Definition
In addition to gag, pol, and env, HIV and SIV genomes contain additional genes (tat, rev, vif, vpr, vpx, vpu, and nef) encoding for regulatory proteins. While Tat and Rev are required both in vitro and in vivo for virus replication, the Vif, Vpr, Vpx, Vpu, and Nef “auxiliary” proteins are usually dispensable for virus growth in vitro, but these auxiliary proteins play essential roles in vivo for virus replication and AIDS pathogenesis through interaction and perturbations of cellular pathways and functions in HIV target cells.
Introduction
The genome of human lentiviruses (HIV-1 and HIV-2) contains more genes than the usual gag, pol, and env genes common to all retroviruses. Indeed, HIV-1 contains additional open reading frames called tat, rev, vif, vpr, vpu, and nef encoding for small regulatory proteins, while the HIV-2 genome has an additional vpr-related vpx gene but usually no vpu. While Tat and Rev proteins are absolutely required both in vitro and in vivo for virus...
This is a preview of subscription content, log in via an institution to check access.
References
Abraham L, Fackler OT. HIV-1 Nef: a multifaceted modulator of T cell receptor signaling. Cell Commun Signal CCS. 2012;10:39.
Basmaciogullari S, Pizzato M. The activity of Nef on HIV-1 infectivity. Front Microbiol. 2014;5:232.
Brégnard C, Benkirane M, Laguette N. DNA damage repair machinery and HIV escape from innate immune sensing. Front Microbiol. 2014;5:176.
Guenzel CA, Hérate C, Benichou S. HIV-1 Vpr-a still “enigmatic multitasker”. Front Microbiol. 2014;5:127.
Jónsson SR, Andrésdóttir V. Host restriction of lentiviruses and viral countermeasures: APOBEC3 and Vif. Viruses. 2013;5:1934–47.
Laguette N, Benkirane M. How SAMHD1 changes our view of viral restriction. Trends Immunol. 2012;33:26–33.
Malim MH, Emerman M. HIV-1 accessory proteins–ensuring viral survival in a hostile environment. Cell Host Microbe. 2008;3:388–98.
Planelles V, Benichou S. Vpr and its interactions with cellular proteins. Curr Top Microbiol Immunol. 2009;339:177–200.
Romani B, Cohen EA. Lentivirus Vpr and Vpx accessory proteins usurp the cullin4-DDB1 (DCAF1) E3 ubiquitin ligase. Curr Opin Virol. 2012;2:755–63.
Roy N, Pacini G, Berlioz-Torrent C, Janvier K. Mechanisms underlying HIV-1 Vpu-mediated viral egress. Front Microbiol. 2014;5:177.
Sauter D. Counteraction of the multifunctional restriction factor tetherin. Front Microbiol. 2014;5:163.
Schaller T, Bauby H, Hué S, Malim MH, Goujon C. New insights into an X-traordinary viral protein. Virology. 2014;5:126.
Strebel K. HIV accessory proteins versus host restriction factors. Curr Opin Virol. 2013;3:692–9.
Tokarev A, Guatelli J. Misdirection of membrane trafficking by HIV-1 Vpu and Nef: Keys to viral virulence and persistence. Cell Logist. 2011;1:90–102.
Yang Z, Greene WC. A new activity for SAMHD1 in HIV restriction. Nat Med. 2014;20:808–9.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2015 Springer Science+Business Media New York
About this entry
Cite this entry
Hérate, C., Benichou, S., Lambelé, M. (2015). HIV “Auxiliary” Proteins. In: Hope, T., Stevenson, M., Richman, D. (eds) Encyclopedia of AIDS. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-9610-6_374-1
Download citation
DOI: https://doi.org/10.1007/978-1-4614-9610-6_374-1
Received:
Accepted:
Published:
Publisher Name: Springer, New York, NY
Online ISBN: 978-1-4614-9610-6
eBook Packages: Springer Reference MedicineReference Module Medicine