On April 22, CDC and the U.S. Department of Agriculture (USDA) reported cases of two domestic cats with confirmed infection with SARS-CoV-2, the virus that causes coronavirus disease 2019 (COVID-19). These are the first reported companion animals (including pets and service animals) with SARS-CoV-2 infection in the United States, and among the first findings of SARS-CoV-2 symptomatic companion animals reported worldwide. These feline cases originated from separate households and were epidemiologically linked to suspected or confirmed human COVID-19 cases in their respective households. Notification of presumptive positive animal test results triggered a One Health* investigation by state and federal partners, who determined that no further transmission events to other animals or persons had occurred. Both cats fully recovered. Although there is currently no evidence that animals play a substantial role in spreading COVID-19, CDC advises persons with suspected or confirmed COVID-19 to restrict contact with animals during their illness and to monitor any animals with confirmed SARS-CoV-2 infection and separate them from other persons and animals at home (1). SARS-CoV-2 is a zoonotic coronavirus that likely originated in bats (2). A small number of animals worldwide, including dogs, cats, zoo tigers and lions, and farmed mink, have been infected naturally with SARS-CoV-2, mostly through suspected human-to-animal transmission † (3). In addition, experimental studies in ferrets, golden Syrian hamsters, Egyptian fruit bats, and cats show that these species can transmit infection to cohoused animals of the same species (4-7). SARS-CoV-2 Clinical Presentation in Domestic Cats On March 24, in Nassau County, New York, a 4-year-old male domestic shorthair (cat A), developed respiratory illness characterized by sneezing, clear ocular discharge, and mild lethargy (Figure). On April 1, the cat was taken to a veterinary clinic; on physical examination the cat was found to be * One Health is a collaborative, multisectoral, and transdisciplinary approach, working at the local, regional, national, and global levels, with the goal of achieving optimal health outcomes recognizing the interconnection between humans, animals, plants, and their shared environment. † https://www.oie.int/scientific-expertise/specific-information-andrecommendations/questions-and-answers-on-2019novel-coronavirus/.

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Obesity has been associated with greater severity of influenza virus infection and impaired host defense. Exercise may confer health benefits even when weight loss is not achieved, but it has not been determined if regular exercise improves immune defense against influenza A virus (IAV) in the obese condition. In this study, diet-induced obese mice and lean control mice exercised for eight weeks followed by influenza viral infection. Exercise reduced disease severity in both obese and non-obese mice, but the mechanisms differed. Exercise reversed the obesity-associated delay in bronchoalveolar-lavage (BAL) cell infiltration, restored BAL cytokine and chemokine production, and increased ciliary beat frequency and IFNα-related gene expression. In non-obese mice, exercise treatment reduced lung viral load, increased Type-I-IFN-related gene expression early during infection, but reduced BAL inflammatory cytokines and chemokines. In both obese and non-obese mice, exercise increased serum anti-influenza virus specific IgG2c antibody, increased CD8+ T cell percentage in BAL, and reduced TNFα by influenza viral NP-peptide-responding CD8+ T cells. Overall, the results suggest that exercise “restores” the immune response of obese mice to a phenotype similar to non-obese mice by improving the delay in immune activation. In contrast, in non-obese mice exercise treatment results in an early reduction in lung viral load and limited inflammatory response.