DC‐SIGN–Mediated Transfer of HIV‐1 Is Compromised by the Ability ofLeishmania infantumto Exploit DC‐SIGN as a Ligand
Author(s) -
Chenqi Zhao,
Réjean Cantin,
Marie Breton,
Barbara Papadopoulou,
Michel J. Tremblay
Publication year - 2005
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/429673
Subject(s) - dc sign , leishmania , biology , leishmania infantum , virology , amastigote , microbiology and biotechnology , leishmania major , dendritic cell , leishmaniasis , immunology , antigen , visceral leishmaniasis , parasite hosting , world wide web , computer science
DC-SIGN (dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin) binds human immunodeficiency virus type 1 (HIV-1) and facilitates transfer of virus to permissive cells. Leishmania parasites also exploit DC-SIGN as a receptor. Here, we report that transfer of HIV-1 to target cells is markedly reduced when DC-SIGN(+) cells are preincubated with Leishmania amastigotes before pulsing with virions. Moreover, binding of HIV-1 to DC-SIGN(+) cells is diminished by the presence of Leishmania amastigotes. Our findings provide novel insight into the complex interactions between HIV-1 and Leishmania parasites. The ability of both HIV-1 and Leishmania parasites to bind to the same cell-surface constituent to gain entry into dendritic cells might have an impact on the immunological and pathological events associated with HIV-1 infection.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom