Abstract:
:In vivo infection with human immunodeficiency virus type 1 (HIV-1) leads to gradual depletion of CD4+ T lymphocytes from the peripheral blood and later from the lymphoid organs. The mechanism of CD4 cell depletion is not known. HIV can only replicate in dividing lymphocytes, but greater than 98% of the lymphocytes in vivo at any given time are resting and are not permissive for productive infection. We found that exposure of resting CD4+ T lymphocytes to HIV-1 transiently upregulated expression of cell surface CD62L (L-selectin), the receptor for homing to lymph nodes, with concomitant enhanced ability of these cells to bind to lymph node high endothelial venules in an ex vivo homing assay (increased approximately 12-fold, P < 0.001) and to home from the blood into lymph nodes following intravenous injection into SCID mice. This suggested the possibility that decreases in numbers of CD4+ T lymphocytes in the blood of HIV-1-infected subjects may reflect enhanced homing of abortively infected, resting lymphocytes into lymph nodes rather than direct virus replication in and killing of these cells, and may explain development of lymphadenopathy at a time when numbers of CD4+ T lymphocytes in the blood fall.
journal_name
Virologyjournal_title
Virologyauthors
Wang L,Robb CW,Cloyd MWdoi
10.1006/viro.1996.8397subject
Has Abstractpub_date
1997-02-17 00:00:00pages
141-52issue
2eissn
0042-6822issn
1096-0341pii
S0042-6822(96)98397-Xjournal_volume
228pub_type
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