HTLV-1 p12 modulates the levels of prion protein (PrP) in CD4 T cells.

INTRODUCTION

Infection with human T cell lymphotropic virus type 1 (HTLV-1) is endemic in Brazil and is linked with pro-inflammatory conditions including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic neuroinflammatory incapacitating disease that culminates in loss of motor functions. The mechanisms underlying the onset and progression of HAM/TSP are incompletely understood. Previous studies have demonstrated that inflammation and infectious agents can affect the expression of cellular prion protein (PrP) in immune cells.

METHODS

Here, we investigated whether HTLV-1 infection affected PrP content in cell lines and primary CD4cells using flow cytometry and western blot assays.

RESULTS

We found that HTLV-1 infection decreased the expression levels of PrP and HTLV-1 encoded p12, an endoplasmic reticulum resident protein also known to affect post-transcriptionally cellular proteins such as MHC-class I and the IL-2 receptor. In addition, we observed a reduced percentage of CD4 T cells from infected individuals expressing PrP, which was reflected by IFN type II but not IL-17 expression.

DISCUSSION

These results suggested that PrP downregulation, linked to both HTLV-1 p12 and IFN-γ expression in CD4 cells, may play a role in the neuropathogenesis of HTLV-1 infection.