Can antiglycolipid antibodies present in HIV-infected individuals induce immune demyelination?

Steven Petratos, Michael F. Gonzales

Research output: Contribution to journalReview ArticleResearchpeer-review

6 Citations (Scopus)


Of the eight clinically defined neuropathies associated with HIV infection, there is compelling evidence that acute and chronic inflammatory demyelinating polyneuropathy (IDPN) have an autoimmune pathogenesis. Many non-HIV infected individuals who suffer from sensory-motor nerve dysfunction have autoimmune indicators. The immunopathogenesis of demyelination must involve neuritogenic components in myelin. The various antigens suspected to play a role in HIV-seronegative IDPN include (i) P2 protein; (ii) sulfatide (GalS); (iii) various gangliosides (especially GM1); (iv) galactocerebroside (GalC); and (v) glycoproteins or glycolipids with the carbohydrate epitope glucuronyl-3-sulfate. These glycoproteins or glycolipids may be individually targeted, or an immune attack may be raised against a combination of any of these epitopes. The glycolipids, however, especially GalS, have recently evoked much interest as mediators of immune events underlying both non-HIV and HIV-associated demyelinating neuropathies. The present review outlines the recent research findings of antiglycolipid antibodies present in HIV-infected patients with and without peripheral nerve dysfunction, in an attempt to arrive at some consensus as to whether these antibodies may play a role in the immunopathogenesis of HIV-associated inflammatory demyelinating polyneuropathy.

Original languageEnglish
Pages (from-to)257-272
Number of pages16
Issue number4
Publication statusPublished - 1 Dec 2000
Externally publishedYes


  • Antibodies
  • Galactocerebroside
  • Gangliosides
  • Human immunodeficiency virus
  • Inflammatory demyelinating polyneuropathy
  • Sulfatide

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