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Journal of Virology, September 2000, p. 7997-8002, Vol. 74, No. 17
Ludwig Boltzmann Institute for AIDS
Research,2 Institute for Hygiene and
Social Medicine,1 and Department of
Otorhinolaryngology,3 University of Innsbruck,
A-6020 Innsbruck, and Institute of Applied Microbiology,
University of Agriculture, A-1190 Vienna,4
Austria
Received 17 February 2000/Accepted 9 June 2000
After the transition from the acute to the chronic phase of human
immunodeficiency virus (HIV) infection, complement mediates long-term
storage of virions in germinal centers (GC) of lymphoid tissue. The
contribution of particular complement receptors (CRs) to virus trapping
in GC was studied on tonsillar specimens from HIV-infected individuals.
CR2 (CD21) was identified as the main binding site for HIV in GC.
Monoclonal antibodies (MAb) blocking the CR2-C3d interaction were shown
to detach 62 to 77% of HIV type 1 from tonsillar cells of an
individual in the presymptomatic stage. Although they did so at a lower
efficiency, these antibodies were able to remove HIV from tonsillar
cells of patients under highly active antiretroviral therapy,
suggesting that the C3d-CR2 interaction remains a primary entrapment
mechanism in treated patients as well. In contrast, removal of HIV was
not observed with MAb blocking CR1 or CR3. Thus, targeting CR2 may
facilitate new approaches toward a reduction of residual virus in GC.
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Detachment of Human Immunodeficiency Virus Type 1 from Germinal Centers by Blocking Complement Receptor Type 2


*
Corresponding author. Mailing address: Institut
für Hygiene und Sozialmedizin, Universität Innsbruck,
Fritz-Pregl-Strasse 3, A-6020 Innsbruck, Austria. Phone: 43 512 507 3424. Fax: 43 512 507 2870. E-mail:
wolfgang.prodinger{at}uibk.ac.at.
Present address: Baxter AG, A-1221 Vienna, Austria.
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