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| Poster #214 SARS-CoV-2 infection of taste bud cells in human ACE2 transgenic mice |
| Kang-Hoon Kim1, Emma Larsson1, Heaven Branch1, Richard Bowen2, Hong Wang1 1Monell Chemical Senses Center, Philadelphia, PA, United States 2Departments of Biomedical Sciences, Colorado State University, Fort Collins, CO, United States |
Taste loss is particularly prevalent with SARS-CoV-2 infection. In the early phase of the COVID-19 pandemic, close to half of patients reported taste loss. While taste function was restored quickly in many patients, a subset of patients suffered from sustained taste loss that lasted longer than several months. How SARS-CoV-2 infection leads to taste dysfunction remains poorly understood. To study the underlying mechanism of taste loss, we used transgenic mouse models that express the human angiotensin-converting enzyme 2 (ACE2), the receptor for SARS-CoV-2 in humans. We used the human ACE2 (hACE2) knock-in and mouse ACE2 knockout strain that has been shown to be susceptible to SARS-CoV-2 infection. Our results show that taste tissues can be infected by SARS-CoV-2, both viral RNAs and proteins can be detected. Antibody staining experiments show that SARS-CoV-2 can infect types II and III taste bud cells that are responsible for sensing sweet, umami, bitter, and sour tastes. In addition, we generated mouse strains that express hACE2 but lack the antiviral gene, interferon regulatory factor 3 (IRF3) or type I interferon receptor 1 (IFNAR1). Recent studies showed that inborn genetic errors in key antiviral genes exist in human populations and are highly enriched in patients with severe COVID-19. Thus, the double-transgenic mouse strains allow us to investigate whether deficiencies in antiviral genes contribute to SARS-CoV-2-induced taste loss. We found that taste tissues of IRF3-knockout mice contained detectable SARS-CoV-2 RNAs at 36 days post infection, while viral RNAs were cleared from taste tissues of mice with functional IRF3. Our results suggest that deficiency in IRF3 leads to prolonged viral infection in taste tissues, which may contribute to long-term post-viral taste loss. |