This article reviews available data and mechanisms regarding the thermal inactivation of a number of important pathogenic animal viruses in comparison with relevant surrogate viruses. Data obtained from over fifty years of research is reviewed with respect to heat inactivation conditions, testing methods, and the mechanisms of virus heat inactivation for the most significant animal virus pathogens. The mechanisms of heat inactivation are described based on fundamental studies of virus particle integrity derived from structural studies of virus cell entry and virus disassembly. The mechanism of the heat inactivation of the ssRNA poliovirus was determined from cell entry studies showing that Polio Virus (PV) heat treatment results in step-wise antigenic changes and eventual exposure of the viral nucleic acids without capsid disassembly. A similar model is apparent for the ssDNA parvovirus, however, these models differ from foot and mouth disease virus showing that thermal inactivation is accompanied by capsid disassembly. Cultured viruses when assayed in solution were generally inactivated by heating to 71 °C for one minute but may be more resistant to dry heat. In general enveloped viruses were more sensitive to heat inactivation than non-enveloped viruses. Amongst the most heat resistant viruses reported were the small DNA viruses including parvoviruses and circoviruses. The important enveloped animal virus pathogens such as highly pathogenic avian influenza and Newcastle disease virus were heat sensitive. However there were few data that showed a direct comparison between the inactivation of different viruses within the same matrix. Graphical representations of virus thermal inactivation kinetics usually show tailing effects and deviation from log-linear inactivation kinetics. Tailing may result from experimental error, virus aggregation, matrix effects, or the transfection of viral nucleic acids.