Plasma samples from 35 individuals,with HIV infection but without clinical
peripheral neuropathy were screened by ELISA for IgM and:IgG antibodies aga
inst peripheral myelin. Eighteen of the 35 samples (51%) showed IgM reactiv
ity and 11 (31%) showed IgG reactivity. By comparison, none of 48 samples f
rom healthy blood donors showed IgM or IgG reactivity. Epitopes reacting wi
th these antibodies were identified by TLC immunostaining as sulphatide (Ga
lS) and the gangliosides GM(1), GD(1a) and GD(1b). Plasma samples from four
people with-HIV infection and neuropathy (HIV+PN), six HIV-seronegative in
dividuals with IgM paraproteinaemic demyelinating neuropathy (IgMPDN) and 1
2 HIV-seronegative individuals with a variety of other neurological disorde
rs (HIV-OND) were also investigated. Two of the four HIV+PN samples showed
IgM reactivity with GalS; and two showed IgG reactivity against GalS. Of th
e six IgMPDN samples, three showed IgM reactivity with GalS. These data ind
icate that antibodies against peripheral myelin glycolipids, in particular
GalS, occur more frequently in HIV infection than in HIV-seronegative indiv
iduals with and without neurological disease, and may contribute to subclin
ical neuropathy in HIV infection.