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Posttranscriptional regulation of US11 in cells infected with a herpes simplex virus 1 recombinant lacking both 222-bp domains containing S-component origins of DNA synthesis.

The US11 gene of herpes simplex virus 1 maps in the unique sequences of the short component of the HSV-1(F) genome approximately 775 bp from the center of the DNA replication origin (OriS) and encodes a virion protein which binds RNA in sequence- and conformation-specific fashion, negatively regulates the accumulation of a prematurely terminated transcript of UL34, associates in the infected cell with the 60S ribosomal subunit, and, late in infection, accumulates in nucleoli. We report the following: (i) Deletion of a 222-bp sequence including OriS (DeltaOriS) negatively affected the accumulation of the US11 protein without decreasing the accumulation of the US11 transcript. (ii) The defect, observed at all times after infection, was multiplicity independent, was unrelated to US11 protein stability, and apparently resulted from a cis-acting element since a coinfecting virus was unable to complement the DeltaOriS virus. (iii) Transcription from the US11 promoter initiated from three sites on the DeltaOriS virus. Transcripts initiated from two of the three initation sites accumulated similarly in cells infected with the DeltaOriS virus or wild-type parent virus. The low-abundance transcript initiating from the third site was apparently unique to the DeltaOriS virus but was not expected to alter the coding capacity of the mRNA. (iv) Infected cells accumulated RNA derived by antisense transcription of the genome domain containing the US11 gene. One transcript accumulated in larger amounts in cells infected with the DeltaOriS virus than in cells infected with parent or repaired virus.