Abstract
Innate immunity plays a critical role in the host response to a viral infection. The innate response has two main functions. First, it triggers effector mechanisms that restrict the infection. Second, it primes development of the adaptive response, which completes the elimination of the pathogen or of infected cells. In vivo, HTLV-1 infects T lymphocytes that participate in adaptive immunity but also monocytes and dendritic cells that are major players in innate immunity. Herein, we will review the interplay between HTLV-1 and innate immunity. Particular emphasis is put on HTLV-1-induced alteration of type-I interferon (IFN-I) function. In vitro, the viral Tax protein plays a significant role in the alteration of IFN synthesis and signaling. Despite this, IFN-I/AZT treatment of Adult T-cell Leukemia/Lymphoma (ATLL) patients leads to complete remission. We will discuss a model in which exogenous IFN-I could act both on the microenvironment of the T-cells to protect them from infection, and also on infected cells when combined with other drugs that lead to Tax down-regulation/degradation.
Highlights
Upon viral infection, several defense mechanisms cooperate to limit propagation of the pathogen within the organism
In line with this hypothesis, stimulation of peripheral blood mononuclear cells (PBMCs) isolated from ACs with -galactosylceramide, the prototypical antigen used for Invariant NKT (iNKT) stimulation, induced ex vivo expansion of iNKT cells as well as decreased proviral load (PVL) in the total PBMCs, indicating that expanded iNKT cells have anti-human T-lymphotropic virus type 1 (HTLV-1) activity [47]
Silencing IRF3 expression in HTLV-1 transfected Jurkat cells resulted in increased HTLV-1 mRNA expression. These results suggest that HTLV-1-infected cells that express viral mRNAs are likely to be impaired for early IFN induction signaling
Summary
Several defense mechanisms cooperate to limit propagation of the pathogen within the organism. Two types of immune responses have been defined: the innate response, a rapidly engaged but transient and poorly specific response, and the adaptive response, a delayed but specific response which allows the development of immune memory
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