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Background <p>Bilateral facial palsy variant Guillain-Barré syndrome (GBS) is a distinct clinical subtype. As an acute immune-mediated polyradiculoneuropathy often triggered by infections, varicella-zoster virus (VZV) is a rare yet significant precipitating factor for this variant. Anti-ganglioside antibodies, particularly anti-GD3, are involved in the pathogenesis of GBS, but their significance in VZV-associated bilateral facial palsy subtype remains incompletely elucidated.</p> Case presentation <p>We report a 46-year-old female who developed acute bilateral facial palsy and limb sensory deficits following VZV infection. Serum anti-ganglioside testing confirmed GD3 IgG positivity, and cerebrospinal fluid analysis revealed albuminocytological dissociation. Nerve conduction studies supported a demyelinating polyneuropathy, and the patient showed significant improvement after intravenous immunoglobulin therapy.</p> Conclusions <p>This case suggests that VZV may act as a potential trigger for GD3 antibody-positive variant GBS. Early immunotherapy may improve outcomes, emphasizing the need for systematic antibody testing in atypical presentations of this variant GBS. Further studies are required to clarify the pathophysiological role of GD3 antibodies in VZV-associated variant GBS.</p>

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Varicella-zoster virus infection triggering GD3 antibody-positive variant Guillain-Barré syndrome: a case report and literature review

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月7日

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  • Yujun Wu,
  • Liyan Gu,
  • Jieyi Liu,
  • Weihua Yan,
  • Jie Wei

摘要

Background

Bilateral facial palsy variant Guillain-Barré syndrome (GBS) is a distinct clinical subtype. As an acute immune-mediated polyradiculoneuropathy often triggered by infections, varicella-zoster virus (VZV) is a rare yet significant precipitating factor for this variant. Anti-ganglioside antibodies, particularly anti-GD3, are involved in the pathogenesis of GBS, but their significance in VZV-associated bilateral facial palsy subtype remains incompletely elucidated.

Case presentation

We report a 46-year-old female who developed acute bilateral facial palsy and limb sensory deficits following VZV infection. Serum anti-ganglioside testing confirmed GD3 IgG positivity, and cerebrospinal fluid analysis revealed albuminocytological dissociation. Nerve conduction studies supported a demyelinating polyneuropathy, and the patient showed significant improvement after intravenous immunoglobulin therapy.

Conclusions

This case suggests that VZV may act as a potential trigger for GD3 antibody-positive variant GBS. Early immunotherapy may improve outcomes, emphasizing the need for systematic antibody testing in atypical presentations of this variant GBS. Further studies are required to clarify the pathophysiological role of GD3 antibodies in VZV-associated variant GBS.