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Rhesus macaque dendritic cells efficiently transmit primate lentiviruses independently of DC-SIGN

  1. Author:
    Wu, L.
    Bashirova, A. A.
    Martin, T. D.
    Villamide, L.
    Mehlhop, E.
    Chertov, A. O.
    Unutmaz, D.
    Pope, M.
    Carrington, M.
    KewalRamani, V. N.

  2. Author Address

    Natl Canc Inst, HIV Drug Resistance Program, Ft Detrick, MD 21702 USA. Natl Canc Inst, HIV Drug Resistance Program, Ft Detrick, MD 21702 USA. Natl Canc Inst, Lab Genom Divers, Ft Detrick, MD 21702 USA. Natl Canc Inst, Basic Res Program, Sci Applicat Int Corp Frederick, Ft Detrick, MD 21702 USA. Populat Council, Ctr Biomed Res, New York, NY 10021 USA. Vanderbilt Univ, Sch Med, Nashville, TN 37232 USA. KewalRamani VN Natl Canc Inst, HIV Drug Resistance Program, Ft Detrick, MD 21702 USA.
    1. Year: 2002
  2. Journal: Proceedings of the National Academy of Sciences of the United States of America
    1. 99
    2. 3
    3. Pages: 1568-1573
  4. Type of Article: Article
  1. Abstract:

    Here, we describe the isolation and characterization of the rhesus macaque homolog for human DC-SIGN, a dendritic cell- specific C-type lectin. mac-DC-SIGN is 92% identical to hu-DC- SIGN. mac-DC-SIGN preserves the virus transmission function of hu-DC-SIGN, capturing and efficiently transducing simian and human immunodeficiency virus to target CD4(+) T cells. Surprisingly, however, mac-DC-SIGN plays no discernable role in the ability of rhesus macaque dendritic cells to capture and transmit primate lentiviruses. Expression and neutralization analyses suggest that this process is DC-SIGN independent in macaque, although the participation of other lectin molecules cannot be ruled out. The ability of primate lentiviruses to effectively use human and rhesus dendritic cells in virus transmission without the cells becoming directly infected suggests that these viruses have taken advantage of a conserved dendritic cell mechanism in which DC-SIGN family molecules are significant contributors but not the only participants.

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