Potential Alternative Receptors for SARS-CoV-2-Induced Kidney Damage: TLR-4, KIM-1/TIM-1, and CD147

Area of Science:

• Nephrology
• Virology
• Immunology

Background:

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to kidney damage, even in patients without prior kidney disease.
• Kidney injury associated with SARS-CoV-2 can be severe, potentially requiring dialysis and hindering patient recovery.
• While angiotensin-converting enzyme 2 (ACE2) was an early focus, emerging evidence suggests direct SARS-CoV-2 infectivity in the kidneys through other pathways.

Purpose of the Study:

• To review the potential involvement of novel viral entry pathways in SARS-CoV-2-associated renal damage.
• To explore toll-like receptor 4 (TLR-4), kidney injury molecule-1/T cell immunoglobulin mucin domain 1 (KIM-1/TIM-1), and cluster of differentiation 147 (CD147) as potential SARS-CoV-2 entry points in the kidney.
• To address unresolved questions regarding SARS-CoV-2 renal infectivity.

Main Methods:

• Literature review of current research on SARS-CoV-2 and kidney injury.
• Analysis of emerging evidence on viral entry mechanisms beyond ACE2.
• Discussion of the roles of TLR-4, KIM-1/TIM-1, and CD147 in SARS-CoV-2 renal pathogenesis.

Main Results:

• Identification of TLR-4, KIM-1/TIM-1, and CD147 as potential alternative receptors for SARS-CoV-2 entry into kidney cells.
• Evidence suggests these novel pathways may contribute to SARS-CoV-2-induced kidney damage.
• The exact mechanisms and significance of these pathways in SARS-CoV-2 renal infectivity require further investigation.

Conclusions:

• Novel viral entry pathways, including TLR-4, KIM-1/TIM-1, and CD147, are implicated in SARS-CoV-2-associated kidney damage.
• Targeting these pathways could offer new therapeutic strategies for managing COVID-19-related kidney injury.
• Further research is crucial to fully elucidate the role of these receptors in SARS-CoV-2 renal pathogenesis.