Human T-cell lymphotropic viruses, types 1 and 2 (HTLV-1 and -2) are genetically and biologically similar. However, their worldwide distribution differs. HTLV-1 has definitively been associated with a human malignant disease, adult T-cell leukemia (ATL), and a less common neurologic condition, HTLV-associated myelopathy/tropical spastic paraparesis (HAM/TSP). There are six subclasses of HTLV-1, each of which is endemic to different regions of the world. No conclusive evidence links HTLV-2 to any known disease.

A. Transmission of HTLV

The distribution of HTLV infection varies greatly with geographic area and socioeconomic group. HTLV transmission occurs primarily by cell-associated virus, via one of three routes. First, in highly endemic regions, mother to fetus or newborn is the most common mode of transmission. This is accomplished via infected lymphocytes either transplacentally or in breast milk. Second, infection can be transmitted sexually by infected lymphocytes contained in semen. Third, any blood products containing intact cells are also a potential source of infection. There is little evidence for transmission by cell-free fluids.

B. Pathogenesis and clinical significance of adult T-cell leukemia Both HTLV-1 and HTLV-2 infect lymphocytes: HTLV-1 has a tropism for CD4 lymphocytes, whereas HTLV-2 preferentially infects CD8 lymphocytes. HTLV-1 infection both stimulates mitosis and immortalizes T lymphocytes, which acquire an “antigen-activated” phenotype. Following infection, the virus becomes integrated in the host cell as a provirus and transforms a polyclonal population of T cells. Although these cells all have an integrated provirus, there is no common integration site in different tumors. No HTLV mRNA is transcribed, and no recognized oncogene is activated. Continued multi plication of T lymphocytes over a period of many years results in the accumulation of many chromosomal aberrations. Peripheral blood smears show lymphoid cells with hyperlobulated nuclei (Figure 1). Selection of monoclonal populations leads to cells that have an increasingly malignant phenotype. HTLV-I seroprevalence rates are strongly age- and sex-dependent, with higher rates associated with older age and with female sex (Figure 2) The majority of infected individuals are asymptomatic carriers who have an estimated 2 to 4 percent chance of developing ATL within their lifetime. ATL typically appears 20 to 30 years after initial infection, when an increasingly larger population of monoclonal malignant ATL cells develops, and infiltration of various visceral organs by these cells occurs. There are accompanying serum chemistry abnormalities, and impairment of the immune system leads to opportunistic infections. Median survival after appearance of acute ATL is about 6 months.

Fig1. Typical “cloverleaf” appearance of nuclei of HTLV-1–infected adult T-cell leukemic cells.

Fig2. Age- and sex-specific seroprevalence of human T-cell lymphotropic virus type I in U.S. blood donors.

C. Pathogenesis and clinical significance of HTLV-associated myelopathy/tropical spastic paraparesis

About 1 to 2 percent of HTLV-1–infected individuals will go on to develop HAM/TSP. HAM/TSP is distinctly different from ATL in that it usually appears only a few years after infection. CNS involvement is indicated by: 1) the presence of anti-HTLV-1 antibody in the cerebrospinal fluid, 2) lymphocytic infiltration and demyelination of the thoracic spinal cord, and 3) brain lesions. The lymphocyte count is normal, although there is a polyclonal nonmalignant fraction with integrated HTLV. HAM occurs with lower frequency than ATL among HTLV-infected populations. It is characterized by progressive spasticity and weakness of the extremities, urinary and fecal incontinence, hyperreflexia, and some peripheral sensory loss.

D. Other manifestions of HTLV-1 infection.

HTLV-1 infections have also been associated with uveitis and retinal vasculitis. In addition, a chronic, severe form of infectious dermatitis can result from vertical transmission of the HTLV-1 virus and has been linked with an earlier onset of HAM/TSP.

E. Laboratory identification

Screening of blood donors for HTLV is done by ELISA or agglutination tests, but the existence of false-positives necessitates confirmatory testing by Western blotting. Test sensitivity is also a problem caused by the low and variable antibody titers in infected individuals. PCR amplification can be used to distinguish between HTLV-1 and HTLV-2 infections and to quantify viral load, which is a marker for the progression to HAM/TSP.

F. Treatment and prevention

The usual agents used in cancer chemotherapy have proven to be ineffective in treating ATL, and attempts to treat HAM/TSP, for the most part, have been equally unsuccessful. Treatment of both dis eases is symptomatic. An estimated 15 to 20 million people world wide are infected with HTLV-1 or -2, and 5 percent of these will eventually develop either ATL or HAM/TSP.

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