SARS-CoV-2, a novel coronavirus with high nucleotide identity to SARS-CoV and SARS-related coronaviruses detected in horseshoe bats, has spread across the world and impacted global healthcare systems and economy 1,2 . A suitable small animal model is needed to support vaccine and therapy development. We report the pathogenesis and transmissibility of the SARS-CoV-2 in golden Syrian hamsters. Immunohistochemistry demonstrated viral antigens in nasal mucosa, bronchial epithelial cells, and in areas of lung consolidation on days 2 and 5 post-inoculation (dpi), followed by rapid viral clearance and pneumocyte hyperplasia on 7 dpi. Viral antigen was also found in the duodenum epithelial cells with viral RNA detected in feces. Notably, SARS-CoV-2 transmitted efficiently from inoculated hamsters to naïve hamsters by direct contact and via aerosols. Transmission via fomites in soiled cages was less efficient. Although viral RNA was continuously detected in the nasal washes of inoculated hamsters for 14 days, the communicable period was short and correlated with the detection of infectious virus but not viral RNA. Inoculated and naturally-infected hamsters showed apparent weight loss, and all animals recovered with the detection of neutralizing antibodies. Our results suggest that SARS-CoV-2 infection in golden Syrian hamsters resemble features found in humans with mild infections.SARS-CoV-2 was first detected from a cluster of pneumonia patients in Wuhan, Hubei Province, China in December 2019. Although 55% of the initial cases were linked to one seafood wholesale market where wild animals were also sold 3 , multiple viral (sustained human-to-human transmissibility by symptomatic and pre-symptomatic patients 4 ) and ecological factors (extensive domestic and international travel during Chinese Lunar New Year) have contributed to the rapid global spread of the virus. The clinical spectrum of patients with the novel coronavirus disease (COVID-19) is wide, 19% of 72,314 symptomatic patients in China progressed to severe and critical illness 5 with an estimated 1.4% symptomatic case fatality risk 6 . There is no approved vaccine or treatment against SARS-CoV-2, and the available interventions including country lock-down and social distancing have severely disrupted the global supply chain and economy.A suitable animal model is essential for understanding the pathogenesis of this disease and for evaluating vaccine and therapeutic candidates. Previous animal studies on SARS-CoV suggested the importance of the interaction between the viral spike protein and the host angiotensin converting enzyme 2 (ACE2) receptors 7-10 as well as age and innate immune status of the animals 11-14 in pathogenesis. As with SARS-CoV, the spike protein of SARS-CoV-2 also utilizes ACE2 receptors that are distributed predominantly in the epithelial cells of the lungs and small intestine to gain entry into epithelial cells for viral replication 1,15 . SARS-CoV-2 showed good binding for human ACE2 but limited binding to murine ACE2 1 , which has limited...

An escalating pandemic by the novel SARS-CoV-2 virus is impacting global health and effective therapeutic options are urgently needed. We evaluated the in vitro antiviral effect of compounds that were previously reported to inhibit coronavirus replication and compounds that are currently under evaluation in clinical trials for SARS-CoV-2 patients. We report the antiviral effect of remdesivir, lopinavir, homorringtonine, and emetine against SARS-CoV-2 virus in Vero E6 cells with the estimated 50% effective concentration at 23.15 μM, 26.63 μM, 2.55 μM and 0.46 μM, respectively. Ribavirin or favipiravir that are currently evaluated under clinical trials showed no inhibition at 100 μM. Synergy between remdesivir and emetine was observed, and remdesivir at 6.25 μM in combination with emetine at 0.195 μM may achieve 64.9% inhibition in viral yield. Combinational therapy may help to reduce the effective concentration of compounds below the therapeutic plasma concentrations and provide better clinical benefits.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein is the main target for neutralizing antibodies. These antibodies can be elicited through immunization or passively transferred as therapeutics in the form of convalescent-phase sera or monoclonal antibodies (MAbs).

L ive poultry markets (LPMs) can serve as hubs for avian influenza virus (AIV) amplification in poultry and pose a risk for human zoonotic infections (1-4). Adopting efficient sampling strategies to monitor AIVs with human zoonotic potential at LPMs is essential for zoonotic disease prevention and pandemic preparedness. Recommendations regarding routine surveillance that would robustly and efficiently inform AIV activity at LPMs have been limited (5). Handling of live poultry interrupts the vending process; moreover, such routine surveillance is difficult to implement. Environmental samples have been collected to monitor AIV activity at LPMs (5-9). There have been limited parallel comparisons of AIV detection rates among poultry and environmental samples (7,10). Without frequent cleaning, the environment often permits AIV accumulation; environmental samples may thus overestimate AIV prevalence in poultry. Subtype-specific detection rates among different environmental samples may also vary. To inform the development of effective sampling strategies for AIV surveillance, we compared monthly detection rates for AIV subtypes H5, H7, and H9 in chickens and various environmental samples at LPMs in Guangzhou, China. The Study During December 2015-July 2018, we performed sampling twice per month at 1 wholesale (52 stalls) and 1 retail (8 stalls) LPM, from 2 randomly selected stalls per sampling event. We collected paired oropharyngeal and cloacal swab samples (n = 3,119 chickens) and environmental samples (n = 3,008) in viral transport medium at the LPMs (Appendix Figure 1, https:// wwwnc.cdc.gov/EID/article/26/3/19-0888-App1. pdf). We randomly collected samples from all chickens at the selected stalls. We rarely observed sick chickens but we sampled them when identified. We also collected environmental samples from 3 key activity areas: poultry holding zones (fecal droppings, drinking water, and poultry feed), slaughtering zones (defeathering machines and surrounding defeathering working areas), and selling zones (chopping boards and display tables) near the selected chickens whenever possible (5-9). (Stalls sampled at the wholesale LPM [wLPM] have only poultry holding zones.) We sampled air using BC-251 cyclone-based NIOSH bioaerosol samplers that fractionate airborne particles into >4 µm, 1-4 µm, and <1 µm size fractions (11). We applied quantitative real-time reverse transcription PCR to detect the matrix gene segment of AIV; we analyzed positive samples by the hemagglutinin gene to determine the AIV subtype (H5, H7, or H9) using specific primers and probes (12,13). H5, H7, and H9 detection rates in environmental samples (median monthly difference 6.2% for H5,