PMID- 19180188
OWN - NLM
STAT- MEDLINE
DCOM- 20090417
LR  - 20211020
IS  - 1553-7374 (Electronic)
IS  - 1553-7366 (Print)
IS  - 1553-7366 (Linking)
VI  - 5
IP  - 1
DP  - 2009 Jan
TI  - Selective transmission of R5 HIV-1 over X4 HIV-1 at the dendritic cell-T cell 
      infectious synapse is determined by the T cell activation state.
PG  - e1000279
LID - 10.1371/journal.ppat.1000279 [doi]
LID - e1000279
AB  - Dendritic cells (DCs) are essential antigen-presenting cells for the induction of 
      T cell immunity against HIV. On the other hand, due to the susceptibility of DCs 
      to HIV infection, virus replication is strongly enhanced in DC-T cell interaction 
      via an immunological synapse formed during the antigen presentation process. When 
      HIV-1 is isolated from individuals newly infected with the mixture of R5 and X4 
      variants, R5 is predominant, irrespective of the route of infection. Because the 
      early massive HIV-1 replication occurs in activated T cells and such T-cell 
      activation is induced by antigen presentation, we postulated that the selective 
      expansion of R5 may largely occur at the level of DC-T cell interaction. Thus, 
      the immunological synapse serves as an infectious synapse through which the virus 
      can be disseminated in vivo. We used fluorescent recombinant X4 and R5 HIV-1 
      consisting of a common HIV-1 genome structure with distinct envelopes, which 
      allowed us to discriminate the HIV-1 transmitted from DCs infected with the two 
      virus mixtures to antigen-specific CD4(+) T cells by flow cytometry. We clearly 
      show that the selective expansion of R5 over X4 HIV-1 did occur, which was 
      determined at an early entry step by the activation status of the CD4(+) T cells 
      receiving virus from DCs, but not by virus entry efficiency or productivity in 
      DCs. Our results imply a promising strategy for the efficient control of HIV 
      infection.
FAU - Yamamoto, Takuya
AU  - Yamamoto T
AD  - Department of Immunology, National Institute of Infectious Diseases, Tokyo, 
      Japan.
FAU - Tsunetsugu-Yokota, Yasuko
AU  - Tsunetsugu-Yokota Y
FAU - Mitsuki, Yu-ya
AU  - Mitsuki YY
FAU - Mizukoshi, Fuminori
AU  - Mizukoshi F
FAU - Tsuchiya, Takatsugu
AU  - Tsuchiya T
FAU - Terahara, Kazutaka
AU  - Terahara K
FAU - Inagaki, Yoshio
AU  - Inagaki Y
FAU - Yamamoto, Naoki
AU  - Yamamoto N
FAU - Kobayashi, Kazuo
AU  - Kobayashi K
FAU - Inoue, Jun-ichiro
AU  - Inoue J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090130
PL  - United States
TA  - PLoS Pathog
JT  - PLoS pathogens
JID - 101238921
RN  - 0 (CXCR4 protein, human)
RN  - 0 (Luminescent Proteins)
RN  - 0 (Receptors, CCR5)
RN  - 0 (Receptors, CXCR4)
RN  - 0 (enhanced green fluorescent protein)
RN  - 0 (fluorescent protein 583)
RN  - 147336-22-9 (Green Fluorescent Proteins)
SB  - IM
MH  - Antigen Presentation
MH  - CD4-Positive T-Lymphocytes/immunology/metabolism/*virology
MH  - Cell Line
MH  - Dendritic Cells/metabolism/*virology
MH  - Flow Cytometry
MH  - Gene Expression Regulation
MH  - Green Fluorescent Proteins/genetics/metabolism
MH  - HIV-1/genetics/*physiology
MH  - Humans
MH  - Immunological Synapses/immunology/*virology
MH  - Luminescent Proteins/genetics/metabolism
MH  - *Lymphocyte Activation
MH  - Microscopy, Fluorescence
MH  - Receptors, CCR5/genetics/*metabolism
MH  - Receptors, CXCR4/genetics/*metabolism
PMC - PMC2627922
COIS- The authors have declared that no competing interests exist.
EDAT- 2009/01/31 09:00
MHDA- 2009/04/18 09:00
PMCR- 2009/01/30
CRDT- 2009/01/31 09:00
PHST- 2008/08/14 00:00 [received]
PHST- 2008/12/23 00:00 [accepted]
PHST- 2009/01/31 09:00 [entrez]
PHST- 2009/01/31 09:00 [pubmed]
PHST- 2009/04/18 09:00 [medline]
PHST- 2009/01/30 00:00 [pmc-release]
AID - 08-PLPA-RA-0928R3 [pii]
AID - 10.1371/journal.ppat.1000279 [doi]
PST - ppublish
SO  - PLoS Pathog. 2009 Jan;5(1):e1000279. doi: 10.1371/journal.ppat.1000279. Epub 2009 
      Jan 30.