Intercellular transmission of HTLV-1: not all mechanisms have been revealed - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue Médecine/Sciences Année : 2015

Intercellular transmission of HTLV-1: not all mechanisms have been revealed

Résumé

HTLV-1 is the etiological agent of Adult T cell Leukemia/Lymphoma (ATLL) and of HTLV-1-Associated Myelopathy/tropical spastic paraparesis (HAM/TSP). It is mainly detected in CD4+ lymphocytes in vivo, but proviral genomes have also been detected although less frequently, in CD8+ T lymphocytes, B lymphocytes, monocytes, macrophages, dendritic cells and other non-lymphoid cells. Virus spread is highly dependent on cell-cell contact. This mode of transmission is correlated with an increased ability of infected cells to migrate, a property linked to cytoskeleton reorganization induced by the viral Tax protein. Cell-to-cell transmission relies on at least three non-exclusive molecular pathways. First, a specialized area, the "virological synapse'' (VS) promotes direct transmission of budding HTLV-1 particles into a synaptic cleft formed between infected and uninfected cells. Second, HTLV-1 particles accumulate at the plasma membrane of infected cells in a biofilm-like extracellular viral assembly that resembles a bacterial biofilm. Viral biofilm is rapidly transmitted to uninfected cells when infected cells contact target cells. Finally, membrane extensions called inter-cellular conduits facilitate HTLV-1 proteins transfer from infected to uninfected target cells, and may stabilize cell-cell contacts. The aim of this review is to summarize the molecular mechanisms of these HTLV-1 transmission pathways.

Dates et versions

hal-01911434 , version 1 (02-11-2018)

Identifiants

Citer

Gerges Rizkallah, Renaud Mahieux, Hélène Dutartre. Intercellular transmission of HTLV-1: not all mechanisms have been revealed. Médecine/Sciences, 2015, 31 (6-7), pp.629-637. ⟨10.1051/medsci/20153106016⟩. ⟨hal-01911434⟩
21 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Mastodon Facebook X LinkedIn More