The animal lentiviruses, equine infectious anemia virus (EIAV) and caprine arthritis and encephalitis virus (CAEV) are being studied to better understand regulation of the lentivirus life cycle and the molecular basis for viral persistence and pathogenesis. The pattern of transcription of the EIAV genome in cultured cells was found to be much more complex than expected on the basis of analysis of the viral genome. A cDNA encoding the tat protein was found to be polycistronic. Surprisingly, the tat open reading frame did not commence with an AUG codon, suggesting that the synthesis of EIAV gene products may be regulated post-transcriptionally. Several other cDNAs active in transactivation assays were isolated and analysis of these clones is in progress. These and other studies localized the functional exon of the tat gene to ORF Sl of the EIAV genome. Virus derived from an infectious molecular clone of EIAV was serially passaged in ponies. Although the virus established an infection. no symptoms typical of EIA were detected. Nucleotide sequence analysis of this clone revealed some differences in its LTR sequences compared to those previously published for noninfectious clones. The pattern of transcription of CAEV has been determined and mRNAs encoding tat and rev have been identified. Defective viral genomes are characteristic of CAEV infections. Analysis of integrated and unintegrated molecular clones of CAEV and CAEV virion RNAs has revealed that deleted genomes can integrate and that their RNA products can be packaged into virions. The genome of the lymphoproliferative disease virus of turkeys (LPDV) is being characterized. Transcriptional control signals within the viral LTR were determined by functional assays, and nucleotide sequencing revealed that LPDV is most closely related to avian leukosis virus. Evidence was obtained indicating that LPDV may induce disease by affecting the expression of K-ras.
