There is compelling evidence that the variant (v) form of CJD first reported in the UK in 1996 〚4〛 is caused by the BSE agent 〚5〛. Studies that are in progress to determine whether or not the vCJD agent is also relatively resistant to inactivation have not yet yielded any results. However, it seems unlikely that the vCJD agent will prove to be significantly different from other TSE agents in this respect.

The BSE-related inactivation studies referred to above were carried out using infected bovine brain-tissue. Further studies have been carried out using brain-tissue from mice infected with the 301V strain of BSE agent that was derived from the serial passage of the BSE agent in VM mice. 301V has been shown to be the most thermostable strain of TSE agent identified so far 〚6〛. It is not completely inactivated by autoclaving at 138 °C for 1 h 〚7〛, and partially survives exposure to hot air at 200 °C for 1 h 〚8〛.

Despite the failure of autoclaving or sodium hydroxide exposure to reliably inactivate TSE agents, it is known that inactivation can be achieved by combining these processes 〚7〛. The use of hot alkaline solutions has even been shown to be effective when 301V is simply boiled for 1 min in 1 M sodium hydroxide 〚9〛.

There is considerable interest in the applicability of the hot alkaline process to problems as diverse as the decontamination of specified risk materials obtained from abattoirs, and its potential to reliably inactivate CJD infectivity that could be unwittingly present on surgical instruments after their use on patients that are in the preclinical, asymptomatic phase of the disease.

In addition to the experiments described above, validation studies have been carried out with regard to the BSE agent to determine the degree of inactivation achieved by the rendering processes that had been used traditionally within the EU 〚10〛. These showed that, in the worst-case scenario, there was almost as much infectivity in the meat and bone meal as there was in the untreated, BSE-spiked raw materials. However, infectivity was not detected in the unfiltered tallow obtained from the same process. This indicates that BSE infectivity does not have a predilection to migrate into tallow during rendering, as has been suggested 〚11〛.

It is widely known that the gelatin manufacturers of Europe are currently carrying out validation studies to address the question as to whether gelatin derived from bovine bones is completely safe for consumption by, or injection into, animals or humans. These have already provided data indicating that the degree of inactivation or removal of infectivity achieved by the traditional acid or alkali processes is sufficient to provide such a reassurance, quite apart from the added confidence arising from the required exclusion of high-risk material from the manufacturing processes. These studies have also shown that the introduction of a step involving a 2-h exposure of acid-treated bone to 0.3 M sodium hydroxide appears to completely eliminate any residual BSE infectivity. 〚12〛 If there were to be any lingering doubts regarding the safety of gelatin, manufacturers could incorporate this brief sodium hydroxide treatment into their production processes to provide a higher degree of reassurance. This treatment would be equally applicable to the alkali extraction system because, in its first stages, it involves exposure to the same conditions that are applied during the acid extraction process.