Overview on HTLV-1 p12, p8, p30, p13: accomplices in persistent infection and viral pathogenesis
- Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA
The human T-lymphotropic virus type-1 (HTLV-1) is etiologically linked to adult T cell leukemia/lymphoma and tropical spastic paraparesis/HTLV-1-associated myelopathy. While the role of Tax and Rex in viral replication and pathogenesis has been extensively studied, recent evidence suggests that additional viral proteins are essential for the virus life cycle in vivo. In this review, we will summarize possible molecular mechanisms evoked in the literature to explain how p12, p8, p30, and p13 facilitate persistent viral infection of the host. We will explore several stratagems used by HTLV-1 accessory genes to escape immune surveillance, to establish latency, and to deregulate cell cycle and apoptosis to participate in virus-mediated cellular transformation.
Keywords: HTLV-1, pathogenesis, immune response, oncogenesis, virus replication
Citation: Bai XT and Nicot C (2012) Overview on HTLV-1 p12, p8, p30, p13: accomplices in persistent infection and viral pathogenesis. Front. Microbio. 3:400. doi: 10.3389/fmicb.2012.00400
Received: 20 July 2012; Paper pending published: 20 August 2012;
Accepted: 31 October 2012; Published online: 11 December 2012.
Edited by:Renaud Mahieux, Ecole Normale Supérieure de Lyon, France
Reviewed by:Cristian Apetrei, University of Pittsburgh, USA
Vincenzo Ciminale, University of Padova, Italy
Copyright: © 2012 Bai and Nicot. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
*Correspondence: Christophe Nicot, Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA. e-mail: email@example.com