Summary auto-generated
This study examined whether human T-lymphotropic virus type I (HTLV-I) preferentially infects or immortalizes specific T-cell subsets. Researchers infected human CD4+ T-cell clones with stable Th1 or Th2 phenotypes with HTLV-I and monitored them for 12 months in culture. Both Th1 and Th2 clones showed identical susceptibility to infection and immortalization, with proviral DNA and viral mRNA present throughout the study period. Infected cells lost their antigen dependence and continuously proliferated in IL-2 medium without additional stimulation. Both cell types expressed elevated levels of activation markers (CD25, HLA-DR, CD44, CD30, CD45RO). HTLV-I altered cytokine production patterns in both subsets: Th1 clones retained IFN-γ but lost IL-2 production, while Th2 clones lost IL-4 expression but gained IFN-γ production. Both produced TNF-α and IL-6. The findings demonstrate that HTLV-I's ability to immortalize T cells is independent of the original Th1 or Th2 phenotype, suggesting the virus modifies infected cells to create a heterogeneous, virus-specific phenotype regardless of their initial characteristics.
Key findings
- HTLV-I infects and immortalizes both Th1 and Th2 T-cell clones equally efficiently, with no preferential tropism
- Infected cells become antigen-independent and proliferate spontaneously in IL-2 medium alone, indicating immortalization
- HTLV-I infection alters cytokine profiles in both cell types: Th1 clones lose IL-2 expression while maintaining IFN-γ, and Th2 clones lose IL-4 expression while gaining IFN-γ
- The virus-driven cytokine pattern in infected cells is independent of their original Th1 or Th2 phenotype
- Both Th1 and Th2 infected clones express activation markers (CD25, HLA-DR, CD44, CD30, CD45RO) and commonly produce TNF-α and IL-6
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Abstract
Human CD4+ Th1 and Th2 clones were infected with human T-lymphotropic virus type I (HTLV-I) and followed up for a 12 month period in culture. PCR analysis showed that proviral DNA and viral mRNA were present in both Th1 and Th2 infected clones, throughout the entire culture period. Thus, HTLV-I exhibited neither preferential tropism nor exerted differential immortalizing activity in Th1 versus Th2 cells. All the infected clones immediately lost their antigen dependency for growth and continuously proliferated in IL-2-conditioned medium without need for additional stimulation. Infected Th1 and Th2 clones equally showed high expression of CD25, HLA-DR, CD44, CD30 and CD45RO. Infection with HTLV-I altered the cytokine profile in Th1 and Th2 clones. Both types of clones produced IL-6 and TNF-alpha. Th1 infected clones retained their ability to secrete IFN-gamma, but lost IL-2 gene expression. Th2 infected clones lost IL-4 gene expression, retained the ability to produce small amounts of IL-5 and acquired IFN-gamma expression.