Mechanisms underlying the diverse pathogenic effects of HLTV-I infection are not well understood. The present studies are designed to investigate interactions between viral products and host cell processes. Previous studies in the LIG involve two HTLV-I infected rabbit cell lines RH/K30 and RH/K34. Upon injection into rabbits, RH/K34 causes lethal experimental leukemia and RH/K30 mediates asymptomatic infection. Molecular clones, K30p and K34p, were derived from the cell lines and functional studies have shown that the molecular clone K30p mediates persistent infection both in vitro and in vivo, whereas K34p does not. The pX region of K30 was shown to play a central role in the ability of the molecular clones to produce persistent infection. Sequence differences between K30p and K34p include two nucleotide substitutions in the pX region that produce replacement substitutions in p13 and p30 products. Clones containing either of the individual pX region substitutions corresponding to the K34 sequence transiently produced low levels of virus. The focus of these studies is to compare functions of p13 and p30 from these two HTLV-1 molecular clones. The yeast two-hybrid system was employed to identify cellular proteins that physically interact with p13 and p30 from K30p and K34p.A cDNA library prepared from RH/K30 was screened with p13 from K30p or p13 from K34p as bait. None of the clones selected in the library screen using p13 from K30p as bait were found to specifically interact. Some of the clones selected had autotranscription activity or they encoded proteosome components that are often observed to give false positive reactions in the yeast two-hybrid system. Two groups of clones were identified as interacting with specifically with p13 from K34p and not p13 from K30p. The clones have been sequenced and alignments have been performed with Genbank sequences. Although both clones showed certain homologies with sequences in the data bank, both cDNA represent novel sequences.
