Short report

Human immunodeficiency virus type 1 envelope proteins traffic toward virion assembly sites via a TBC1D20/Rab1-regulated pathway

Dikla Nachmias¹, Ella H Sklan^2*, Marcelo Ehrlich^1* and Eran Bacharach^1*

• * Corresponding authors: Ella H Sklan sklan@post.tau.ac.il - Marcelo Ehrlich marceloe@post.tau.ac.il - Eran Bacharach eranbac@post.tau.ac.il

Author Affiliations

¹ Department of Cell Research and Immunology, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel

² Department of Clinical Immunology and Microbiology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel

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Retrovirology 2012, 9:7 doi:10.1186/1742-4690-9-7

Published: 19 January 2012

Abstract

Background

The cellular activity of many factors and pathways is required to execute the complex replication cycle of the human immunodeficiency virus type 1 (HIV-1). To reveal these cellular components, several extensive RNAi screens have been performed, listing numerous 'HIV-dependency factors'. However, only a small overlap between these lists exists, calling for further evaluation of the relevance of specific factors to HIV-1 replication and for the identification of additional cellular candidates. TBC1D20, the GTPase-activating protein (GAP) of Rab1, regulates endoplasmic reticulum (ER) to Golgi trafficking, was not identified in any of these screens, and its involvement in HIV-1 replication cycle is tested here.

Findings

Excessive TBC1D20 activity perturbs the early trafficking of HIV-1 envelope protein through the secretory pathway. Overexpression of TBC1D20 hampered envelope processing and reduced its association with detergent-resistant membranes, entailing a reduction in infectivity of HIV-1 virion like particles (VLPs).

Conclusions

These findings add TBC1D20 to the network of host factors regulating HIV replication cycle.