Abstract:
:The pathogenesis of the decline of CD4 lymphocyte counts accompanying the typical course of HIV-1 infection is not completely defined and might be related to a differential susceptibility of naive and memory cells to HIV-1 exposure. Here, we examined the effects induced by heat-inactivated HIV-1 virions on these lymphocyte populations. Exposure of CD45RA naive T cells to inactivated viral particles induced a marked decrease of both mitogenic responses and activation-induced apoptosis. Conversely, the growth of CD45RO cells was less severely restrained. Analysis of intracellular levels of cell cycle regulatory proteins revealed an arrest at the G1/S restriction point of the naive but not memory subset. This effect was associated with alterations in phosphotyrosine profile and with a marked decrease of ERK and NJK kinase activation. Finally, up-regulation of the cAMP-dependent protein kinase A (PKA) activity induced by mitogens was not affected by virus. Altogether, these findings show that interaction of HIV-1 with the T cell surface is sufficient to inhibit the proliferative response of the CD4CD45RA subset by disturbing proximal TCR signaling. This mechanism would affect renewal of naive lymphocytes, contributing in such a way to the impairment of T cell turnover during the course of HIV-1 infection.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Masci AM,Paz FL,Borriello A,Cassano S,Della Pietra V,Stoiber H,Matarese G,Della Ragione F,Zappacosta S,Racioppi Ldoi
10.1002/(SICI)1521-4141(199906)29:06<1879::AID-IMMkeywords:
subject
Has Abstractpub_date
1999-06-01 00:00:00pages
1879-89issue
6eissn
0014-2980issn
1521-4141journal_volume
29pub_type
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