Human T-cell lymphotropic virus type 2 (HTLV-2) infection has been shown to be endemic among intravenous drug users in parts of North America, Europe and Southeast Asia and in a number of Amerindian populations. Despite a 65% genetic similarity and common host humoral response, the human T-cell lymphotropic viruses type 1 (HTLV-1) and 2 display different mechanisms of host interaction and capacity for disease development. While HTLV-1 pathogenicity is well documented, HTLV-2 etiology in human disease is not clearly established. From an evolutionary point of view, its introduction and integration into the germ cell chromosomes of host species could be considered as the final stage of parasitism and evasion from host immunity. The extraordinary abundance of endogenous viral sequences in all vertebrate species genomes, including the hominid family, provides evidence of this invasion. Some of these gene sequences still retain viral characteristics and the ability to replicate and hence are potentially able to elicit responses from the innate and adaptive host immunity, which could result in beneficial or pathogenic effects. Taken together, this data may indicate that HTLV-2 is more likely to progress towards endogenization as has happened to the human endogenous retroviruses millions of years ago. Thus, this intimate association (HTLV-2/human genome) may provide protection from the immune system with better adaptation and low pathogenicity.
Keywords: Endogenization; HTLV-2; Human retroviruses; Viral pathogenicity.
© 2020 The Authors.