Human T-cell Leukemia/lymphotropic Virus-1 is estimated to infect at least 5-10 million individuals. The HTLV-1 is endemic in Japan, Latin America, the Caribbean, parts of sub-Saharan Africa, and central Australia. HTLV-1 prevalence in some highly populated regions including India, the Maghreb, some regions of China are yet to be established due to inconsistent data.
HTLV-1 is a retrovirus, and as such, the viral RNA genome is reverse transcribed into double-stranded DNA, before viral DNA is integrated into the host genomic DNA.
The integrated virus, called provirus, is transcribed and serves as a template to produce new viral particles.

A characteristic of HTLV-1 infection, especially in the chronic phase, is the virus increases or maintains its copy number not via the production of free viral particles but via the clonal expansion of infected cells.
HTLV-1 infection requires absolute cell-to-cell contact and cell-free virions generally do not cause infection.
Proviral sequences are extremely stable during the chronic phase of infection because they are maintained by DNA replication mediated by the DNA polymerase of the host cells, which is much less error-prone compared to the viral reverse transcriptase.
HTLV-1 sporadically causes severe diseases, such as Adult T-cell Leukemia / lymphoma (ATL), and some inflammatory diseases, such as Human T-Lymphotropic Virus-1-associated myelopathy (HAM)/tropical spastic paraparesis (TSP).
HTLV-1 can be transmitted from carrier mother to the baby mainly through breast feeding. Transmission by sex is also notable in some populations. Transfer of infected lymphocytes (eg. by blood transfusion and organ transplant is another mode of transmission.

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