Abstract
Viruses such as lentiviruses that are responsible for long lasting infections have to evade several levels of cellular immune mechanisms to persist and efficiently disseminate in the host. Over the past decades, much evidence has emerged regarding the major role of accessory proteins of primate lentiviruses, human immunodeficiency virus and simian immunodeficiency virus, in viral evasion from the host immune defense. This short review will provide an overview of the mechanism whereby the accessory protein Vpu contributes to this escape. Vpu is a multifunctional protein that was shown to contribute to viral egress by down-regulating several mediators of the immune system such as CD4, CD1d, NTB-A and the restriction factor BST2. The mechanisms underlying its activity are not fully characterized but rely on its ability to interfere with the host machinery regulating protein turnover and vesicular trafficking. This review will focus on our current understanding of the mechanisms whereby Vpu down-regulates CD4 and BST2 expression levels to favor viral egress.
Highlights
Viral egress and replication rely on a complex interplay between viral and cellular proteins
The genome of lentiviruses encodes for several accessory proteins such as Nef, Vif, Vpr, Vpx, and Vpu, in addition to the structural and enzymatic proteins Gag, Pol, and Env and the regulatory proteins Tat and Rev (Malim and Bieniasz, 2012). These accessory proteins are, not common to all lentiviruses: Nef and Vpr are specific of primate lentiviruses (HIV-1, HIV-2, and SIV),Vpx is expressed by HIV-2 and its closely related SIVsmm and SIVmac, Vpu is expressed by HIV-1 strains and a few strains of SIV
We showed that Vpu-mediated down-regulation of BST2 and viral release require HRS, and unveiled an increased affinity of BST2 for HRS upon Vpu expression (Janvier et al, 2011)
Summary
Viral egress and replication rely on a complex interplay between viral and cellular proteins. Vpu is a multifunctional protein that was shown to contribute to viral egress by down-regulating several mediators of the immune system such as CD4, CD1d, NTBA and the restriction factor BST2.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
