The modelling of infectious diseases in experimental animals provides useful information on the pathogenesis of the disease. A recent article by Wiles and co-authors discuss the limitations of animal models for investigation into bacterial diseases1. However, we believe that the picture is considerably more complicated for viral pathogens. The fact that many bacteria can multiply without a host cell, whereas viruses always require a host cell for replication, underlines one aspect of the complexity of viral pathogenesis. In addition, although we have experimental models for several viral diseases, in many instances, the pathogenic process in experimental animals is different from that observed in the natural host. For example, the foot and mouth disease virus causes vesicular disease in its natural hosts, including cattle, swine and other ruminants. In mice, however, the virus causes encephalitis, therefore it is difficult to judge the consequence of viral infection as compared with the course of disease in the natural host. Although the generation of transgenic mice can provide some advantages, the involvement and co-operation of other receptors or molecules cannot be addressed with these transgenic models.
As is well established, several factors in the environment, other than host itself, influence the outcome of a viral disease. It is therefore difficult to reproduce all of these factors under controlled laboratory conditions. For example, an influenza virus can jump between species such as chicken, swine, cattle, horse and human, and can do so at any time. While jumping between species, the virus undergoes mutations to adapt to a new host. The domestication of the above animal species in south-east Asian countries has been an important reason for the emergence of novel influenza viruses in this region. In addition, the severity of the virus infection in humans can also depend on the propagation of the virus in other hosts before spreading to humans.
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