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• W2156838006 abstract "ABSTRACT Infection by the human T-cell leukemia virus type 1 (HTLV-1) is thought to cause dysregulated T-cell proliferation, which in turn leads to adult T-cell leukemia/lymphoma. Early cellular changes after HTLV-1 infection have been difficult to study due to the poorly infectious nature of HTLV-1 and the need for cell-to-cell contact for HTLV-1 transmission. Using a series of reporter systems, we show that HeLa cells cease proliferation within one or two division cycles after infection by HTLV-1 or transduction of the HTLV-1 tax gene. HTLV-1-infected HeLa cells, like their tax -transduced counterparts, expressed high levels of p21 CIP1 / WAF1 and p27 KIP1 , developed mitotic abnormalities, and became arrested in G 1 in senescence. In contrast, cells of a human osteosarcoma lineage (HOS) continued to divide after HTLV-1 infection or Tax expression, albeit at a reduced growth rate and with mitotic aberrations. Unique to HOS cells is the dramatic reduction of p21 CIP1 / WAF1 and p27 KIP1 expression, which is in part associated with the constitutive activation of the phosphatidylinositol-3-kinase (PI3K)-protein kinase B (Akt) pathway. The loss of p21 CIP1 / WAF1 and p27 KIP1 in HOS cells apparently allows HTLV-1- and Tax-induced G 1 arrest to be bypassed. Finally, HTLV-1 infection and Tax expression also cause human SupT1 T cells to arrest in the G 1 phase of the cell cycle. These results suggest that productive HTLV-1 infection ordinarily leads to Tax-mediated G 1 arrest. However, T cells containing somatic mutations that inactivate p21 CIP1 / WAF1 and p27 KIP1 may continue to proliferate after HTLV-1 infection and Tax expression. These infected cells can expand clonally, accumulate additional chromosomal abnormalities, and progress to cancer." @default.
• W2156838006 created "2016-06-24" @default.
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• W2156838006 date "2008-09-01" @default.
• W2156838006 modified "2023-10-18" @default.
• W2156838006 title "Human T-Cell Leukemia Virus Type 1 Infection Leads to Arrest in the G ₁ Phase of the Cell Cycle" @default.
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• W2156838006 doi "https://doi.org/10.1128/jvi.00091-08" @default.
• W2156838006 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2519625" @default.
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