The most well characterized are adult T-cell lymphoma (ATL) and HTLV-I-associated myelopathy/Tropical spastic paraparesis (HAM/TSP), both of which are only diagnosed in individuals testing positive to HTLV-1 infection.

[10] HTLV-1 is believed to have originated from the simian T-lymphotropic virus type 1 (STLV-1), a retrovirus prevalent among numerous nonhuman primates in intertropical Africa.

This theory is supported by the significant genetic diversity of HTLV-1 subtypes in Africa, potentially arising from repeated zoonotic transmissions during human interactions with STLV-1 endemic nonhuman primates.

Within areas where HTLV-I is found, its occurrence varies considerably, with endemic clusters often situated near populations with lower prevalence.

This pattern might be influenced by the founder effect, suggesting prolonged viral transmission within isolated groups, but this theory warrants further investigation.

Areas broadly regarded as having endemic regions include Japan, Iran, the Americas, the Caribbean, Melanesia, Central and West Africa, and Australia.

Globally, there remains a lack of robust data from populous countries like India and Nigeria and most of North and East Africa.

[citation needed] Although little serologic data exist, the prevalence of infection is thought to be highest among blacks living in the Southeast.

[13][14][citation needed] It is also high among the Inuit of Northern Canada, in Japan, northeastern Iran,[15] Peru, the Pacific coast of Colombia and Ecuador, and the Caribbean.

[citation needed] The risk to a fetus while inside the womb is minimal, given the virtual absence of viral particles in human plasma.

The least common is parenteral transmission through blood transfusion, with an infection rate of 44-63% estimated in one study, and needle sharing among intravenous drug users.

With proper prophylaxis (e.g. breastfeeding counseling for mothers, condom use, and donor blood screening), rates of transmission can be effectively reduced.

HTLV-I entry is mediated through the interaction of the surface unit of the virion envelope glycoprotein (SU) with its cellular receptor GLUT1, a glucose transporter, on target cells.

[citation needed] In the central Australian Aboriginal population, HTLV-1 is thought to be related to their extremely high rate of death from sepsis.

[8] Treatment of opportunistic infections varies depending on the type of disease and ranges from careful observation to aggressive chemotherapy and antiretroviral agents.

[citation needed] Adult T cell lymphoma is a common complication of HTLV infection and requires aggressive chemotherapy, typically R-CHOP.

Therapies studied include corticosteroids, plasmapheresis, cyclophosphamide, and interferon, which may produce a temporary symptomatic improvement in myelopathy symptoms.

Recently, however, a study of valproic acid combined with zidovudine showed a major decrease in the viral load of baboons infected with HTLV-1.

[citation needed] Allogenic bone marrow transplantation has been investigated to treat HTLV-1 disease with varied results.

One case report describes an HTLV-1-infected woman who developed chronic refractory eczema, corneal injury, and adult T-cell leukemia.