@article{fdi:010068190,
  title = {{T}he potency of {N}ef-mediated {SERINC}5 antagonism correlates with the prevalence of primate lentiviruses in the wild},
  author = {{H}eigele, {A}. and {K}miec, {D}. and {R}egensburger, {K}. and {L}anger, {S}. and {P}eiffer, {L}. and {S}turzel, {C}. {M}. and {S}auter, {D}. and {P}eeters, {M}artine and {P}izzato, {M}. and {L}earn, {G}. {H}. and {H}ahn, {B}. {H}. and {K}irchhoff, {F}.},
  editor = {},
  language = {{ENG}},
  abstract = {{T}he cellular factor serine incorporator 5 ({SERINC}5) impairs {HIV}-1 infectivity but is antagonized by the viral {N}ef protein. {W}e analyzed the anti-{SERINC}5 activity of {N}ef proteins across primate lentiviruses and examined whether {SERINC}5 represents a barrier to cross-species transmissions and/or within-species viral spread. {HIV}-1, {HIV}-2, and {SIV} {N}efs counteract human, ape, monkey, and murine {SERINC}5 orthologs with similar potency. {H}owever, {HIV}-1 {N}efs are more active against {SERINC}5 than {HIV}-2 {N}efs, and chimpanzee {SIV} ({SIV}cpz) {N}efs are more potent than those of their monkey precursors. {A}dditionally, {N}efs of {HIV} and most {SIV}s rely on the dileucine motif in the {C}-terminal loop for anti-{SERINC}5 activity, while the {N}ef from colobus {SIV} ({SIV}col) evolved different inhibitory mechanisms. {W}e also found a significant correlation between anti-{SERINC}5 potency and the {SIV} prevalence in the respective ape and monkey species. {T}hus, {N}ef-mediated {SERINC}5 antagonism may determine the ability of primate lentiviruses to spread within natural hosts.},
  keywords = {{AFRIQUE}},
  booktitle = {},
  journal = {{C}ell {H}ost and {M}icrobe},
  volume = {20},
  numero = {3},
  pages = {381--391},
  ISSN = {1931-3128},
  year = {2016},
  DOI = {10.1016/j.chom.2016.08.004},
  URL = {https://www.documentation.ird.fr/hor/fdi:010068190},
}