Programme(s) to which this project applies:
|☑ MPhil/PhD||☒ MRes[Med]||☒ URIS|
The Coronavirus disease 2019 (COVID-19) pandemic was suspected to be zoonotic and originated from a novel beta-coronavirus (CoV) that has now been officially named as SARS-CoV-2. The rapid dissemination of SARS-CoV-2 was related to highly efficient person-to-person transmission in both hospital and community settings. SARS-CoV-2 has been globally spread by travellers, and often by contacts with asymptomatic carriers. It remains unclear why host immune responses are insufficient in controlling early pathogenesis and transmission of COVID-19. It is, therefore, crucial to dissect the immune mechanisms of SARS-CoV-2 pathogenesis to promote the control of the pandemic and the development of an effective vaccine against COVID-19. Several elegant studies demonstrated that SARS-CoV-2 and SARS-CoV use the same cellular entry receptor angiotensin-converting enzyme 2 (ACE2) to initiate infection, despite that only 40% of amino acid are identical in the receptor binding domain (RBD) external subdomain. Since some coronaviruses also use ACE2 as the cellular receptor but they have not caused any major outbreaks, it is suspected that other host factors may contribute to the highly efficient zoonotic and person-to-person transmission besides ACE2. Currently, the mechanism underlying early immunopathogenesis of COVID-19 remains unclear and is yet to be fully determined.
To define the role of host immune responses in acute SARSCoV-2 pathogenesis.
Research Plan and Methodology:
-To determine mechanism underlying rapid dysfunction of dendritic cells (DC)
-To determine the role of anti-spike IgG/MAb-mediated acute lung injury
-To determine T cell responses essential for cell-mediated immune protection
Prof ZW Chen, Department of Microbiology
Professor Zhiwei Chen, Department of Microbiology/ AIDS InstituteBiography
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