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Our knowledge of molecular events of virus replication in infected cells is related to the genome structure and transcription and to the function of virus coded proteins based on studies in vitro. On other hand, classical investigations of virus pathogenesis take advantage of morphological studies at the level of light and/or electron miscroscopy, using labeled monospecific and/or monoclonal antibodies. On the example of 4 herpesviruses (pseudorabies virus, herpes simplex virus 1, murine herpesvirus and Epstein Barr virus), from which 2 are human pathogens while the another 2 are natural animal pathogens, the former are Alphaherpesviruses, while the latter are members of the subfamily of Gammaherpesviruses, the author interpretes the molecular results aiming to explain the behaviour of corresponding viruses in vivo. A striking discrepance promoting the authors way of thinking was that some virion components or proteins encoded by the virus are not essential for replication in vitro, even though they are inevitable tools of its virulence in vivo. The same is true for evasion proteins, helping the virus to avoid the immune response, which may be deleted in the course passaging.
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