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Preparing populations for health threats, including threats from new or re-emerging infectious diseases is recognised as an important public health priority. The development, production and application of emergency vaccinations are the important measures against such threats. Vaccines are cost-effective tools to prevent disease, and emergency vaccines may be the only means to prevent a true disaster for global society in the event of a new pandemic with potential to cause morbidity and mortality comparable to the Spanish flu, the polio epidemics in the 1950s, or the SARS outbreak in 2003 if its spread had not been contained in time. Given the early recognition of a new threat, and given the advances of biotechnology, vaccinology and information systems, it is not an unrealistic goal to have promising prototype vaccine candidates available in a short time span following the identification of a new infectious agent; this is based on the assumption that the emerging infection is followed by natural immunity. However, major bottlenecks for the deployment of emergency vaccine are lack of established systems for fast-track regulatory approval of such candidates and limited international vaccine production capacity. In the present discussion paper, we propose mechanisms to facilitate development of emergency vaccines in Europe by focusing on public–private scientific partnerships, fast-track approval of emergency vaccine by regulatory agencies and proposing incentives for emergency vaccine production in private vaccine companies.

The widespread medical and veterinary importance of Coronaviruses provided the initial reason for studying these viruses at the molecular level. However, two unusual features of the viral life cycle are of particular interest for “pure” molecular biology. First, the intracellular budding site of Coronaviruses, apparently associated with the restricted intracellular distribution of the E1 glycoprotein1 suggests that this protein may provide a model to study the transport and sorting of membrane proteins of the endoplasmic reticulum and Golgi apparatus. Secondly, the unusual “nested set” structure of the viral RNA’s2,3,4,5(Spaan et al., this volume) implies a replication mechanism unlike that of other RNA viruses.

A reaction stimulated by elongation factor 2 (EF-2) is necessary for the formation of the initial peptide-bond in poly(U)-directed peptide synthesis on yeast ribosomal subunits. The stimulation is inhibited by fusidic acid or diphtheria toxin together with NAD. It is assumed that the reaction of EF-2 represents translocation: in the presence of EF-2 almost twice the amount of N-acetyl-phenylalanyl-tRNA is bound to ribosomes and moreover, upon addition of puromycin a considerable stimulation of N-acetyl-phenylalanyl-puromycin formation is found. Contradictory data in the literature on this subject may be due to nonenzymatic translocation caused by a high monovalent cation concentration in the ribosome preparations or to an unspecific method for the extraction of N-acetyl-phenylalanyl-puromycin.

One of the most striking differences between coronaviruses and other enveloped RNA viruses is that they bud into intracellular membranes. Only bunyaviruses behave similarly (1). Coronavirions have been observed in the lumens of endoplasmic reticulum (ER) and Golgi apparatus from cells infected with various coronaviruses such as mouse hepatitis virus (MHV) (2–5), avian infectious bronchitis virus (IBV) (6) and porcine enteric Coronavirus (7) The assembled virions then appear in smooth-walled vesicles en route to the plasma membrane (PM) where they are probably released from the cell by exocytosis (4,8).

Temperature-sensitive (ts) mutants of mouse hepatitis virus (MHV-A59) are drastically attenuated in their pathogenic properties: intracerebral inoculation of mice with mutants results in more prolonged infection of the central nervous system without clinical signs (Koolen et al., 1983, Virology 125, 393–402). This was surprising in the case of mutant ts–342 which was “leaky” and grew well in tissue culture cells at 37°C. We have studied the replication of mutant ts–342 in primary cultures of mouse brain Open image in new window Fig. 1 Growth kinetics of MHV-A59 and its mutant ts-342 in Sac(−) cells (A) or in mouse brain cells (B). The cells were infected with 50 PFU/cell. cells, derived from approximately 14-day-old Balb/c mouse embryos. Cultures became confluent after seven days. The cells were identified as astrocytes since they contained glial fibrillary acidic protein (GFAP).