Influenza and Other Respiratory Virus Weekly Activity Report, November 1, 2008, Week 44

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, October 25, 2008, Week 43

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, October 18, 2008, Week 43

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, October 18, 2008, Week 42

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, October 11, 2008, Week 41

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, May 29, 2009, revised Week 20

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, May 30, 2009, revised Week 21

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, June 13, 2009, revised Week 23

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, June 6, 2009, Week 22

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, June 27, 2009, Week 25

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, June 20, 2009, Week 24

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, July 4, 2009, Week 26

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Influenza and Other Respiratory Virus Weekly Activity Report, July 11, 2009, Week 27

Weekly report of the Iowa Influenza Surveillance Network produced by the Iowa Department of Public Health.

Possible etiologies for tropical spastic paraparesis and human T lymphotropic virus I-associated myelopathy

The epidemiology of tropical spastic paraparesis/human T lymphotropic virus I (HTLV-I)-associated myelopathy (TSP/HAM) is frequently inconsistent and suggests environmental factors in the etiology of these syndromes. The neuropathology corresponds to a toxometabolic or autoimmune process and possibly not to a viral disease. Some logical hypotheses about the etiology and physiopathology of TSP and HAM are proposed. Glutamate-mediated excitotoxicity, central distal axonopathies, cassava, lathyrism and cycad toxicity may explain most cases of TSP. The damage caused to astrocytes and to the blood-brain barrier by HTLV-I plus xenobiotics may explain most cases of HAM. Analysis of the HTLV-I/xenobiotic ratio clarifies most of the paradoxical epidemiology of TSP and HAM. Modern neurotoxicology, neuroimmunology and molecular biology may explain the neuropathology of TSP and HAM. It is quite possible that there are other xenobiotics implicated in the etiology of some TSP/HAMs. The prevention of these syndromes appears to be possible today.

Autoimmunity and molecular mimicry in tropical spastic paraparesis/human T-lymphotropic virus-associated myelopathy

Viruses share antigenic sites with normal host cell components, a phenomenon known as molecular mimicry. It has long been suggested that viral infections might trigger an autoimmune response by several mechanisms including molecular mimicry. More than 600 antiviral monoclonal antibodies generated against 11 different viruses have been reported to react with 3.5% of cells specific for uninfected mouse organs. The main pathological feature of tropical spastic paraparesis/human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (TSP/HAM) is a chronic inflammation of the spinal cord characterized by perivascular cuffing of mononuclear cells accompanied by parenchymal lymphocytic infiltration. We detected the presence of autoantibodies against a 98- to 100-kDa protein of in vitro cultured human astrocytes and a 33- to 35-kDa protein from normal human brain in the serum of HTLV-I-seropositive individuals. The two cell proteins exhibited molecular mimicry with HTLV-I gag and tax proteins in TSP/HAM patients, respectively. Furthermore, the location of 33- to 35-kDa protein cross-reaction correlated with the anatomical spinal cord areas (in the rat model) in which axonal damage has been reported in several cases of TSP/HAM patients. Our experimental evidence strongly suggests that the demyelinating process occurring in TSP/HAM may be mediated by molecular mimicry between domains of some viral proteins and normal cellular targets of the spinal cord sections involved in the neurodegeneration.