M K Sharief1, R Hentges, M Ciardi. 1. Department of Clinical Neurochemistry, National Hospital for Neurology and Neurosurgery, London, United Kingdom.
Abstract
BACKGROUND: The syndrome of progressive muscular atrophy decades after acute paralytic poliomyelitis (post-polio syndrome) is not well understood. The theory that physiologic changes and aging cause the new weakness does not explain the immunologic abnormalities reported in some patients. An alternative explanation is persistent or recurrent poliovirus infection. METHODS: We assessed the intrathecal antibody response to poliovirus and intrathecal production of interleukin-2 and soluble interleukin-2 receptors in 36 patients with the post-polio syndrome and 67 controls (including 13 who had had poliomyelitis but had no new symptoms and 18 with amyotrophic lateral sclerosis). Intrathecal antibody responses to measles, mumps, herpes simplex, and varicella zoster viruses were also determined. RESULTS: Oligoclonal IgM bands specific to poliovirus were detected in the cerebrospinal fluid of 21 of the 36 patients with the post-polio syndrome (58 percent) but in none of the control group (P less than 0.0001). In quantitative studies there was evidence of increased intrathecal synthesis of IgM antibodies to poliovirus only among the patients with the post-polio syndrome; there was no increased synthesis of IgM to measles, mumps, herpes simplex, or varicella zoster viruses. The patients with post-polio syndrome had significantly higher mean (+/- SD) (cerebrospinal fluid levels of interleukin-2 and soluble interleukin-2 receptors than the controls (8.1 +/- 5.3 vs. 1.4 +/- 0.8 U per milliliter and 159.6 +/- 102.9 vs. 10.7 +/- 6.2 U per milliliter, respectively). The intrathecal synthesis of IgM antibodies to poliovirus correlated with the cerebrospinal fluid concentrations of interleukin-2 (P less than 0.0005) and soluble interleukin-2 receptors (P less than 0.001). CONCLUSIONS: An intrathecal immune response against poliovirus is present in many patients with the post-polio syndrome. In some of these patients the recrudescence of muscle weakness may be caused by persistent or recurrent infection of neural cells with the poliovirus.
BACKGROUND: The syndrome of progressive muscular atrophy decades after acute paralytic poliomyelitis (post-polio syndrome) is not well understood. The theory that physiologic changes and aging cause the new weakness does not explain the immunologic abnormalities reported in some patients. An alternative explanation is persistent or recurrent poliovirus infection. METHODS: We assessed the intrathecal antibody response to poliovirus and intrathecal production of interleukin-2 and soluble interleukin-2 receptors in 36 patients with the post-polio syndrome and 67 controls (including 13 who had had poliomyelitis but had no new symptoms and 18 with amyotrophic lateral sclerosis). Intrathecal antibody responses to measles, mumps, herpes simplex, and varicella zoster viruses were also determined. RESULTS: Oligoclonal IgM bands specific to poliovirus were detected in the cerebrospinal fluid of 21 of the 36 patients with the post-polio syndrome (58 percent) but in none of the control group (P less than 0.0001). In quantitative studies there was evidence of increased intrathecal synthesis of IgM antibodies to poliovirus only among the patients with the post-polio syndrome; there was no increased synthesis of IgM to measles, mumps, herpes simplex, or varicella zoster viruses. The patients with post-polio syndrome had significantly higher mean (+/- SD) (cerebrospinal fluid levels of interleukin-2 and soluble interleukin-2 receptors than the controls (8.1 +/- 5.3 vs. 1.4 +/- 0.8 U per milliliter and 159.6 +/- 102.9 vs. 10.7 +/- 6.2 U per milliliter, respectively). The intrathecal synthesis of IgM antibodies to poliovirus correlated with the cerebrospinal fluid concentrations of interleukin-2 (P less than 0.0005) and soluble interleukin-2 receptors (P less than 0.001). CONCLUSIONS: An intrathecal immune response against poliovirus is present in many patients with the post-polio syndrome. In some of these patients the recrudescence of muscle weakness may be caused by persistent or recurrent infection of neural cells with the poliovirus.
Authors: P Muir; U Kämmerer; K Korn; M N Mulders; T Pöyry; B Weissbrich; R Kandolf; G M Cleator; A M van Loon Journal: Clin Microbiol Rev Date: 1998-01 Impact factor: 26.132
Authors: C Iñiguez; A Jiménez-Escrig; J M Gobernado; M Nocito; P Gonzalez-Porque Journal: J Neurol Neurosurg Psychiatry Date: 1995-04 Impact factor: 10.154