New insights into HTLV entry

International audiencen.

Current concepts regarding the HTLV-1 receptor complex

The identity of the Human T lymphotropic Virus type 1 (HTLV-1) receptor remained an unsolved puzzle for two decades, until the recent demonstration that three molecules, Glucose Transporter 1, Neuropilin-1 and Heparan Sulfate Proteoglycans are involved in HTLV-1 binding and entry. Despite these advances, several questions remain unanswered, including the precise role of each of these molecules during virus entry. In light of the most recent data, we propose a model of the HTLV-1 receptor complex and discuss its potential impact on HTLV-1 infection

TRAF5-mediated Tax ubiquitination modulates IKK phosphorylation but not binding to NEMO

International audienc

Molecular Aspects of HTLV-1 Entry: Functional Domains of the HTLV-1 Surface Subunit (SU) and Their Relationships to the Entry Receptors

The initial step in retroviral infection involves specific interactions between viral envelope proteins (Env) and specific receptors on the surface of target cells. For many years, little was known about the entry receptors for HTLV-1. During this time, however, functional domains of the HTLV-1 Env were identified by analyzing the effects of neutralizing antibodies and specific mutations in Env on HTLV-1 infectivity. More recent studies have revealed that HTLV-1 infectivity involves interactions with three different molecules: heparan sulfate proteoglycans (HSPG), the VEGF-165 receptor Neuropilin 1 (NRP-1) and glucose transporter type 1 (GLUT1). Here, we revisit previously published data on the functional domains of Env in regard to the recent knowledge acquired about this multi-receptor complex. We also discuss the similarities and differences between HTLV-1 and other deltaretroviruses in regards to receptor usage

Exclusion from the Golgi and very low levels of HTLV-2 Tax ubiquitination do not prevent IKK-gamma/NEMO relocalization and NF-κB activation

International audiencen.

Predominant role of Tax sumoylation in Tax-induced NF-kB activation in T cells

International audiencen.