Herpes simplex virus-type adenovirus infected cells

Halford WP, Kemp CD, Isler JA, Davido D.I. Schaffer PA (2001) ICPO, ICP4, or VP16 expressed from adenovirus vectors induces reactivation of latent herpes simplex virus type I in primary cultures of latently infected trigeminal ganglion cells. J Virol 75 6143- 6153 He B, Gross M, Roizman B (1997) The gamma(l)34.5 protein of herpes simplex virus 1 complexes with protein phosphatase 1 alpha to dephosphorylate the alpha subunit of the eukaryotic translation initiation factor 2 and preclude the shutoff of protein synthesis by double-stranded RNA-aetivated protein kinase. Proc Natl Acad Sci USA 94 843-848... 

As already indicated adsorption, penetration, and uncoating of AAV do not require helper virus and purified DNA is infectious but requires helper. However, in the absence of helper no DNA or RNA synthesis is detected. Therefore, a helper function (s) appears to be required to initiate AAV-specific nucleic acid synthesis. Co-infection with herpes simplex virus type 1 (HSV-1) also serves to allow AAV DNA or RNA synthesis (Boucher et al., 1971 Rose and Koczot, 1972). The extent of AAV nucleic acid synthesis appeared to be comparable with either HSV or adenovirus as the helper. AAV DNA synthesized in the presence of HSV has been reported to be infectious (Boucher et al., 1971). Additionally, AAV antigens in cells co-infected with HSV are detectable by means of a fluorescent antibody staining technique (Atchison, 1970 Blacklow et al, 1970 Blacklow et al, 1971 Johnson et al., 1972). However, no infectious particles can be recovered with HSV as the helper. Interestingly, antisera to both AAV-specific SDS-polypeptides and virion protein stain the infected cells. 

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