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

Nada J Habeichi1,2,3,4, Ghadir Amin1,2,5, Bachir Lakkis6

  • 1Department of Pharmacology and Toxicology, American University of Beirut Faculty of Medicine, 1107-2020 Beirut, Lebanon.

Frontiers in Bioscience (Landmark Edition)
|January 30, 2024
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause kidney damage, even in healthy individuals. This review explores novel pathways like toll-like receptor 4 (TLR-4) involved in SARS-CoV-2 renal infectivity.

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.
Keywords:
COVID-19acute kidney injuryrenal diseaseviral infection

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