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1. A Human Milk Factor Susceptible to Cathepsin D Inhibitors Enhances Human Immunodeficiency Virus Type 1 Infectivity and Allows Virus Entry into a Mammary Epithelial Cell Line

Author

Nicole Van Tieghem, Nicole Moguilevsky, Corinne Liesnard, Lise Thiry, Kamal El Messaoudi, and Alex Bollen

Subjects
viruses, Lymphocyte, Immunology, Gene Expression, Cathepsin D, Galactosylceramides, HIV Envelope Protein gp120, Biology, Microbiology, CXCR4, Virus, chemistry.chemical_compound, Receptors, HIV, Viral entry, Virology, Pepstatins, Tumor Cells, Cultured, medicine, Animals, Humans, Breast, RNA, Messenger, skin and connective tissue diseases, Cathepsin, Infectivity, virus diseases, Epithelial Cells, Molecular biology, Virus-Cell Interactions, Milk, medicine.anatomical_structure, chemistry, Insect Science, HIV-1, RNA, Viral, Female, Pepstatin
Abstract

Human immunodeficiency virus type 1 (HIV-1) growth in lymphocyte cultures was increased when the virus inoculum was incubated in breast milk. The enhancing effect of milk was abolished by anti-cathepsin D antibody or by pepstatin A, a cathepsin D inhibitor. The cathepsin D-producing CD4-negative MCF7 mammary cells supported the growth of some HIV-1 isolates. An MCF7 line chronically producing HIV-1 IIIb was obtained. Cathepsin D may induce conformational modification of viral gp120, allowing direct interaction with a coreceptor. We demonstrated the presence of CXCR4 mRNA in MCF7 cells.

Published
2000
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