Heat shock activation of human T cell leukemia/lymphoma virus type I (HTLV-I) in HTLV-I-transformed cells (MT-2) is associated with down-regulation of cellular heat shock protein (HSP27/28).

Important note: Information in this article was accurate in 1994. The state of the art may have changed since the publication date.

Heat shock activation of human T cell leukemia/lymphoma virus type I (HTLV-I) in HTLV-I-transformed cells (MT-2) is associated with down-regulation of cellular heat shock protein (HSP27/28).

Diss Abstr Int [B]; 53(12):6238 1993. Unique Identifier : AIDSLINE ICDB/94696171
Sun D; Univ. of Maryland Baltimore Professional Schools

Abstract: Temperature elevation constitutes a beneficial component of host defense against viral pathogens. However, virally infected cells may exhibit altered cellular tolerance to thermal stress. Additionally, increased viral oncoprotein expression in virally infected cells during thermal stress may contribute to cellular neoplastic transformation. Downregulation of cellular HSP27/28 is inversely associated with the oncogenicity of adenovirus-transformed cells (Zantema et al, 1989). We investigated the effect of thermal stress on the replication of human T-cell lymphotropic leukemia/lymphoma virus type I (HTLV-I) and the expression of cellular HSP27/28 in MT-2 cells, an HTLV-I-transformed human lymphoid cell line. We found that viability of MT-2 cells was reduced by 75% over control levels after 3-hr thermal stress. Normal peripheral blood mononuclear cell (PBMC) viability was reduced by only 9% (p less than 0.01). Metabolic [3H]leucine labeling and immunoblotting of MT-2 cells showed a decrease of HSP27/28 expression during 5 hr of thermal stress. Northern blotting also demonstrated a decrease of HSP27/28 mRNA transcription. However, the production of HSP27/28 in PBMCs was increased. Thermal stress results in a rapid increase in the phosphorylated form of HSP27/28 in both MT-2 and uninfected lymphoid CEM cells during 1-hr thermal stress. The expression of the HSP70 protein family increased during thermal stress in both MT-2 cells and PBM cells. HTLV-I replication in MT-2 cells was markedly increased as detected by viral p24 antigen expression and reverse transcriptase (RT) activity during 5 hr of thermal stress at 42 C. There were strong negative correlations between the reduced production of cellular HSP27/28 and the increased production of HTLV-I p24 (r = -0.9390, p less than 0.01), and RT activity (r = -0.9429, p less than 0.01) in MT-2 cells during 5-hr thermal stress. The results suggest that (1) the downregulation of cellular HSP27/28 in MT-2 cells during thermal stress is associated with increased HTLV-I proliferation, and (2) early posttranslational phosphorylation of HSP27/28 could be a determinant of the ability of MT-2 cells to survive hyperthermia. (Full text available from University Microfilms International, Ann Arbor, MI, as Order No. AAD93-08925)

Keywords: *Cell Transformation, Neoplastic *Down-Regulation (Physiology) *Heat Heat-Shock Proteins/*METABOLISM Human HTLV-I/*PHYSIOLOGY HTLV-I Infections/GENETICS/*METABOLISM *Virus Replication THESIS
941030
M94A0896

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