The Achilles Heel of the Trojan Horse Model of HIV-1 trans-Infection

PLoS Pathogens

Marielle Cavrois¹  Jason Neidleman¹  Warner C. Greene¹ 

[1] Gladstone Institute of Virology and Immunology, San Francisco, California, United States of America

关键词: Virions;    HIV-1;    T cells;    T helper cells;    Cell membranes;    Synapses;    T cell receptors;    Horses;   

DOI  :  10.1371/journal.ppat.1000051

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

To ensure their survival, microbial pathogens have evolved diverse strategies to subvert host immune defenses. The human retrovirus HIV-1 has been proposed to hijack the natural endocytic function of dendritic cells (DCs) to infect interacting CD4 T cells in a process termed trans-infection. Although DCs can be directly infected by certain strains of HIV-1, productive infection of DCs is not required during trans-infection; instead, DCs capture and internalize infectious HIV-1 virions in vesicles for later transmission to CD4 T cells via vesicular exocytosis across the infectious synapse. This model of sequential endocytosis and exocytosis of intact HIV-1 virions has been dubbed the “Trojan horse” model of HIV-1 trans-infection. While this model gained rapid favor as a strong example of how a pathogen exploits the natural properties of its cellular host, our recent studies challenge this model by showing that the vast majority of virions transmitted in trans originate from the plasma membrane rather than from intracellular vesicles. This review traces the experimental lines of evidence that have contributed to what we view as the “rise and decline” of the Trojan horse model of HIV-1 trans-infection.

【 授权许可】

CC BY