{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T20:33:48Z","timestamp":1791146028316,"version":"4.1.0"},"reference-count":71,"publisher":"American Society for Microbiology","issue":"22","license":[{"start":{"date-parts":[[2009,11,15]],"date-time":"2009-11-15T00:00:00Z","timestamp":1258243200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2009,11,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Human T-lymphotropic virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia\/lymphoma, and it encodes a number of nonstructural proteins that are involved in virus replication and immune evasion. The viral protein p12 previously has been characterized to interfere with major histocompatibility complex class, ICAM-1, and ICAM-2 expression, and it activates STAT5. Using a previously established T-cell line immortalized with an HTLV-1 molecular clone deleted for p12, we assessed the role of p12 in regulating cellular growth and virus transmission. These cells were complemented for p12 expression by the transduction of a lentivirus vector expressing p12. We report that p12 conferred a selective growth advantage in vitro and increased the colony formation of human T cells in soft-agar assays. Consistently with previous studies, p12<jats:sup>\u2212<\/jats:sup>and p12<jats:sup>+<\/jats:sup>cell lines produced similar amounts of virus particles released into the supernatant of cultured cells, although we found that p12 expression greatly enhanced virus transmission. Moreover, we found that interleukin-2 (IL-2) stimulation also increased HTLV-1 transmission whether p12 was expressed or not, and inversely, that the inhibition of Jak signaling significantly reduced HTLV-1 transmission. Intriguingly, IL-2\/Jak signaling was not associated with changes in viral gene expression, viral RNA encapsidation, the maturation of the virus particle, cell-cell adherence, or Gag polarization and virological synapse formation. We do demonstrate, however, that IL-2 stimulation and p12 expression significantly increased the rate of syncytium formation, revealing a novel role for IL-2 signaling and Jak activation in HTLV-1 virus transmission.<\/jats:p>","DOI":"10.1128\/jvi.00952-09","type":"journal-article","created":{"date-parts":[[2009,9,3]],"date-time":"2009-09-03T00:45:59Z","timestamp":1251938759000},"page":"11467-11476","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":23,"title":["Novel Role for Interleukin-2 Receptor-Jak Signaling in Retrovirus Transmission"],"prefix":"10.1128","volume":"83","author":[{"given":"J. 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