Jang, Kyung-Lib; (1991) The effect of HSV infection on cellular transcription factors. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

Infection with herpes simplex virus (HSV) suppresses most cellular gene expression rapidly in the early stage of virus infection. However, this virus also increases gene expression from a few cellular genes such as those encoding heat shock proteins. It is not clear how such effects occur. Alu repeats were induced at the transcriptional level by the action of HSV immediate early (IE) protein ICP27. This effect was mediated through increasing the activity of transcription factor IIIC (TFIIIC) which is the limiting factor for RNA polymerase III (po1III) transcription. This increased activity of TFIIIC appeared to occur by increasing its abundance. Also, other viral transactivators such as adenovirus (Ad) E1A protein, pseudorabies virus (PRV) immediate- early protein, and human immunodeficiency virus (HIV) Tat protein showed the same effect on the expression of Alu repeats to that seen in HSV infection. On the other hand, HSV also produced profound effects on the RNA polymerase II transcription system. HSV increased the activity of a few cellular transcription factors such as AP-1 and NFkB. In contrast, no increase in the activity of several other transcription factors such as Oct-1, Sp1, or ATF was observed. The up-regulation of AP-1 activity appeared to occur through increasing the concentration of c-Jun and possibly c-Fos probably at the transcriptional level by the action of the HSV IE protein ICPO. The significance of the induced pol III gene expression during infection with various viruses is discussed. Also, it is suggested these HSV-induced cellular proto-oncogenes play a role in the regulation of viral and cellular gene expression during lytic infection, and particularly during the processes of cell transformation and herpes virus latency.

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