The ability of rabbit hemorrhagic disease virus to agglutinate human erythrocytes and to attach to rabbit epithelial cells of the upper respiratory and digestive tracts was shown to depend on the presence of ABH blood group antigens. Indeed, agglutination was inhibited by saliva from secretor individuals but not from nonsecretors, the latter being devoid of H antigen. In addition, erythrocytes of the rare Bombay phenotype, which completely lack ABH antigens, were not agglutinated. Native viral particles from extracts of infected rabbit liver as well as virus-like particles from the recombinant virus capsid protein specifically bound to synthetic A and H type 2 blood group oligosaccharides. Both types of particles could attach to adult rabbit epithelial cells of the upper respiratory and digestive tracts. This binding paralleled that of anti-H type 2 blood group reagents and was inhibited by the H type 2-specific lectin UEA-I and polyacrylamide-conjugated H type 2 trisaccharide. Young rabbit tissues were almost devoid of A and H type 2 antigens, and only very weak binding of virus particles could be obtained on these tissues. Rabbit hemorragic disease virus (RHDV) is a noncultivablecalicivirus that infects rabbits and causes epidemics of an acute fatal hepatitis. The disease is characterized by high morbidity and mortality rates for adult animals. Death is the result of a widespread circulation dysfunction associated with disseminated intravascular coagulation and necrotizing hepatitis lesions (14, 24). Large quantities of virus particles are found in several organs, especially the liver, which is considered the major site of virus replication (6,14,19,27). The viral genome consists of a single-stranded RNA of nearly 7.5 kb, packaged in a small icosahedral capsid (3, 15). The capsid protein has an estimated molecular mass of 60 kDa (VP60) (16), and expression of the corresponding cDNA in insect cells infected with a recombinant baculovirus yields a protein that spontaneously assembles into virus-like particles (VLPs). These VLPs are both antigenically and morphologically similar to native RHDV particles (11,23). Yet very little is known about the pathogenesis of naturally occurring RHDV infections, and identification of the cellular receptor(s) used by the virus to establish infection would lead to a better understanding of the pathogenesis of RHDV.RHDV is known to agglutinate human erythrocytes (2, 25), and previous studies demonstrated that its hemagglutinin receptor on human red blood cells corresponds to a developmental antigen which is not expressed on fetal cells and is mainly carried by polyglycosylceramides (26). The glycolipid nature of the receptor on human red blood cells suggests that the carbohydrate moiety could be recognized by the virus capsid protein. Carbohydrate antigens of the histo-blood group family are developmental antigens that can be shared among various mammal species, and the presence of some of these antigens has been detected on epithelial cells of the rabbit digestive tract (1,17,21...

No abstract

New vaccine strategies are needed for the prevention of leptospirosis, a widespread human and animal disease caused by pathogenic leptospires. Our previous work determined that a protein leptospiral extract conferred cross-protection in a gerbil model of leptospirosis. The 31-to 34-kDa protein fraction of Leptospira interrogans serovar autumnalis was shown sufficient for this purpose. In the present study, N-terminal sequencing of a 32-kDa fraction and Southern blotting of genomic DNA with corresponding degenerated oligonucleotide probes identified two of its constituents: hemolysis-associated protein 1 (Hap1) and the outer membrane Leptospira protein 1 (OmpL1). Adenovirus-mediated Hap1 vaccination induces significant protection against a virulent heterologous Leptospira challenge in gerbils, whereas a similar OmpL1 construct failed to protect the animals. These data indicate that Hap1 could be a good candidate for developing a new generation of vaccines able to induce broad protection against leptospirosis disease.

No abstract

Many studies have implicated fresh water as a source of leptospirosis outbreaks. To estimate the survival and the preservation of the virulence of pathogenic Leptospira spp. maintained in water, we selected five still waters with various pH and mineral profiles. The water samples were artificially inoculated with a culture of a pathogenic strain belonging to serovar Icterohaemorrhagiae. Samples were stored for 20 months at 4, 20 or 30 °C. The survival and preservation of virulence of this pathogenic strain was estimated by subculturing these stored samples. After 14 and 20 months of storage, the strain Icterohaemorrhagiae was re-isolated, and its virulence was determined using an animal model. In these waters, the mean survival was 130 days for storage at 4 °C, 263 days at 20 °C, and 316 days at 30 °C. Unexpectedly, the mean survival was 344 days for a final pH < 7 and 129 days for pH ≥ 7. Moreover, the pathogenic strain remained fully virulent and was able to induce a lethal disease in gerbils even when the pH of the contaminated waters decreased to <6. These data showed that despite unfavourable storage conditions such as cold, nutrient-poor acidic waters, the survival and virulence of pathogenic Leptospira spp. was fully preserved over at least 20 months.