Defective processing of human adenovirus 2 late transcription unit mRNAs during abortive infections in monkey cells.
Growth of human adenoviruses is severely restricted in monkey cells. We examined the synthesis of mRNAs from the Ad2 late transcription unit (LTU) in abortively infected monkey cells at late times in infection. All L2, L3, and L5 mRNAs were absent or drastically reduced in abortive infections. Most L1 and L4 mRNAs were also greatly decreased in abortive infections; however, a single large messenger was produced from each of the L1 and L4 families, at levels approaching those found in productive infections. The pattern of i-leader containing mRNAs was also changed in abortive infections. These defects could be corrected in monkey cells by the presence of SV40 T antigen or an altered adenoviral DNA binding protein. These defects in late gene expression in abortive infections could not be attributed to differences in transcription along the LTU or levels of DNA replication. In abortively infected cells, nuclear levels of L5 mRNA were decreased 2 to 6 fold, while cytoplasmic levels were decreased over 200-fold. These findings imply a general defect in processing of viral mRNAs, most likely due to defective splicing and/or transport, during abortive infections.
Ross
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Kaplan Cancer Center, New York University Medical Center, New York 10016.
Ziff
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D000260:Adenoviruses, Human / Q000235:genetics* / Q000502:physiology; D000818:Animals; D001483:Base Sequence; D015152:Blotting, Northern; D002460:Cell Line; D004261:DNA Replication; D004279:DNA, Viral / Q000096:biosynthesis; D000882:Haplorhini; D006367:HeLa Cells; D006801:Humans; D012323:RNA Processing, Post-Transcriptional; D012333:RNA, Messenger / Q000378:metabolism; D012367:RNA, Viral / Q000378:metabolism*; D014158:Transcription, Genetic; D014779:Virus Replication / Q000235:genetics
D004279:DNA, Viral; D012333:RNA, Messenger; D012367:RNA, Viral