Research into the antibody detection technology of mink plasmacytosis and its current applications / 病毒学报

Mink plasmacytosis, caused by Aleutian Mink Disease Virus (AMDV), poses a threat to the development of the animal fur industry. Neutralizing antibodies against AMDV may result in a persistent infection rather than providing protection for minks. To date,no specific methods to prevent or cure this disease have been developed. In order to eliminate mink plasmacytosis, antibody detection technology has been used globally as a dominant approach to screen for AMDV-positive minks. This paper introduces the classical technology, counterimmunoelectrophoresis and emerging technology in terms of AMDV antibody detection,and provides a glimpse into the future development of these technologies.

Sequencing Analyses of the Hypervariable Region within the VP2 Gene of a Strain of the Aleutian Mink Disease Virus / 病毒学报

To analyze the molecular mechanisms of cross-host transmission of the Aleutian mink disease vi rus (ADV), the hypervariable region fragment of the VP2 gene of the ADV in Jilin Province (China) was amplified. Sequencing analyses showed diversity at residue 174 by comparison with other VP2 genes in GenBank. The phylogenetic tree indicated that the ADV-JL strain had a close relationship with the highly pathogenic strain from Denmark: ADV-K. Results implied that residue 174 may be associated with ADV infectivity.

Eenie, Meenie, Miney, Moe, who is responsible for the antibody-dependent enhancement of Aleutian mink disease parvovirus infection? / 病毒学报

Aleutian mink disease parvovirus (AMDV) causes a persistent infection associated with immune complex disease, hypergammaglobulinemia, and high levels of antiviral antibodies. Despite the presence of an antibody, the virus is not cleared in vivo. Pre-existing antibodies may enhance viral infections, by Fc-receptor-mediated antibody-dependent enhancement (ADE), but the mechanism that underlies ADE has not been fully defined. Three models have been proposed, including: (1) interactions between antibody and FcR, complement C3 fragment and CR, or between C1q and C1qR, which promotes viral attachment to cells; (2) suppression of IFN-gamma-mediated host-cell antiviral gene expression by the upregulation of negative regulators of pathogen pattern recognition; and (3) the promotion of early IL-10 secretion. In addition, the role of cytokine IL-6 in ADE mediated disease development is discussed, to facilitate a better understanding of the pathogenesis of AMDV infection, as well as give insights into rational vaccine design approaches.