Mink, on a farm with about 15,000 animals, became infected with SARS-CoV-2. Over 75% of tested animals were positive for SARS-CoV-2 RNA in throat swabs and 100% of tested animals were seropositive. The virus responsible had a deletion of nucleotides encoding residues H69 and V70 within the spike protein gene as well as the A22920T mutation, resulting in the Y453F substitution within this protein, seen previously in mink. The infected mink recovered and after free-testing of 300 mink (a level giving 93% confidence of detecting a 1% prevalence), the animals remained seropositive. During further follow-up studies, after a period of more than 2 months without any virus detection, over 75% of tested animals again scored positive for SARS-CoV-2 RNA. Whole genome sequencing showed that the viruses circulating during this re-infection were most closely related to those identified in the first outbreak on this farm but additional sequence changes had occurred. Animals had much higher levels of anti-SARS-CoV-2 antibodies in serum samples after the second round of infection than at free-testing or during recovery from initial infection, consistent with a boosted immune response. Thus, it was concluded that following recovery from an initial infection, seropositive mink were readily re-infected by SARS-CoV-2. Author summary Early on, in the course of SARS-CoV-2 infections among mink in Denmark, we identified a farm, with about 15,000 mink, that had virus-infected animals. At this time, we found that a very high proportion of the mink had been infected and made antibodies against the virus. In contrast to the three previously infected farms, the mink were allowed to recover (the mink had shown few signs of disease and only low mortality) and our testing demonstrated the absence of circulating virus. Continued screening, in the following weeks, supported the absence of infection in the mink but the maintenance of antibodies against the virus. However, less than 3 months after the initial infection, we again identified the presence of virus in some dead mink from this farm and in many live mink. The viruses responsible for this second wave of infection were slightly different from those found in the first wave but were closer to each other than to the SARS-CoV-2s found on other mink farms. The antibody levels in mink during this second wave of infection were much higher than observed after the initial infection. We concluded that the initial round of infection in mink was insufficient to confer protection against re-infection.
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