期刊
JOURNAL OF INFECTIOUS DISEASES
卷 182, 期 3, 页码 785-791出版社
OXFORD UNIV PRESS INC
DOI: 10.1086/315790
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U01AI041530] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [N01DE072621] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK047322] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI41530] Funding Source: Medline
- NIDCR NIH HHS [DE72621] Funding Source: Medline
- NIDDK NIH HHS [DK47322] Funding Source: Medline
Most human immunodeficiency virus type 1 (HIV-1) infections are acquired via mucosal surfaces, and transmitted viruses are nearly always macrophage-tropic, suggesting that mucosal macrophages participate in early HIV-1 infection. Mucosal lymphocytes isolated from normal human intestine expressed CD4 (14,530 +/- 7970 antibody-binding sites [ABSs]/cell), CCR5 (2730 +/- 1524 ABSs/cell), and CXCR4 (2507 +/- 1840 ABSs/cell), but intestinal macrophages, which also expressed CD4 (2959 +/- 2695 ABSs/cell), displayed no detectable CCR5 or CXCR4 ABS. The absence of CCR5 on intestinal macrophages was not due to expression of the Delta 32 deletion allele because matched-blood monocytes expressed CCR5. CCR5(+)CXCR4(+) intestinal lymphocytes supported both R5 (BaL) and X4 (IIIB) HIV-1 replication, whereas the CCR5(-)CXCR4(-) macrophages were not permissive to either isolate or other laboratory isolates (ADA and DJV) and primary isolates (MDR 24 and JOEL). In the intestinal mucosa, lymphocytes, not macrophages, are the likely target cell for R5 (and X4) HIV-1 and are the major source of HIV-1 production during early infection.
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