Can cilia provide an entry gateway for SARS-CoV-2 to human ciliated cells?

Area of Science:

• Nephrology
• Virology
• Pathology

Background:

• The COVID-19 pandemic, caused by SARS-CoV-2, presents a global health crisis with limited approved treatments.
• Previous coronavirus outbreaks (SARS-CoV, MERS-CoV) were associated with severe acute kidney injury (AKI), contributing to high mortality rates.
• Emerging evidence indicates significant renal involvement in COVID-19 patients, underscoring the need to understand SARS-CoV-2's impact on kidney function.

Purpose of the Study:

• To review the current literature on kidney damage in COVID-19 patients.
• To explore potential mechanisms of SARS-CoV-2-induced AKI, drawing parallels with other coronavirus strains.
• To propose a hypothesis linking SARS-CoV-2 cellular infection to the primary cilium in kidney cells.

Main Methods:

• Literature review of existing studies on COVID-19, SARS-CoV-2, and kidney injury.
• Analysis of proposed mechanisms for AKI in COVID-19, including hyperinflammation and cytotoxic effects.
• Examination of the role of angiotensin-converting enzyme-2 (ACE2) and collectrin in SARS-CoV-2 infection and kidney pathology.

Main Results:

• COVID-19 is associated with substantial kidney damage, potentially increasing mortality rates, especially in patients with pre-existing conditions.
• Two primary theories for AKI in COVID-19 are proposed: secondary effects of reduced oxygen and hyperinflammation, or direct cytotoxic effects.
• The expression of ACE2 and collectrin in kidneys, and the known targeting of cilia by coronaviruses, suggest a potential mechanism for viral entry and kidney damage.

Conclusions:

• Kidney damage is a significant concern in COVID-19, contributing to higher mortality.
• The precise mechanisms of SARS-CoV-2-induced AKI require further investigation.
• A potential link between SARS-CoV-2 cellular infection and the primary cilium warrants further research into COVID-19 pathogenesis.