PMID- 23271952
OWN - NLM
STAT- MEDLINE
DCOM- 20130521
LR  - 20220330
IS  - 1545-7885 (Electronic)
IS  - 1544-9173 (Print)
IS  - 1544-9173 (Linking)
VI  - 10
IP  - 12
DP  - 2012
TI  - Siglec-1 is a novel dendritic cell receptor that mediates HIV-1 trans-infection 
      through recognition of viral membrane gangliosides.
PG  - e1001448
LID - 10.1371/journal.pbio.1001448 [doi]
LID - e1001448
AB  - Dendritic cells (DCs) are essential antigen-presenting cells for the induction of 
      immunity against pathogens. However, HIV-1 spread is strongly enhanced in 
      clusters of DCs and CD4(+) T cells. Uninfected DCs capture HIV-1 and mediate 
      viral transfer to bystander CD4(+) T cells through a process termed 
      trans-infection. Initial studies identified the C-type lectin DC-SIGN as the 
      HIV-1 binding factor on DCs, which interacts with the viral envelope 
      glycoproteins. Upon DC maturation, however, DC-SIGN is down-regulated, while 
      HIV-1 capture and trans-infection is strongly enhanced via a 
      glycoprotein-independent capture pathway that recognizes sialyllactose-containing 
      membrane gangliosides. Here we show that the sialic acid-binding Ig-like lectin 1 
      (Siglec-1, CD169), which is highly expressed on mature DCs, specifically binds 
      HIV-1 and vesicles carrying sialyllactose. Furthermore, Siglec-1 is essential for 
      trans-infection by mature DCs. These findings identify Siglec-1 as a key factor 
      for HIV-1 spread via infectious DC/T-cell synapses, highlighting a novel 
      mechanism that mediates HIV-1 dissemination in activated tissues.
FAU - Izquierdo-Useros, Nuria
AU  - Izquierdo-Useros N
AD  - AIDS Research Institute IrsiCaixa, Institut d'Investigacio en Ciencies de la 
      Salut Germans Trias i Pujol, Universitat Autonoma de Barcelona, Badalona, Spain. 
      nizquierdo@irsicaixa.es
FAU - Lorizate, Maier
AU  - Lorizate M
FAU - Puertas, Maria C
AU  - Puertas MC
FAU - Rodriguez-Plata, Maria T
AU  - Rodriguez-Plata MT
FAU - Zangger, Nadine
AU  - Zangger N
FAU - Erikson, Elina
AU  - Erikson E
FAU - Pino, Maria
AU  - Pino M
FAU - Erkizia, Itziar
AU  - Erkizia I
FAU - Glass, Barbel
AU  - Glass B
FAU - Clotet, Bonaventura
AU  - Clotet B
FAU - Keppler, Oliver T
AU  - Keppler OT
FAU - Telenti, Amalio
AU  - Telenti A
FAU - Krausslich, Hans-Georg
AU  - Krausslich HG
FAU - Martinez-Picado, Javier
AU  - Martinez-Picado J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20121218
PL  - United States
TA  - PLoS Biol
JT  - PLoS biology
JID - 101183755
RN  - 0 (Gangliosides)
RN  - 0 (Lipid Bilayers)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Liposomes)
RN  - 0 (Sialic Acid Binding Ig-like Lectin 1)
SB  - IM
CIN - PLoS Biol. 2012;10(12):e1001454. PMID: 23271956
MH  - Dendritic Cells/drug effects/*metabolism/*virology
MH  - Exosomes/drug effects/metabolism
MH  - Gangliosides/*metabolism
MH  - Gene Silencing/drug effects
MH  - HEK293 Cells
MH  - HIV Infections/*immunology/pathology/virology
MH  - HIV-1/*physiology
MH  - Humans
MH  - Immunological Synapses/drug effects
MH  - Lipid Bilayers/*metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Liposomes/metabolism
MH  - Sialic Acid Binding Ig-like Lectin 1/*metabolism
MH  - Up-Regulation/drug effects
MH  - Virion/drug effects/metabolism
PMC - PMC3525531
COIS- I have read the journal's policy and have the following conflicts: A patent 
      application based on this work has been filed (EP11382392.6, 2011). The authors 
      declare that no other competing financial interests exist.
EDAT- 2012/12/29 06:00
MHDA- 2013/05/23 06:00
PMCR- 2012/12/18
CRDT- 2012/12/29 06:00
PHST- 2012/05/09 00:00 [received]
PHST- 2012/10/31 00:00 [accepted]
PHST- 2012/12/29 06:00 [entrez]
PHST- 2012/12/29 06:00 [pubmed]
PHST- 2013/05/23 06:00 [medline]
PHST- 2012/12/18 00:00 [pmc-release]
AID - PBIOLOGY-D-12-01770 [pii]
AID - 10.1371/journal.pbio.1001448 [doi]
PST - ppublish
SO  - PLoS Biol. 2012;10(12):e1001448. doi: 10.1371/journal.pbio.1001448. Epub 2012 Dec 
      18.