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Jan 31, 2023

TRS Seminar Series on Coronaviruses (2023-01-31)

School of Biomedical Sciences is pleased to invite you to join the following seminar:

Title: Anosmia and long term neurological disease in SARS-CoV-2-infected mice
Speaker: Professor Stanley Perlman, Professor of Microbiology and Immunology, and of Pediatrics, University of Iowa Distinguished Professor, The University of Iowa

Date: 31 January 2023 (Tuesday)
Time: 10:00 am – 11:00 am

Zoom link
Meeting ID: 923 9947 8891
Password: 914939

Supported by:

  • Department of Microbiology, School of Clinical Medicine, HKUMed
  • Theme-based Research Program (T11-709/21-N) on "Ecology, Molecular Virology and Pathogenesis of SARS-CoV-2"
  • State Key Laboratory of Emerging Infectious Diseases, HKU
  • Center for Virology, Vaccinology and Therapeutics (CVVT), InnoHK@HKUMed



Professor Stanley Perlman received his Ph.D. in Biophysics from M.I.T., Cambridge, Massachusetts and his M.D. from the University of Miami, Miami, Florida. He was trained in Pediatrics and Pediatric Infectious Diseases at Boston Children’s Hospital, Boston, Massachusetts. He is a member of the VRBPAC of the FDA and the COVID-19 Advisory Committee of the ACIP (Advisory Committee on Immunization Practices). His current research efforts are focused on coronavirus pathogenesis, including virus-induced demyelination and the Severe Acute Respiratory Syndrome (SARS), the Middle East Respiratory Syndrome (MERS) and COVID-19. His laboratory has developed several novel animal models useful for studying pathogenesis and evaluating vaccines and anti-viral therapies. His studies are directed at understanding why aged patients and mice developed more severe disease than younger individuals after infection with SARS-CoV or SARS-CoV-2 and also on why there is a male predominance in patients with more severe disease after infection with SARS-CoV, MERS-CoV or SARS-CoV-2. His laboratory has developed several mouse models for COVID-19. Among other topics, his research is now focusing on the loss of sense of smell (anosmia) and taste (ageusia) and neurological disease in patients with acute SARS-CoV-2 infection and long COVID-19.


Loss of olfactory function has been commonly reported in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infections. Recovery from anosmia is not well understood. Previous studies showed that sustentacular cells, and occasionally, olfactory sensory neurons (OSNs) in the olfactory epithelium (OE) are infected in SARS-CoV-2-infected patients and experimental animals. Here, we show that SARS-CoV-2 infection of sustentacular cells induces inflammation characterized by infiltration of myeloid cells to the olfactory epithelium and variably increased expression of proinflammatory cytokines. We observed widespread damage to, and loss of cilia on, OSNs, accompanied by downregulation of olfactory receptors and signal transduction molecules involved in olfaction. A consequence of OSN dysfunction was a reduction in the number of neurons in the olfactory bulb expressing tyrosine hydroxylase, consistent with reduced synaptic input. We also identified long term behavioral defects in SARS-CoV-2 infected mice, and changes in gene expression in the substantia nigra, an area of the brain affected in Parkinson’s Disease. Together, these results begin to define the downstream effects of sustentacular cell infection, provide insight into olfactory dysfunction in COVID-19-associated anosmia and identify neurological defects in infected mice.


Should you have any enquiries, please feel free to contact Miss Angela Wong at 3917 9216.