Recent studies have shown that decreased TFIIB levels do not affect transcription levels within cells, this is thought to be partially because over 90% of mammalian promoters do not contain a BRE or TATA box. However, it has been shown that TFIIB is vital to the in vitro transcription and regulation of the herpes simplex virus. This is thought to be due to similarity TFIIB has to cyclin A. In order to undergo replication, viruses often stop host cells progression through the cell cycle, using cyclins and other proteins. As TFIIB has a similar structure to cyclin A it has been suggested that depleted levels of TFIIB could have antiviral effects.