Replication and pathogenesis of the human T-cell leukemia/lymphotropic retroviruses.
The broad outlines of mechanisms of tumorigenesis by the HTLV-I family of viruses are beginning to emerge. The viruses encode at least three genes in addition to the genes (gag, pol, and env) required for virus replication. These additional genes encoded for by the X region are likely to affect in a specific fashion the growth of lymphocytes. The tat gene appears to mimick at least part of the response of mature lymphocytes to recognition of the cognate antigen. That is, in T-lymphocytes the tatI gene seems to induce the IL-2 and IL-2 receptor genes (W. Greene et al. 1986). The alternative reading-frame proteins, pp21 and pp27, have some similarity of cellular proteins that are associated with G0 to G1 transitions and may contribute to the transformed phenotype in cooperation with the tat gene. The expression of viral genes in infected lymphocytes, the tat gene and pp21 and pp27 proteins, and possibly other viral genes (since the coding capacity of the X region is not exhausted by the tat and pp21 and pp27 proteins) may be sufficient to account for the transformation of T cells in culture. A secondary change in the infected cells in culture is not required to explain the outgrowth of cells which are clonal with respect to the site of viral genomic integration, as selection of the most rapidly growing infected cell could account for this observation. The case of infected patients is more complex. Infection of T cells with the HTLV-I or -II virus is not sufficient to produce malignant disease.(ABSTRACT TRUNCATED AT 250 WORDS)
D017977:Deltaretrovirus / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology*; D006800:Deltaretrovirus Infections / Q000209:etiology; D005786:Gene Expression Regulation; D005814:Genes, Viral; D006801:Humans; D014170:Transformation, Genetic; D014779:Virus Replication