Analysis of expression of selected genes Kaposi's sarcoma associated Herpesvirus (KSHV) in cell TIVE-LTC exposed in the tat protein of human immunodeficiency virus (HIV-1).

Abstract

Introduction: Patients with human immunodeficiency virus (HIV) are at increased risk of developing malignancies linked to Kaposi's sarcoma-associated herpesvirus (KSHV), including Kaposi's sarcoma (KS). Notably, AIDS-associated Kaposi's sarcoma (AIDS-KS) has become more aggressive than other forms of KS, suggesting the existence of synergistic interaction between the products of KSHV and HIV-1. The biological cycle of KSHV is divided into latent and lytic phases. The vFLIP and LANA proteins expressed in the latent phase and the lytic proteins Rta, vGPCR and K1, exhibit oncogenic properties. It is plausible that HIV-1 Tat protein significantly modify the gene expression of KSHV due to its ability in stimulating angiogenesis and other inflammatory phenomena, providing phenotypic changes that contribute to the development of AIDS-associated KS. For a better understanding of the effects of HIV-1 tat protein in KSHV-infected cells, through the analysis of the Real Time Quantitative reverse transcriptase polymerase chain reactions (qRT-PCR), the present paper described the changes in the gene expression encoding vFLIP, LANA, Rta, vGPCR and K1 in Telomerase-immortalized human umbilical vein endotelial cell line - Long Term KSHV infected (TIVE-LTC) exposed to recombinant HIV-1 Tat protein for 12, 24, 48 and 72 hours. Results: In descriptive terms, the fold change of latent genes during exposure to the recombinant HIV-1 Tat protein regarding denatured tat protein, increased after 12 and 24h for LANA and after 24 and 72h for vFLIP. For lytic genes, the fold change consistently increased until 48h and decreased in the next 12 hours for ORF-50. While for ORF-K1 the fold change increased after 12 and 24 hours and did not change after 48 and 72 hours. Conclusions: The experimental model used to evaluate gene expression showed important limitations and therefore, the variations found in the analysis of gene expression of KSHV to a possible effect of exposure of TIVE-LTC to recombinant HIV-1 Tat protein could not be reliably assigned.