Immunoelectron microscopical labelling of a glycolipid in the envelopes of brain cell-derived budding viruses, Semliki Forest, influenza and measles, using a monoclonal antibody directed chiefly against galactocerebroside resulting from Semliki Forest virus infection

Pathak, S.; Illavia, Shirin J.; Khalili-Shirazi, Azadeh; Webb, H. E.

doi:10.1016/0022-510x(90)90140-i

Cited by 14 publications

(5 citation statements)

References 20 publications

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“…It has been suggested that low levels of anti‐GalS antibodies may be common constituents of the normal human immune repertoire and may be secreted by the CD5 positive subset of B cells, similar to other naturally occurring IgM anticarbohydrate antibodies 31 . These B cells may be activated by GalS incorporated into the envelope of a budding virus, 32 by cross‐reactive foreign antigens or by antigen complexes and may be excessively produced by expanded B cell clones in monoclonal gammopathies.…”

Section: Discussionmentioning

confidence: 99%

High‐titre IgM anti‐sulfatide antibodies in individuals with IgM paraproteinaemia and associated peripheral neuropathy

et al. 2000

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The common association between monoclonal gammopathy and peripheral neuropathy was studied in seven patients with demyelinating polyneuropathy and IgM paraproteinaemia. Plasma samples from these individuals were thoroughly tested for antiperipheral nerve myelin (PNM) antibodies and then screened for glycoprotein and glycolipid reactivity by western immunoblotting and thin-layer chromatography (TLC) immunostaining. Three of the seven samples showed strong IgM anti-PNM and antisulfatide (GalS) antibody reactivity. Two of these three plasma samples showed extraordinarily high antisulfatide IgM antibody titres, ranging from 1 x 104 to 1 x 106 arbitrary units/L. These same samples also showed intense myelin staining of sciatic nerve sections (paraffin and cryostat) and teased nerve fibres. No axonal immunoreactivity was observed. These results suggest that high titre IgM antisulfatide antibodies may play a pathogenetic role in the immune demyelination associated with IgM paraproteinaemia.

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Section: Discussionmentioning

confidence: 99%

High‐titre IgM anti‐sulfatide antibodies in individuals with IgM paraproteinaemia and associated peripheral neuropathy

et al. 2000

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“…Viral infections have also been suggested to play a role in the development of autoimmune diseases through a process called “molecular mimicry”: Antibodies generated against viruses, e.g., Theiler’s murine encephalomyelitis virus, SFV, IAV, MV and rubella virus also bind various lipid-like structures, including the myelin component galactocerebroside, which may contribute to myelin destruction [ 180 , 181 , 182 , 183 , 184 ]. On the plus side, cross-reactive immunity arising from a common host cell-membrane-derived glycolipid component present in the viral envelopes of different viruses may protect against other viral infections.…”

Section: Viral-induced Apoptosis and Morbiditymentioning

confidence: 99%

Ceramide and Related Molecules in Viral Infections

Beckmann

Becker

2021

IJMS

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Ceramide is a lipid messenger at the heart of sphingolipid metabolism. In concert with its metabolizing enzymes, particularly sphingomyelinases, it has key roles in regulating the physical properties of biological membranes, including the formation of membrane microdomains. Thus, ceramide and its related molecules have been attributed significant roles in nearly all steps of the viral life cycle: they may serve directly as receptors or co-receptors for viral entry, form microdomains that cluster entry receptors and/or enable them to adopt the required conformation or regulate their cell surface expression. Sphingolipids can regulate all forms of viral uptake, often through sphingomyelinase activation, and mediate endosomal escape and intracellular trafficking. Ceramide can be key for the formation of viral replication sites. Sphingomyelinases often mediate the release of new virions from infected cells. Moreover, sphingolipids can contribute to viral-induced apoptosis and morbidity in viral diseases, as well as virus immune evasion. Alpha-galactosylceramide, in particular, also plays a significant role in immune modulation in response to viral infections. This review will discuss the roles of ceramide and its related molecules in the different steps of the viral life cycle. We will also discuss how novel strategies could exploit these for therapeutic benefit.

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“…[69][70][71][72] It has been suggested that low levels of anti-GalS antibodies may be common constituents of the normal human immune repertoire and may be secreted by the CD5-positive subset of B cells, similar to other naturally occurring anticarbohydrate IgM antibodies. 73 These B cells might be activated by GalS incorporated into the envelope of a budding virus, 74 by cross-reactive foreign antigens or antigen complexes, and may be excessively produced by expanded B cell clones in monoclonal gammopathies.…”

Section: Anti-gals Antibodiesmentioning

confidence: 99%

“…158 This antibody also labels SFV, influenza, and measles virus, which replicate in the same brain cell cultures from which the SFV is derived. 74 This indicates that budding viruses take similar glycolipid into their coat if the original host cell of replication is the same.…”

Section: Viral Buddingmentioning

confidence: 99%

“…GalS may become incorporated into viral envelope protein during the course of productive infection (i.e. cells containing GalS within their membrane) and the viral budding process 74 . The integration of GalS into the viral membrane may be the trigger for the immune system to begin synthesizing autoantibodies against the carbohydrate moiety of the molecule.…”

Section: The Autoimmune Hypothesismentioning

confidence: 99%

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

Petratos

Gonzales

2000

Neuropathology

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Neuropathology 2000; 20, 257-272 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 sensorymotor 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) P 2 protein; (ii) sulfatide (GalS); (iii) various gangliosides (especially GM 1 ); (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 HIVinfected 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.

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Immunoelectron microscopical labelling of a glycolipid in the envelopes of brain cell-derived budding viruses, Semliki Forest, influenza and measles, using a monoclonal antibody directed chiefly against galactocerebroside resulting from Semliki Forest virus infection

Cited by 14 publications

References 20 publications

High‐titre IgM anti‐sulfatide antibodies in individuals with IgM paraproteinaemia and associated peripheral neuropathy

High‐titre IgM anti‐sulfatide antibodies in individuals with IgM paraproteinaemia and associated peripheral neuropathy

Ceramide and Related Molecules in Viral Infections

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

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