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Background: The clinical features of myositis related with Human T-cell leukemia virus type 1 (HTLV-1) remains unclear despite epidemiological studies suggesting inflammatory myopathy associated with the virus. Case presentation: Here, we described the clinical presentations, muscle biopsy studies and laboratory results of two siblings with HTLV-1-associated myelopathy / tropical spastic paraparesis (HAM/TSP) who were affected with lumbar lordosis. Computed tomography (CT) scans demonstrated marked paraspinal muscle atrophy in both patients. Immunohistochemical studies of biopsy tissue obtained from one of the patients revealed inflammatory change of the muscle. Upon oral prednisolone therapy, the patient showed improvement in muscle strength and serum creatine kinase (CK) level. Conclusion: Myopathy or specifically axial myopathy should be considered as clinical symptom when treating the patients with HTLV-1 infection. [ABSTRACT FROM AUTHOR]

An abstract of the research paper titled,"Gene expression and glycan profiling of CD4+T cells in HAM/TSP," is presented.

An abstract of the article "Neural Bystander Damage by Infiltrating Virusinfected T Cells and the Cytotoxic T Lymphocytes in HTLV-I-Associated Neurological Disease," by Eiji Matsuura from 15th International Conference on Human Retroviruses held in Belgium from June 5-8, 2011 is presented.

An abstract of the article " HLA-A24-restricted HTLV-I-specific CTL Response Reduces the HTLV-I Proviral Load but the HLA Increases the Risk of HAM/ TSP," by Ryuji Kubota and colleagues from 15th International Conference on Human Retroviruses held in Belgium from June 5-8, 2011 is presented.

An abstract of the article "Reduced Tim-3 Expression on HTLV-I Tax-specific Cytotoxic T Lymphocytes in HTLV-I Infection," by Nashwa H Abdelbary and colleagues from 15th International Conference on Human Retroviruses held in Belgium from June 5-8, 2011 is presented.

An abstract of the article "Histopathologic differences between human T-lymphotropic virus type 1 (HTLV-1)-positive and HTLV-1-negative polymyositis," by Hazem M. Abdullah and colleagues is presented.

Background: Although human T-lymphotropic virus type 1 (HTLV-1) infection is a prerequisite for the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), specific provirus mutations in HAM/TSP have not yet been reported. In this study, we examined whether HAM/TSP patients had the disease-specific genomic variants of HTLV-1 by analyzing entire sequences of HTLV-1 proviruses in these patients, including familial cases. In addition, we investigated the genetic variants of host restriction factors conferring antiretroviral activity to determine which mutations may be related to resistance or susceptibility to HAM/TSP., Results: The subjects included 30 patients with familial HAM/TSP (f-HAM/TSP), 92 patients with sporadic HAM/TSP (s-HAM/TSP), and 89 asymptomatic HTLV-1 carriers (ACs). In all 211 samples, 37 samples (18%) were classified into transcontinental subtype and 174 samples (82%) were classified as Japanese subtype. Among three groups, the percentage of transcontinental subtype in f-HAM/TSP, s-HAM/TSP and ACs was 33, 23 and 7%, respectively. The frequency of transcontinental subtype was significantly higher in both f-HAM/TSP (p < 0.001) and s-HAM/TSP (p < 0.001) than in ACs. Fifty mutations in HTLV-1 sequences were significantly more frequent in HAM/TSP patients than in ACs, however, they were common only in transcontinental subtype. Among these mutations, ten common mutations causing amino acid changes in the HTLV-1 sequences were specific to the transcontinental subtype. We examined host restriction factors, and detected a rare variant in TRIM5α in HAM/TSP patients. The patients with TRIM5α 136Q showed lower proviral loads (PVLs) than those with 136R (354 vs. 654 copies/10 4 PBMC, p = 0.003). The patients with the 304L variant of TRIM5α had significantly higher PVLs than those with 304H (1669 vs. 595 copies/10 4 PBMC, p = 0.025). We could not find any HAM/TSP-specific mutations of host restriction factors., Conclusions: Transcontinental subtype is susceptible to HAM/TSP, especially in familial cases. Ten common mutations causing amino acid changes in the HTLV-1 gene were specific to the transcontinental subtype. TRIM5α polymorphisms were associated with PVLs, indicating that TRIM5α could be implicated in HTLV-1 replication.