Increased MHC H-2K gene transcription in cultured mouse embryo cells after adenovirus infection

The class I major histocompatibility complex (MHC) antigens are highly polymorphic¹ cell-surface proteins² whose expression is essential for the cellular immune response against virus-infected, abnormal and foreign cells^3,4. Transformation of primary rat cell cultures by the oncogenic adenovirus 12 (Ad 12) results in suppression of the transplantation antigens⁵, thus enabling the transformed cells to escape the immune response and efficiently form tumours in vivo⁶. In contrast, transformation of the same cells with the non-oncogenic adenovirus 5 (Ad5) does not suppress the transplantation antigens⁵ and, consequently, they elicit an effective (MHC-restricted) immune response⁶. Here, however, we show that infection of mouse embryo cells with both viruses initially increases the level of transcripts from the H-2K^b transplantation antigen gene. Both the adenovirus E1a (12S RNA) and E1b genes are required for activation of the H-2K gene and measurement of the relative rate of transcription indicates that the increase in the level of H-2K messenger RNA following infection is at least in part due to a gene-specific transcriptional activation. The newly transcribed H-2K^b mRNA is then properly transported to the cytoplasm