Like HIV infection, infection with HTLV is also worldwide, as noted in Figure 12.25. However, unlike HIV, sequence conservation is the rule in viral infections throughout the world, with the
Figure 12.25 Worldwide distribution of HTLV-I. (Adapted from Wigdahl and Brady, 1996, with per- mission of the authors and publisher.)
overall nucleotide divergence of strains being only about 4%, depending on the region of the genome analyzed (cf. Ferreira et al., 1997). HTLV transmission occurs at birth due to infection in mothers or later in life through sexual contact, blood transfusion, and needle sharing, modes quite similar to the transmission of HIV infections. Like HIV, HTLV as a cause of human lym- phomas was first reported less than two decades ago (Poiesz et al., 1980). While HIV has an incubation or latent period, usually of several years during which no clinical disease is evident, the incubation period for the development of adult T-cell leukemia/lymphoma after infection with HTLV is probably in the order of decades (Wiktor and Blattner, 1991). Generally, the clini- cal course of the disease is short, but several variants that induce a chronic disease picture have also been described (cf. Wiktor and Blattner, 1991).