A morbillivirus causing mass mortality in seals.

During an outbreak of a serious apparently infectious disease among harbour seals (Phoca vitulina), which started in the Kattegat area in April 1988 and rapidly spread to the North sea, the Wadden sea and the Baltic sea, greater than 17,000 animals died within a period of eight months. In August 1988 it was realized that the clinical symptoms and pathological lesions were similar to those found in canine distemper: apart from general depression and fever, the animals suffered from severe respiratory, gastrointestinal and central nervous disease and a variety of viral, bacterial and parasitic infections were frequently encountered, suggesting a severe malfunctioning of the immune system. At different expert meetings, held in several of the countries involved, possible explanations for the deaths were not only attributed to an infectious agent, but also to effects of overpopulation and environmental pollution. Seroepizootiological studies and the failure of vaccination experiments suggested that a herpesvirus and a picornavirus, which had been isolated from dead seals at the beginning of the outbreak, were opportunistic infections occurring in animals suffering from another infection rather than being the primary cause of the outbreaks. Serological studies were then extended to other viruses of carnivores, known to cause similar symptoms. Screening of a large panel of seal sera from the Netherlands, Denmark, FRG, Sweden and the UK, collected before and during the outbreak, in a virus neutralization test for the presence of canine distemper virus (CDV) neutralizing antibodies, indicated that CDV or a closely related morbillivirus was the primary cause of the disease outbreak.(ABSTRACT TRUNCATED AT 250 WORDS

Induction of neutralizing antibody in mice against poliovirus type II with monoclonal anti-idiotypic antibody.

Syngeneic monoclonal anti-idiotope antibody Ab2,2-17C3SCC was raised against an idiotope on a protective monoclonal antibody with specificity for poliovirus type II. Ab2,2-17C3SCC detects a paratope-related interspecies IdX. Ab2,2-17C3SCC purified from supernatant fluids of hybridoma cells by protein A-Sepharose was injected into 4- to 6-wk-old BALB/c mice. The sera of the mice were screened for the expression of antibodies bearing the corresponding idiotope. Immunization of mice with Ab2,2-17C3SCC induced antibodies of complementary specificity. Furthermore, micro VN tests suggest that Ab2,2-17C3SCC can substitute for antigen in the induction of anti-polio neutralizing antibodies, and hence can function as a monoclonal anti-idiotypic vaccine

SARS

Five years after the first severe acute respiratory syndrome (SARS) outbreak, several candidate SARS-coronavirus (CoV) vaccines are at various stages of preclinical and clinical development. Based on the observation that SARSCoV infection is efficiently controlled upon passive transfer of antibodies directed against the spike (S) protein of SARS-CoV, vaccines containing the S protein have been formulated. Animals immunized with inactivated whole virus vaccines or live-recombinant vaccines expressing the SARS-CoV S protein (e.g., using rabies virus, vesicular stomatitis virus, bovine parainfluenza virus type 3, adenovirus, or attenuated vaccinia virus MVA as a vector), as well as mice immunized with DNA vaccines expressing the S protein gene all developed neutralizing antibodies to SARS-CoV and were protected against SARS-CoV challenge.Although much effort has been focused on developing a SARS vaccine, the commercial viability of such a vaccine for SARS-CoV will ultimately depend on whether the virus re-emerges in the near future. This vaccine should induce highly cross-reactive neutralizing antibodies to protect against newly emerging viruses related to SARS-CoV and protect both the gastrointestinal and respiratory tract in the absence of significant side effects. Given the fact that in the previous outbreak mainly the elderly succumbed to the infection, special attention should be given to vaccines that are able to efficiently protect aged individuals

Authors' response to Hogan

In response to our Perspective on nonhuman primate models for SARS, which accompanied the article by Lawler et al., Robert Hogan questions the usefulness of nonhuman primates as good models for SARS.As demonstrated by several groups, SARS coronavirus (SARS-CoV) replicates to high titers in the respiratory tract of a surprisingly broad range of animal species, albeit showing remarkable differences in cell tropism. We have argued that efficient infection of type 1 and 2 pneumocytes as seen in macaques and humans—most likely due to the similarities in the spike protein binding domains of the host SARS-CoV receptor ACE2—is a prerequisite for the SARS-CoV infection–induced pathology observed in humans. So far there is no strong evidence that a similar tropism is observed in other animal species.[...

Authors' response to Hogan

In response to our Perspective on nonhuman primate models for SARS, which accompanied the article by Lawler et al., Robert Hogan questions the usefulness of nonhuman primates as good models for SARS.As demonstrated by several groups, SARS coronavirus (SARS-CoV) replicates to high titers in the respiratory tract of a surprisingly broad range of animal species, albeit showing remarkable differences in cell tropism. We have argued that efficient infection of type 1 and 2 pneumocytes as seen in macaques and humans—most likely due to the similarities in the spike protein binding domains of the host SARS-CoV receptor ACE2—is a prerequisite for the SARS-CoV infection–induced pathology observed in humans. So far there is no strong evidence that a similar tropism is observed in other animal species.[...