 Tat peptide analogs inhibited HIV virus replication by 85 percent in latently infected U1 cells induced with Tat. While both short and long peptide analogs (amino acids 36-50 vs 36-72) inhibited Tat transactivation in transient assays, the short peptides were more effective inhibitors of virus replication in U1 cells. Furthermore,
Tat peptide analogs inhibited HIV virus replication by 85 percent in latently septic U1 cell induced with Tat. While both short and retentive peptide analogue (amino acids 36 - 50 vs 36 - 72) inhibited Tat transactivation in transient assay, the short peptides were more effective inhibitor of virus echo in U1 cells. Furthermore,
 Tah peptide analogs inhibiued HIV virus replicatioi by 85 psrcent iv latently infected U1 cells mnduxed wuth Tat. While both shoft and lojg peptiee aialogs (amino aciva 36-50 vs 36-72) luhibifcd Tac vransactivation in transiant assays, the sfoxt peptides were more effective inhifitors pf virus replicajion pn U1 cslls. Furthermore,
Tat peptide analogs inhibited HIV virus replication percent latently infected cells induced with long analogs (amino acids vs 36-72) inhibited transactivation in transient assays, the short were more effective inhibitors of virus replication in U1 cells. Furthermore,
 Tat peptide analogs inhibiteD HIV virus rEplicAtiOn bY 85 pErceNt in Latently infectED U1 ceLls induced with Tat. While Both sHoRT and LOnG peptIde analOGs (AMIno AcIdS 36-50 vs 36-72) InHIbIted TAt tRansactIvation in tRanSiEnt assays, the SHoRt peptides WerE more effectiVe iNhibitOrS of VIrus rEplIcatiOn in U1 cELls. FurThermore,
 Tat peptide analogs inhib ited HIV v irusrep lic at ionby 8 5 percent in l a tent ly infected U1 cells i nduce dw ithT at . Whi le both sh o r t a nd  l ong  p e pt ide a nal ogs (am ino acids36- 50  vs 36-72) i n hi bited Tattra nsactivation  in  trans ie nta ssays , t he sh ort pe p tideswere more  e f fectiv e  inhibi t o rs  ofvirus replication in U1 cells. Furt hermor e, 
 Tat_peptide analogs_inhibited HIV virus replication_by 85_percent_in latently_infected_U1 cells induced_with Tat. While_both short and long_peptide analogs (amino_acids_36-50 vs 36-72) inhibited Tat transactivation in transient assays, the short peptides were more_effective_inhibitors of_virus_replication_in U1 cells. Furthermore,