Human immunodeficiency virus type 1 causes productive infection of macrophages in primary placental cell cultures

Kathleen A. Mc Gann, Ronald Collman, Dennis L. Kolson, Francisco Gonzalez-Scarano, George Coukos, Christos Coutifaris, Jerome F. Strauss, Neal Nathanson

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48 Scopus citations

Abstract

To characterize the role of the placenta in vertical transmission of human immunodeficiency virus type 1 (HIV-1), the susceptibility of primary human placental cultures and of transformed trophoblast cell lines to infection by several HIV-1 isolates was examined. Placental cultures supported the replication of all strains tested, including lymphocyte-, macrophage-, and amphotropic isolates. All viruses replicated to modestlevels, with production of both viral antigen and infectious virus in the culture supernatants. Placental cells demonstrated a pattern of permissiveness for HIV-1 isolates distinct from that seen with lymphocytes, blood-derived macrophages, or T cell lines. Immunofluorescent staining showed that 5%-10% of the cultured placental cells expressed viral antigens, and double labeling revealed that the HIV-positive cells were macrophages not trophoblasts. None of the trophoblast cell lines (JEG-3, Jar, BeWo, HP-W1) could be infected by HIV. These results support the hypothesis that infection ofthe placenta could playa role in maternofetal transmission of HIV-1 and suggest that the placental macrophage is likely to be the primary cell type responsible.

Original languageEnglish (US)
Pages (from-to)746-753
Number of pages8
JournalJournal of Infectious Diseases
Volume169
Issue number4
DOIs
StatePublished - Apr 1994

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

Cite this

Mc Gann, K. A., Collman, R., Kolson, D. L., Gonzalez-Scarano, F., Coukos, G., Coutifaris, C., Strauss, J. F., & Nathanson, N. (1994). Human immunodeficiency virus type 1 causes productive infection of macrophages in primary placental cell cultures. Journal of Infectious Diseases, 169(4), 746-753. https://doi.org/10.1093/infdis/169.4.746