Owing to the rapid decline of the European mink (Mustela lutreola) in France, a national conservation action plan has been initiated, in which scientific research to improve understanding of the causes of the decline is one of the primary objectives. In order to investigate the possible role of Aleutian disease parvovirus (ADV) in decline of the species, a serologic survey was conducted from March 1996 to March 2002 in 420 free-ranging individuals of six species of small carnivores distributed in eight dé partements of southwestern France. Antibodies to ADV were detected in 17 of 75 American mink (Mustela vison), 12 of 99 European mink, 16 of 145 polecats (Mustela putorius), four of 17 stone martens (Martes foina), one of 16 pine martens (Martes martes), and three of 68 common genets (Genetta genetta). Seroprevalence was significantly higher in American mink than in other species. Seropositive individuals with gamma globulin levels Ͼ20% were observed in four European mink, four American mink, two stone martens, and one pine marten. Geographic distribution of positive animals indicates the virus has spread to all areas where European mink are found. Furthermore, a trend of increasing prevalence seems to appear in Mustela sp. sympatric with American mink. Although further investigations are necessary to evaluate the role of ADV in decline of European mink, evidence of the virus in the wild at the levels found in our study has implications for conservation of this species.

When mink kits were infected neonatally with a highly virulent strain of Aleutian disease virus (ADV), 100% of both Aleutian and non-Aleutian genotype mink died of interstitial pneumonia characterized by permissive ADV infection of alveolar type H cells. Treatment of infected kits with either mink anti-ADV gamma globulin or mouse monoclonal antibodies against ADV structural proteins reduced mortality by 50 to 75% and * Corresponding author. sen, unpublished results), the accumulated information suggested that perhaps maternally transferred antibodies masked the development of pneumonia. By using immunofluorescence, Southern blot analysis, and strand-specific in situ hybridization, we previously showed that the acute pneumonia is caused by cytopathic replication of ADV in lung alveolar type II cells of newborn ADV antibody-negative mink kits. This infection is associated with high levels of viral antigen, viral DNA, the viral replicative forms (RFs) of DNA, and viral mRNA in each infected cell (7). In contrast, in mink infected as adults, viral replication and transcription are dramatically altered. The target cells lie within lymphoid organs (probably lymphocytes), and ADV expression is markedly restricted at the cellular level. That is to say, the level of viral RF DNA and mRNA is decreased by a factor of 10 to 100 and intranuclear viral protein, which is easily detected in infected mink kits, cannot be detected (6). One difference between adult and newborn mink is the rapid development of anti-ADV antibodies in adults, and we previously speculated that the restricted pattern seen in adults might be a result of the anti-ADV antibody responise (6). Similarly, we wondered whether the failure to observe pneumonia in ADV antibody-positive kits was due to some effect of maternally transferred antibodies. In the present study, we directly examnined the effect of passive anti-ADV antibodies on the replication of ADV and development of disease in neonatally infected mink kits. Our results showed that antibodies restrict viral replication at the cellular level, preventing the acute but not the chronic disease caused by ADV.

No abstract

No abstract

Aleutian disease virus (ADV) infection was analyzed in vivo and in vitro to compare virus replication in cell culture and in mink. Initial experiments compared cultures of Crandell feline kidney (CRFK) cells infected with the avirulent ADV-G strain or the highly virulent Utah I ADV. The number of ADV-infected cells was estimated by calculating the percentage of cells displaying ADV antigen by immunofluorescence (IFA), and several parameters of infection were determined. Infected cells contained large quantities of viral DNA (more than 105 genomes per infected cell) as estimated by dot-blot DNA-DNA hybridization, and much of the viral DNA, when analyzed by Southern blot hybridization, was found to be of a 4.8-kilobase-pair duplex monomeric replicative form (DM DNA). Furthermore, the cultures contained 7 to 67 fluorescence-forming units (FFU) per infected cell, and the ADV genome per FFU ratio ranged between 2 x 103 and 164 x 103. Finally, the pattern