A human milk factor susceptible to cathepsin D inhibitors enhances human immunodeficiency virus type 1 infectivity and allows virus entry into a mammary epithelial …

K El Messaoudi, LF Thiry, C Liesnard… - Journal of …, 2000 - Am Soc Microbiol
K El Messaoudi, LF Thiry, C Liesnard, N Van Tieghem, A Bollen, N Moguilevsky
Journal of Virology, 2000Am Soc Microbiol
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 …
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.
American Society for Microbiology