Abstract:
:The expression of HLA class II genes is under the control of a transcriptional activator, CIITA, encoded by the AIR-1 locus. Here we show that CIITA inhibits HIV-1 LTR transactivation mediated by Tat. The inhibition occurred when CIITA and Tat were transiently expressed in cells after transfection and, most importantly, when tat cDNA was transfected in cells expressing CIITA in a constitutive fashion and at physiological levels. Furthermore, CIITA inhibited the HIV-1 LTR transactivation mediated by extracellular Tat protein. CIITA inhibition of Tat function could be reversed by overexpression of Cyclin T1, the cellular cofactor used by Tat to facilitate elongation of viral transcripts. CIITA inhibition of Tat function had a dramatic effect on HIV-1 productive infection of human T cells because CIITA(+) T cells supported very poorly, if any, viral replication. These results indicate that sustained expression of CIITA in HIV-1-susceptible targets may down-regulate viral expression both in cells actively replicating the virus and in silently infected cells requiring exogenous Tat to reactivate virus from latency.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Accolla RS,Mazza S,De Lerma Barbaro A,De Maria A,Tosi Gdoi
10.1002/1521-4141(2002010)32:10<2783::AID-IMMU2783keywords:
subject
Has Abstractpub_date
2002-10-01 00:00:00pages
2783-91issue
10eissn
0014-2980issn
1521-4141journal_volume
32pub_type
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