@article{fdi:010054734,
  title = {{N}ef-mediated suppression of {T} cell activation was lost in a lentiviral lineage that gave rise to {HIV}-1},
  author = {{S}chindler, {M}. and {M}unch, {J}. and {K}utsch, {O}. and {L}i, {H}. and {S}antiago, {M}.{L}. and {B}ibollet {R}uche, {F}. and {M}uller {T}rutwin, {M}.{C}. and {N}ovembre, {F}.{J}. and {P}eeters, {M}artine and {C}ourgnaud, {V}al{\'e}rie and {B}ailes, {E}. and {R}oques, {P}. and {S}odora, {D}.{L}. and {S}ilvestri, {G}. and {S}harp, {P}.{M}. and {H}ahn, {B}.{H}. and {K}irchhoff, {F}.},
  editor = {},
  language = {{ENG}},
  abstract = {{H}igh-level immune activation and {T} cell apoptosis represent a hallmark of {HIV}-1 infection that is absent from nonpathogenic {SIV} infections in natural primate hosts. {T}he mechanisms causing these varying levels of immune activation are not understood. {H}ere, we report that nef alleles from the great majority of primate lentiviruses, including {HIV}-2, downmodulate {TCR}-{CD}3 from infected {T} cells, thereby blocking their responsiveness to activation. {I}n contrast, nef alleles from {HIV}-1 and a subset of closely related {SIV}s fail to downregulate {TCR}-{CD}3 and to inhibit cell death. {T}hus, {N}ef-mediated suppression of {T} cell activation is a fundamental property of primate lentiviruses; that likely evolved to maintain viral persistence in the context of an intact host immune system. {T}his function was lost during viral evolution in a lineage that gave rise to {HIV}-1 and may have predisposed the simian precursor of {HIV}-1 for greater pathogenicity in humans.},
  keywords = {},
  booktitle = {},
  journal = {{C}ell},
  volume = {125},
  numero = {6},
  pages = {1055--1067},
  ISSN = {0092-8674},
  year = {2006},
  DOI = {10.1016/j.cell.2006.04.033},
  URL = {https://www.documentation.ird.fr/hor/fdi:010054734},
}