Abstract
BackgroundAnimal models of COVID-19 have been rapidly reported after the start of the pandemic. We aimed to assess whether the newly created models reproduce the full spectrum of human COVID-19.MethodsWe searched the MEDLINE, as well as BioRxiv and MedRxiv preprint servers for original research published in English from January 1 to May 20, 2020. We used the search terms (COVID-19) OR (SARS-CoV-2) AND (animal models), (hamsters), (nonhuman primates), (macaques), (rodent), (mice), (rats), (ferrets), (rabbits), (cats), and (dogs). Inclusion criteria were the establishment of animal models of COVID-19 as an endpoint. Other inclusion criteria were assessment of prophylaxis, therapies, or vaccines, using animal models of COVID-19.ResultThirteen peer-reviewed studies and 14 preprints met the inclusion criteria. The animals used were nonhuman primates (n = 13), mice (n = 7), ferrets (n = 4), hamsters (n = 4), and cats (n = 1). All animals supported high viral replication in the upper and lower respiratory tract associated with mild clinical manifestations, lung pathology, and full recovery. Older animals displayed relatively more severe illness than the younger ones. No animal models developed hypoxemic respiratory failure, multiple organ dysfunction, culminating in death. All species elicited a specific IgG antibodies response to the spike proteins, which were protective against a second exposure. Transient systemic inflammation was observed occasionally in nonhuman primates, hamsters, and mice. Notably, none of the animals unveiled a cytokine storm or coagulopathy.ConclusionsMost of the animal models of COVID-19 recapitulated mild pattern of human COVID-19 with full recovery phenotype. No severe illness associated with mortality was observed, suggesting a wide gap between COVID-19 in humans and animal models.
Highlights
Animal models of COVID-19 have been rapidly reported after the start of the pandemic
SARS-CoV-2 is a beta coronavirus that binds with a high affinity to angiotensin-converting enzyme (ACE) 2 receptor and uses the transmembrane serine protease (TMPRSS) 2 as co-receptor to gain entry to cells [10,11,12]
ACE2 and TMPRSS2 are co-expressed in many tissues and organs, the nasal epithelial cells and alveolar type II cells of the lungs, which may explain
Summary
Animal models of COVID-19 have been rapidly reported after the start of the pandemic. We aimed to assess whether the newly created models reproduce the full spectrum of human COVID-19. Coronavirus disease 2019 (COVID-19) is a febrile respiratory illness due to a novel viral pathogen severe acute respiratory syndrome–coronavirus 2 (SARS-CoV-2) [1, 2]. SARS-CoV-2 is a beta coronavirus that binds with a high affinity to angiotensin-converting enzyme (ACE) 2 receptor and uses the transmembrane serine protease (TMPRSS) 2 as co-receptor to gain entry to cells [10,11,12]. SARS-CoV-2-induced COVID-19 has led to a pandemic that overwhelmed the capacity of most national health systems, resulting in a global health crisis [19]. An estimated 11,280 million persons in 188 countries were infected, of which 531,000 died [20]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
