Search

Human T‐lymphotropic virus type‐1 (HTLV‐1) was the first discovered human oncogenic retrovirus, the etiological agent of two serious diseases have been identified as adult T‐cell leukaemia/lymphoma malignancy and HTLV‐1‐associated myelopathy/tropical spastic paraparesis (HAM/TSP), a debilitating chronic neuro‐myelopathy. Despite more than 40 years of molecular, histopathological and immunological studies on HTLV‐1‐associated diseases, the virulence and pathogenicity of this virus are yet to be clarified. The reason why the majority of HTLV‐1‐infected individuals (∼95%) remain asymptomatic carriers is still unclear. The deterioration of the immune system towards oncogenicity and autoimmunity makes HTLV‐1 a natural probe for the study of malignancy and neuro‐inflammatory diseases. Additionally, its slow worldwide spreading has prompted public health authorities and researchers, as urged by the WHO, to focus on eradicating HTLV‐1. In contrast, neither an effective therapy nor a protective vaccine has been introduced. This comprehensive review focused on the most relevant studies of the neuro‐inflammatory propensity of HTLV‐1‐induced HAM/TSP. Such an emphasis on the virus‐host interactions in the HAM/TSP pathogenesis will be critically discussed epigenetically. The findings may shed light on future research venues in designing and developing proper HTLV‐1 therapeutics. [ABSTRACT FROM AUTHOR]

Summary: Human T lymphotropic virus type‐1 (HTLV‐1) is a well‐known human oncovirus, associated with two life‐threatening diseases, adult T cell leukaemia/lymphoma (ATL) and HTLV‐1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). The study of this oncogenic virus is significant from two different aspects. First, HTLV‐1 can be considered as a neglected public health problem, which may spread slowly worldwide. Second, the incidence of HTLV‐1 associated diseases due to oncogenic effects and deterioration of the immune system towards autoimmune diseases are not fully understood. Furthermore, knowledge about viral routes of transmission is important for considering potential interventions, treatments or vaccines in endemic regions. In this review, novel characteristics of HTLV‐1, such as the unusual infectivity of virions through the virological synapse, are discussed in the context of the HTLV‐1 associated diseases (ATL and HAM/TSP). [ABSTRACT FROM AUTHOR]

Abstract: Aim: Human T lymphotropic virus type 1 (HTLV‐1) infection with high prevalence in the north‐east of Iran, particularly in Mashhad, can lead to adult T‐cell leukemia (ATL) and HTLV‐1‐associated myelopathy/tropical spastic paraparesis (HAM/TSP) and a variety of autoimmune diseases. The aim of the study was to examine the presence of autoimmune markers in HTLV carries. Methods: Serum samples were obtained from blood donors in Mashhad, northeastern Iran. One hundred and five HTLV‐1 positive (cases) and 104 age‐ and sex‐matched HTLV‐1 negative donors (controls) were assessed for presence of serum autoimmune markers by enzyme‐linked immunosorbent assay. Results: The mean ages of cases and controls were 40.8 ± 9.4 and 41.5 ± 9.3 years, respectively (P = 0.5). In the case group, 81.9% and in the control group 83.7% were male (P = 0.74). The frequency of positive antinuclear antibodies and anticyclic citrullinated peptide antibodies in the serum of the two groups were not significantly different (P = 0.68 and P = 0.62, respectively). Only one antineutrophil cytoplasmic antibody‐positive case (1%) was observed in the group and no anti‐phospholipid immunoglobulin G positivity was observed. The frequency of rheumatoid factor (RF) was greater in case group than in the control group, although the difference was not significant (P = 0.08). The amount of RF in all 12 RF positive sera were higher than normal levels (33–37 IU/mL). Conclusion: Because we failed to detect any significant relation between serum autoimmune markers and HTLV‐1 infection, and because of the relatively low prevalence of autoimmune diseases, it could be concluded that healthy HTLV‐1 carriers do not produce rheumatologic‐related auto‐antibodies more than the healthy population. [ABSTRACT FROM AUTHOR]