Abstract
The HIV-1, HIV-2 and SIV Nef protein are known to modulate the expression of several cell surface receptors and molecules to escape the immune system, to alter T cell activation, to enhance viral replication, infectivity and transmission and overall to ensure the optimal environment for infection outcome. Consistent and continuous efforts have been made over the years to characterize the modulation of expression of each of these molecules, in the hope that a better understanding of these processes essential for HIV infection and/or pathogenesis will eventually highlight new therapeutic targets. In this article we provide an extensive review of the knowledge gained so far on this important and evolving topic.
Highlights
Receptor down-modulation is a strategy broadly used by many viruses to escape the immune system and establish the best environment for their replication and spread [1,2,3,4,5]
The CD4 co-receptor is necessary for T cell activation upon recognition of the MHC-II:antigen complex and is required for productive signaling that leads to the immune response to pathogen infection [29]
MHC-II is expressed on antigen-presenting cells (APCs) such as macrophages and dendritic cells and binds to the T cell and CD4 receptors present on T-helper lymphocytes to play a fundamental role in the immune response
Summary
Receptor down-modulation is a strategy broadly used by many viruses to escape the immune system and establish the best environment for their replication and spread [1,2,3,4,5]. The down-modulation of surface receptors and molecules is considered one of the most important and conserved functions of the HIV-1 Nef protein, with relevance for pathogenicity.
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