Advances in the treatment of human T-cell lymphotropic virus type-I associated myelopathy

Mashkani, Baratali; Jalili Nik, Mohammad; Rezaee, Seyed Abdolrahim; Boostani, Reza

doi:10.1080/14737175.2023.2272639

Cited by 2 publications

(1 citation statement)

References 249 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…239 The reverse transcriptase, integrase, and protease inhibitors are utilised in the treatment of HTLV-1-associated diseases. [240][241][242] Zidovudine, an HIV reverse transcriptase inhibitor, is commonly used for treating HTLV-1-associated diseases. 237,[243][244][245] However, previous studies have mainly focused on ATLL subjects rather than HAM/TSP patients, and clinical trials administering AZT to HAM/TSP patients have produced conflicting results.…”

Section: Therapeutic Approaches For Ham/tspmentioning

confidence: 99%

Novel insights into human T‐lymphotropic virus type‐1 (HTLV‐1) pathogenesis‐host interactions in the manifestation of HTLV‐1‐associated myelopathy/tropical spastic paraparesis

Ahmadi Ghezeldasht,

Mosavat,

Rezaee

2024

Reviews in Medical Virology

Self Cite

View full text Add to dashboard Cite

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.

show abstract