ArticleClinical and experimental immunology1993
CR1 (CD35) and CR3 (CD11b/CD18) mediate infection of human monocytes and monocytic cell lines with complement-opsonized HIV independently of CD4.
Article in Clinical and experimental immunology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 70 citations in OpenAlex.
- The grand escape - how pathogens outsmart the human complement system.Immunobiology · 2025Review
- Long-Term Elite Controllers of HIV-1 Infection Exhibit a Deep Perturbation of Monocyte Homeostasis.International journal of molecular sciences · 2025Article
- How Broadly Neutralising Antibodies Are Redefining Immunity to Influenza.Antibodies (Basel, Switzerland) · 2025Review
- Article
- Conserved and Distinct Elements of Phagocytosis in Human andInternational journal of molecular sciences · 2021Review
- Antibody dependent enhancement: Unavoidable problems in vaccine development.Advances in immunology · 2021Article
- Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein DuringFrontiers in immunology · 2018Article
- Evasion Mechanisms Used by Pathogens to Escape the Lectin Complement Pathway.Frontiers in microbiology · 2017Review
- Mice expressing human CR1/CD35 have an enhanced humoral immune response to T-dependent antigens but fail to correct the effect of premature human CR2 expression.Immunobiology · 2012Article
- A weak neutralizing antibody response to hepatitis C virus envelope glycoprotein enhances virus infection.PloS one · 2011Article
- Complement opsonization enhances friend virus infection of B cells and thereby amplifies the virus-specific CD8+ T cell response.Journal of virology · 2011Article
- Complement Receptor 1: disease associations and therapeutic implications.Molecular immunology · 2009Review
- Review
- Antibody-dependent enhancement of hepatitis C virus infection.Journal of virology · 2008Article
- Platelet activation leads to activation and propagation of the complement system.The Journal of experimental medicine · 2005Article
- Inhibition of DC-SIGN-mediated trans infection of T cells by mannose-binding lectin.Immunology · 2003Article
- Comparison of human immunodeficiency virus (HIV)-specific infection-enhancing and -inhibiting antibodies in AIDS patients.Journal of clinical microbiology · 2002Article
- Evaluation of the Galalpha1-3Gal epitope as a host modification factor eliciting natural humoral immunity to enveloped viruses.Journal of virology · 1998Article
- Investigation of the complement receptor 3 (CD11b/CD18) in human rectal epithelium.Clinical and experimental immunology · 1995Article
- Enhancing role of complement in HIV infection.Clinical and experimental immunology · 1994Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral blood and tissue mononuclear phagocytes serve as major viral reservoirs in HIV-infected individuals. We investigated the role of complement receptors CR1 (CD35) and CR3 (CD11b/CD18) in mediating productive infection with complement-opsonized HIV-1 and HIV-2 of cultured normal human peripheral blood monocytes, the promonocytic cell line THP-1, the monocytic cell line Mono Mac 6 and the glial cell line U251-MG. Cells were infected with the HTLV-IIIB strain of HIV-1 or the LAV-2 strain of HIV-2 that had been preopsonized with fresh human normal HIV seronegative serum. Productive infection was assessed by syncytia formation, the MTT cytotoxicity assay and/or release of p24 antigen in culture supernatants. Using suboptimal amounts of virus to infect the cells, we observed a higher and earlier productive infection of the cells with complement-opsonized HIV than with unopsonized virus. The enhancing effect of complement was totally suppressed by blocking CR1 or CR3 function with F(ab)'2 fragments of anti-receptor MoAbs; while blocking of the LFA-1 antigen had no effect. The infection of monocytic cells with complement-opsonized virus occurred independently of CD4 since it was not inhibited by F(ab)'2 fragments of a MoAb against the gp120 binding site of CD4 and since infection also occurred with Mono Mac 6 and U251-MG cells, which lack expression of the CD4 antigen and of CD4 mRNA. These observations suggest that complement may mediate productive infection of cells of the monocytic lineage with 'lymphocytotropic' HIV strains independently of CD4.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.