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Aim: Disruption of the internal circadian rhythm pathway could lead to a range of diseases. In this study, we aim to evaluate the circadian rhythm pathway by assessing the interaction between CLOCK and CSNK1D genes in HTLV-1 carriers in comparison with healthy individuals. Materials & methods:CLOCK and CSNK1D gene expression was assessed using the RT-qPCR. Pathogenesis-related signaling networks were designed and analyzed using the obtained results. Results: There was no significant difference in age between the groups. CLOCK and CSNK1D gene expression levels were significantly higher in carriers than in healthy individuals (p = 0.04, p = 0.03, respectively). Conclusion: In addition to introducing potential biological markers, obtained results could be a good idea to further investigate this signaling pathway in the future. [ABSTRACT FROM AUTHOR]

A high proviral load (PVL) is recognized as a risk factor for human T cell leukemia virus-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), but there is a lack of prospective studies evaluating whether or not HTLV-1 carriers with high PVL are at risk of developing HAM/TSP or other HTLV-1-related diseases. Here, we compare the incidence of clinical manifestations and the cytokine levels in 30 HTLV-1 carriers with high (> 50,000 copies/106 PBMC) and an equal number of subjects with low proviral load. Participants were followed for 3 to 16 years (median of 11 years). The PVL, IFN-γ, TNF, and IL-10 levels were quantified at entry and at the end of the follow-up. Among the self-reported symptoms in the initial evaluation, only the presence of paresthesia on the hands was more frequent in the group with high PVL (p < 0.04). The production of IFN-γ was higher in the group with high PVL group (median of 1308 versus 686 pg/ml, p < 0.011) when compared with the control group in the first assessment. There was no difference in the occurrence of urinary symptoms or erectile dysfunction, periodontal disease, Sicca syndrome, and neurologic signs between the two groups during the follow-up. The observation that none of the HTLV-1 carriers with high PVL and with exaggerated inflammatory response progressed to HAM/TSP indicates that other factors in addition to the PVL and an exaggerated immune response are involved in the pathogenesis of HAM/TSP. [ABSTRACT FROM AUTHOR]

The authors have previously developed a logistic regression equation to predict the odds that a human T-cell lymphotropic virus type 1 (HTLV-1)–infected individual of specified genotype, age, and provirus load has HTLV-1–associated myelopathy/tropical spastic paraparesis (HAM/TSP) in southern Japan. This study evaluated whether this equation is useful predictor for monitoring asymptomatic HTLV-1–seropositive carriers (HCs) in the same population. The authors genotyped 181 HCs for each HAM/TSP-associated gene (tumor necrosis factor [TNF]- α - 863A/C, stromal cell-derived factor 1 (SDF-1) + 801G/A, human leukocyte antigen [HLA]-A * 02, HLA-Cw * 08, HTLV-1 tax subgroup) and measured HTLV-1 provirus load in peripheral blood mononuclear cells using real-time polymerase chain reaction (PCR). Finally, the odds of HAM/TSP for each subject were calculated by using the equation and compared the results with clinical symptoms and laboratory findings. Although no clear difference was seen between the odds of HAM/TSP and either sex, family history of HAM/TSP or adult T-cell lenkemia (ATL), history of blood transfusion, it was found that brisk patellar deep tendon reflexes, which suggest latent central nervous system compromise, and flower cell-like abnormal lymphocytes, which is the morphological characteristic of ATL cells, were associated with a higher odds of HAM/TSP. The best-fit logistic regression equation may be useful for detecting subclinical abnormalities in HCs in southern Japan. Journal of NeuroVirology (2006) 12 , 171–177. [ABSTRACT FROM AUTHOR]