Eenie, Meenie, Miney, Moe, who is responsible for the antibody-dependent enhancement of Aleutian mink disease parvovirus infection?.
- Author:
Hong-Wei ZHU
;
Xiu-Mei XING
;
Yong-Jun WEN
- Publication Type:Journal Article
- MeSH:
Aleutian Mink Disease;
immunology;
virology;
Aleutian Mink Disease Virus;
genetics;
immunology;
Animals;
Antibodies, Viral;
immunology;
Antibody-Dependent Enhancement;
Mink;
immunology;
virology
- From:
Chinese Journal of Virology
2014;30(4):450-455
- CountryChina
- Language:Chinese
-
Abstract:
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.
