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<p>Neurological complications of COVID-19 encompass acute syndromes and persistent post-acute sequelae, yet their mechanistic basis remains incompletely defined. Integrated clinical, neuropathological, neuroimaging, and molecular evidence indicates that SARS-CoV-2–associated neurological injury is driven predominantly by receptor-mediated immune and vascular mechanisms rather than widespread productive central nervous system infection. Angiotensin-converting enzyme 2 (ACE2) remains the principal viral entry receptor, while neuropilin-1 (NRP1) facilitates neurovascular and olfactory access in specific contexts. In contrast, CD147 and dipeptidyl peptidase-4 (DPP4) appear to exert indirect modulatory roles through endothelial dysfunction and immune activation rather than acting as dominant neurotropic entry receptors. Toll-like receptors, particularly TLR2, TLR4, and TLR7, amplify neuroinflammatory signaling and contribute to blood–brain barrier disruption, microvascular injury, and sustained microglial activation. Cerebrospinal fluid biomarkers and neuroimaging findings consistently support a dual-pathway model combining limited direct viral presence with predominant immune-mediated injury. Current therapeutic strategies targeting receptor-mediated entry and neuroinflammation remain largely investigational, underscoring the need for biomarker-guided and phase-specific interventions. These findings refine the mechanistic framework of NeuroCOVID and identify translational priorities for acute and long-term neurological management.</p>

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Receptor-mediated mechanisms underlying neurological complications in COVID-19: from viral entry to neuroinflammation

  • 期刊论文

  • 发表日期：

    2026年3月9日

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  • Digbijoy Nath,
  • Abdullah Al Noman,
  • Sanjana Pradhan,
  • Pranab Dev Sharma,
  • Sahidur Ahmed,
  • Firuza Begum,
  • Md Al Hafiz,
  • Emad M. Abdallah

摘要

Neurological complications of COVID-19 encompass acute syndromes and persistent post-acute sequelae, yet their mechanistic basis remains incompletely defined. Integrated clinical, neuropathological, neuroimaging, and molecular evidence indicates that SARS-CoV-2–associated neurological injury is driven predominantly by receptor-mediated immune and vascular mechanisms rather than widespread productive central nervous system infection. Angiotensin-converting enzyme 2 (ACE2) remains the principal viral entry receptor, while neuropilin-1 (NRP1) facilitates neurovascular and olfactory access in specific contexts. In contrast, CD147 and dipeptidyl peptidase-4 (DPP4) appear to exert indirect modulatory roles through endothelial dysfunction and immune activation rather than acting as dominant neurotropic entry receptors. Toll-like receptors, particularly TLR2, TLR4, and TLR7, amplify neuroinflammatory signaling and contribute to blood–brain barrier disruption, microvascular injury, and sustained microglial activation. Cerebrospinal fluid biomarkers and neuroimaging findings consistently support a dual-pathway model combining limited direct viral presence with predominant immune-mediated injury. Current therapeutic strategies targeting receptor-mediated entry and neuroinflammation remain largely investigational, underscoring the need for biomarker-guided and phase-specific interventions. These findings refine the mechanistic framework of NeuroCOVID and identify translational priorities for acute and long-term neurological management.