Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 118, Issue 18, Pages -Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.2025601118
Keywords
SARS-CoV-2; virology; transmission; genetics; coronavirus
Categories
Funding
- National Institute of Allergy and Infectious Diseases [HHSN272201400008C/AI/NIAID]
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Ferrets are relevant for laboratory studies on respiratory viruses, but no evidence of natural transmission of SARS-CoV-2 from infected humans to ferrets was observed in the study. Unique mutations in ferrets may contribute to their susceptibility to SARS-CoV-2. Therefore, domestic ferrets are considered to be at low risk of natural infection from currently circulating SARS-CoV-2.
Ferrets (Mustela putorius furo) are mustelids of special relevance to laboratory studies of respiratory viruses and have been shown to be susceptible to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and onward transmission. Here, we report the results of a natural experiment where 29 ferrets in one home had prolonged, direct contact and constant environmental exposure to two humans with symptomatic disease, one of whom was confirmed positive for SARS-CoV-2. We observed no evidence of SARS-CoV-2 transmission from humans to ferrets based on viral and antibody assays. To better understand this discrepancy in experimental and natural infection in ferrets, we compared SARS-CoV-2 sequences from natural and experimental mustelid infections and identified two surface glycoprotein Spike (S) mutations associated with mustelids. While we found evidence that angiotensin-converting enzyme II provides a weak host barrier, one mutation only seen in ferrets is located in the novel S1/S2 cleavage site and is computationally predicted to decrease furin cleavage efficiency. These data support the idea that host factors interacting with the novel S1/S2 cleavage site may be a barrier in ferret SARS-CoV-2 susceptibility and that domestic ferrets are at low risk of natural infection from currently circulating SARS-CoV-2. We propose two mechanistically grounded hypotheses for mustelid host adaptation of SARS-CoV-2, with possible effects that require additional investigation.
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