A mechanism of resistance to HIV-1 entry: inefficient interactions of CXCR4 with CD4 and gp120 in macrophages.
To test the hypothesis that inefficient interactions of CXCR4 with CD4 and gp120 could affect HIV-1 entry, we incubated macrophages, monocytes, and lymphocytes with gp120 and coimmunoprecipitated CD4 by using anti-CXCR4 antibodies. CD4 was efficiently coimmunoprecipitated in lymphocytes and monocytes but not in macrophages. Overexpression of CD4 in macrophages resulted in detection of CD4-CXCR4 and gp120-CD4-CXCR4 complexes in parallel with the restoration of macrophage fusion susceptibility. These results suggest a mechanism of resistance to entry of some X4 HIV-1 strains into macrophages and a method for dissection of the initial stages of HIV entry.
Dimitrov
D S
DS
NCI-FCRDC, NIH, Frederick, Maryland, 21702-1201, USA.
Norwood
D
D
Stantchev
T S
TS
Feng
Y
Y
Xiao
X
X
Broder
C C
CC
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D015704:CD4 Antigens / Q000276:immunology*; D015699:HIV Envelope Protein gp120 / Q000276:immunology*; D015497:HIV-1 / Q000502:physiology*; D006367:HeLa Cells; D006801:Humans; D007113:Immunity, Innate; D008264:Macrophages / Q000276:immunology* / Q000821:virology*; D019718:Receptors, CXCR4 / Q000276:immunology*; D014779:Virus Replication / Q000276:immunology
D015704:CD4 Antigens; D015699:HIV Envelope Protein gp120; D019718:Receptors, CXCR4