Abstract

Human T-cell leukemia virus (HTLV) is a human retrovirus of the subfamily Retroviridae, genus Deltaretrovirus, with four known types, all originating from zoonotic transmissions from closely related simian T-cell leukemia viruses (STLVs). HTLV-1 causes adult T-cell leukemia-lymphoma (ATL), HTLV-associated myelopathy (HAM), uveitis, and autoimmune diseases and is prevalent in sub-Saharan Africa, the Caribbean basin, Latin America, Australia, and Japan. HTLV-2 causes HAM but not malignancy and infects indigenous peoples of the Amazon and central Africa, and injection drug users in the United States and Europe. HTLV-3 and HTLV-4 have been isolated from only a few humans living in central Africa and represent recent transmissions of STLVs from gorillas and apes. Other than structural genes encoding core and envelope proteins, HTLV-1 and HTLV-2 genomes code for the regulatory proteins Tax and HBZ, which induce the proliferation of infected lymphocytes that may lead to ATL and HAM. Diagnosis relies on the detection of HTLV antibodies through screening and confirmatory assays along with polymerase chain reaction to detect proviral DNA. HTLV-1–related ATL occurs in 2% to 4% of infected individuals and responds poorly to traditional chemotherapy; zidovudine and α-interferon are effective in some clinical subtypes. HTLV-1 and HTLV-2 HAM is thought to be due to aberrant immunologic control of the retroviral infection and is difficult to treat. Prevention of HTLV infection requires interdiction of breastfeeding by HTLV-infected mothers, prevention of sexual transmission, and interventions to prevent parenteral transmission by blood transfusion, organ transplantation, and injection drug use.

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