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HIV infection of CD45RA + and CD45RO + CD4 + T cells
Author(s) -
HELBERT M. R.,
WALTER J.,
L'AGE J.,
BEVERLEY P. C. L.
Publication year - 1997
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1997.280-ce1170.x
Subject(s) - biology , immunology , syncytium , population , antigen , virology , microbiology and biotechnology , virus , medicine , environmental health
HIV preferentially infects the RO + memory subset of CD4 + lymphocytes, and these cells are lost earlier in HIV infection than their RA + counterparts. Although both populations express similar amounts of CD4 and bind the HIV envelope glycoprotein (gp120) equally well, calcium signals and CD4 down‐regulation subsequent to gp120 binding are not the same in both populations. Data suggest these disparities are mediated by differential tyrosine kinase (TK) regulation. Syncytium formation is enhanced in RO + cells, partly a consequence of increased leucocyte function antigen‐1 (LFA‐1) expression and, again, partly due to altered TK regulation. After in vitro HIV infection, reverse transcription is not detected in RA + cells, is minimal in the RO + class II − population, but progresses well in RO + class II + . Infection followed by mitogen stimulation permits reverse transcription in all cells. HIV infection of RO + cells is enhanced moderately at multiple points in the virus life cycle.

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