Am. J. Respir. Cell Mol. Biol., Vol 16, No. 4, 04 1997, 421-428.
Mediation of entry of human immunodeficiency virus-1 into alveolar macrophages by CD4 without facilitation by surfactant-associated protein-A
LA Guay, JG Sierra-Madero, CK Finegan and EA Rich
Department of Pediatrics, Case Western Reserve University, Cleveland, Ohio 44106-4984, USA.
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-1(JR-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-1(JR-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.
