Mediation of Entry of Human Immunodeficiency Virus-1 into Alveolar Macrophages by CD4 without Facilitation by Surfactant-associated Protein-A

Laura A. Guay, Juan G. Sierra-Madero, Candace K. Finegan, Elizabeth A. Rich

Research output: Contribution to journalArticlepeer-review

Abstract

The mechanism of uptake of human immunodeficiency virus-1 (HIV-1) into alveolar macrophages (AM), freshly isolated blood monocytes (MN), and cultured MN (CM) was investigated focusing on the role of CD4 and of surfactant-associated protein A (SP-A). By radioimmunoassay which obviated the problems of auto- and nonspecific fluorescence of more differentiated macrophages, each of the macrophage populations studied expressed CD4. Semiquantitative polymerase chain reaction was performed to assess uptake of HIV-1JR-FL into cells. OKT4a (directed against CD4) blocked uptake of HIV-1 into CM, AM, and MN by 67 to 100%. OKT4 (directed against another epitope of CD4) had a smaller and less consistent effect (0-90%), and control antibodies showed minimal effects and only at supersaturating concentrations. SP-A had no effect on uptake of HIV-1 into AM. SP-A also had no consistent effect on production of HIV-1JR-FL by AM infected in vitro (p24 antigen ELISA). Thus CD4 is the major receptor for HIV-1 in mononuclear phagocytes, including AM, and SP-A does not modulate entry.

Original languageEnglish (US)
Pages (from-to)421-428
Number of pages8
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Volume16
Issue number4
StatePublished - 1997
Externally publishedYes

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Pulmonary and Respiratory Medicine

Fingerprint Dive into the research topics of 'Mediation of Entry of Human Immunodeficiency Virus-1 into Alveolar Macrophages by CD4 without Facilitation by Surfactant-associated Protein-A'. Together they form a unique fingerprint.

Cite this