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Published on: January 19, 2018
[The recent advances of HAM/TSP research]
13rd Department of Internal Medicine, Faculty of Medicine, Kagoshima University.
Insights
Human T-lymphotropic virus type 1 (HTLV-I) infection affects millions. Certain human leukocyte antigen (HLA) alleles, like HLA-A*02, significantly reduce the risk of developing HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP).
Area of Science:
- Retroviruses and human T-lymphotropic virus (HTLV) research.
- Immunogenetics and disease susceptibility.
- Neurovirology and molecular pathology.
Context:
- HTLV-I is a human retrovirus with global epidemiological data indicating millions of carriers and thousands of patients with associated diseases.
- Human T-lymphotropic virus type 1 (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a neurological disorder linked to HTLV-I infection.
- Previous research localized HTLV-I proviral DNA and mRNA to specific immune cells in the spinal cords of HAM/TSP patients.
Purpose:
- To summarize global epidemiological data on HTLV-I carriers and related disorders.
- To investigate the cellular localization of HTLV-I proviral DNA and mRNA in HAM/TSP patients.
- To explore the role of human leukocyte antigen (HLA) alleles in HTLV-I proviral load and HAM/TSP susceptibility.
Summary:
- Epidemiological data suggest over 2.2 million HTLV-I carriers, 1,200 adult T-cell leukemia (ATL) patients, and 3,000 HAM/TSP patients worldwide.
- HTLV-I proviral DNA and mRNA were localized to specific immune cells (OPD 4-positive cells) in the spinal cords of HAM/TSP patients.
- A novel technique detected HTLV-I tax protein in cerebrospinal fluid and peripheral blood mononuclear cells of HAM/TSP patients.
- The study identified HLA-A*02 as a protective allele against HAM/TSP, halving the odds and reducing proviral load in carriers.
- HLA-DRB1*0101 was associated with increased HAM/TSP susceptibility, particularly when the protective HLA-A*02 allele was absent.
Impact:
- Provides crucial insights into the pathogenesis of HAM/TSP by identifying specific cellular targets and viral proteins.
- Highlights the significant role of host genetic factors (HLA alleles) in determining susceptibility and disease progression of HTLV-I infection.
- Demonstrates the potential for genetic screening to identify individuals at higher risk for developing HAM/TSP.
- Advances understanding of retroviral disease mechanisms and host-pathogen interactions.
Abstract:
The ninth international conference on HTLVs and related disorders was held on April 5-9, 1999 at Kagoshima, Japan under the conference chairperson, Dr. Mitsuhiro Osame. In this meeting, world-wide epidemiological data on HTLV-I carriers, ATL patients, and HAM/TSP patients were summarized as shown in the table. The total number of them was supposed to be more than 2.2 millions, 1,200, and 3,000, respectively. To elucidate the localization of HTLV-I proviral DNA directly, double staining using immunohistochemistry and PCR in situ hybridization in the spinal cords of HAM/TSP patients were performed. HTLV-I proviral DNA was localized only to OPD 4-positive cells (Matsuoka et al, 1998). The localization of HTLV-I messenger RNA was the same (Moritoyo et al, 1996). A novel technique to detect HTLV-I tax protein was also developed. In HAM/TSP patients, 0.04-1.16% of the CSF cells and 0.02-0.54% of PBMCs were positive for HTLV-I tax protein (Moritoyo et al, 1999). It was also hypothesized that HLA alleles control HTLV-I proviral load and thus influence susceptibility to HAM/TSP. Two hundred and thirty-two cases of HAM/TSP were compared with 201 randomly selected HTLV-I seropositive asymptomatic blood donors. It was shown that, after infection with HTLV-I, the class I allele HLA-A*02 halves the odds of HAM/TSP (p < 0.0001), preventing 28% of potential cases of HAM/TSP. Furthermore, HLA-A*02 positive healthy HTLV-I carriers have a proviral load one-third that (p = 0.0114) of HLA-A*02 negative HTLV-I carriers. An association of HLA-DRB1*0101 with disease susceptibility was also identified, which doubled the odds of HAM/TSP in the absence of the protective effect of HLA-A*02 (Jeffery and Usuku et al, 1999).
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