior lead to the emergence of Ebola virus disease., Author Summary Multiple Ebola virus disease outbreaks have occurred over the past 40 years, yet we still do not know the geographical distributions, definitive host species, and suitable habitats for animal-to-human transmission of different ebolaviruses. Each Ebola virus disease outbreak has started with at least one transmission event from a wildlife host to a human, also known as a spillover event. While researchers have studied these events in regards to Ebola virus disease outbreaks, many studies neglect that there are multiple ebolaviruses and that these viruses may differ in their spillover events. We characterize the specific ecological contexts of different ebolavirus spillover events based on recorded index case infections. Comparing the environmental contexts of these cases and using ecological niche modelling, we find that two ebolaviruses have different suitable habitats for spillover. The different habitats and contexts of the two ebolaviruses involved in the majority of outbreaks, Ebola virus and Sudan virus, indicate that we must further investigate virus-specific differences in ebolaviruses and their hosts.