The Adenovirus Productive Cycle

The adenovirus productive cycle has most usually been studied following infection of established lines of human cells, such as HeLa, with sufficiently high multiplicities of a human serotype to achieve a 

The program of viral gene expression that defines a productive infection has been subject to intense scrutiny, but will be described only briefly here the interested reader is referred to Tooze (1980), Ziff (1980), or Flint (1982) for more detailed information. Early genes, defined as those expressed prior to the onset of viral DNA replication, are expressed as six transcriptional units ElA, ElB, E2, E3, E4, 

The positions of several mutations discussed in the text are also indicated the 

In addition to the early and late genes that are expressed as mRNA and are transcribed by the host cells RNA polymerase form II, the adenoviral genome encodes two small RNA species, termed VA-RNAi and VA-RNAu. These viral genes are transcribed by RNA polymerase III. Transcription of both occurs during the early phase of infection, but that of the VA-RNAi gene accelerates once an infection enters the late phase (Soderlund et al., 1976). Indeed, VA-RNAi is produced in much larger quantities than VA-RNAn and accumulates in the cytoplasm (Mathews and Pettersson, 1978), where it is essential for the efficient translation of viral mRNA species (Thimmappaya et al., 1982). 

Indeed, the whole question of the variable responses of mammalian cells to different human adenovirus serotypes is poorly understood, despite the fascinating range of interactions displayed. The variable abilities of cells derived from different species, or different tissues, to support adenovirus replication is generally interpreted in terms of the presence, or lack of, cellular factors that the virus needs to complete various steps in the replication cycle. More precisely, putative factors that permit human adenovirus replication in human cells may be present in, say, murine cells, but sufficiently divergent that they fail to interact optimally with the relevant viral components. Thus, an understanding in molecular terms of the steps in the viral replication cycle that are blocked in non- or semipermissive cells should provide important information about the host cell components utilized by the virus and, thus, the molecular interactions among viral and cellular products. 

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