Abstract 347P
Background
In this study, we summarize the chemokines that are involved in malignant HTLV-1 associated disease, adult T cell leukemia/lymphoma (ATLL) progression. The interaction of virus and host were evaluated in chemokine level.
Methods
The expression of CCR6, CXCR-3, the HTLV-1 proviral load (PVL), HTLV-1-Tax, and HBZ were assessed in 12 asymptomatic HTLV-1carriers (ACs), 12 healthy controls (HCs) and 12 ATLL patients. We applied quantitative real-time PCR (qRT-PCR) and TaqMan method.
Results
As per results, the level of CXCR3 gene expression in ATLL patients compared to HTLV-1 virus carriers and healthy people showed a significant difference (P=0.00 and P=0.008). Also, the mean expression of CCR6 genes in ATLL patients compared to HTLV-1 virus carriers had a significant difference of P=0.04, but in the ATLL group there was no significant difference compared to the healthy group.
Conclusions
Our study results illustrate that the expression of chemokine receptors is directly related to the course and stages of the disease as well as the prognosis of the disease. In carriers, compared to healthy individuals, we still have a higher level of expression of chemokine. In addition, with the progression of the conflict and the progression to malignancy and involvement of T lymphocytes (the producer of these chemokines) as shown in our study, we can conclude that with decreased levels of these chemokine receptors can lead to malignancy with a poor prognosis. Our findings confirm previous studies that Tax protein may not be expressed in ATLL patients. Additionally, an oncoprotein may involve in inducing malignancy, but in the absence of Tax, HTLV-1-HBZ protein implicated in the maintenance of mechanism of the virus to escape from the host cell immune system. We also found an increase in virus load as HTLV-1 carriers move toward. So these chemokines could be suggested as influential targets for the prognosis and proper therapy of ATLL.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
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