English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

While human T cell leukemia virus type 1 (HTLV-1) is an etiological agent of adult T-cell leukemia (ATL), its close relative HTLV-2 is not associated with any leukemia. HTLV-1 and HTLV-2 encode Tax1 and Tax2 proteins, respectively, which are essential for immortalization of T-cells by the respective viruses, thereby persistent infection. Tax1 and Tax2 have more than 75% amino acid similarities, but we show here that Tax1 and Tax2 have multiple distinct activities. Tax1 induced IL-2-independent growth of a T-cell line CTLL-2 more efficiently than Tax2. By contrast, Tax2 immortalized human T-cells in the presence of IL-2 more efficiently than Tax1. These results suggest that HTLV-1 and HTLV-2 have distinct IL-2 requirements to immortalize T-cells. We also found that Tax1 altered cellular oxidative stress response. Arsenite, a pro-oxidant, induced stress granule (SG) formation, which functions as a protective role against oxidant-induced cell damages, but the formation was inhibited by Tax1. We will discuss these findings in terms of the HTLV-1-specific pathogenesis.

Distinct activities of HTLV-1 Tax1 from HTLV-2 Tax2 play key roles in pathogenesis