AFRICAN SWINE FEVER VIRUS CD2-LIKE PROTEIN MEDIATES MONOCYTE INFECTION-INHIBITION

Authors: Zsak, Laszlo; Burrage, Thomas; Neilan, John; Lu, Zhiqiang; Kutish, Gerald; Rock, Daniel

Submitted to: Conference Research Workers Disease Meeting
Publication Type: Proceedings
Publication Acceptance Date: 11/16/2004
Publication Date: 11/16/2004
Citation: Zsak, L., Burrage, T.G., Neilan, J.G., Lu, Z., Kutish, G.F., Rock, D.L. 2004. African swine fever virus cd2-like protein mediates monocyte infection-inhibition [abstract]. Conference Research Workers Disease Meeting. p. 197

Interpretive Summary:

Technical Abstract: Antibody-mediated immune mechanisms independent of virus neutralization have been shown to be important in immunity to African swine fever (ASF). Monocyte infection-inhibition (M-II), a novel antibody-mediated mechanism that interferes with ASFV replication in infected macrophages has been described. M-II antibody titers in convalescent swine serum correlate with protective immunity to virus challenge suggesting a significant role for it in antibody-mediated protection. Viral protein(s) mediating this effect are unknown. Notably, hemadsorption-inhibiting antibodies, directed against the CD2-like protein of ASFV, also correlate with protection. To examine the possibility that CD2-like protein may also be responsible for M-II, a Malawi CD2 gene deletion mutant (M-D-CD2) and a chimeric Malawi virus containing the CD2-like gene from a heterologous virus isolate Pr4, (M-PCD2) were constructed and evaluated in M-II assays. M-II was observed using parental Malawi virus and anti-Malawi convalescent swine serum (log 5.6) but was reduced a 1,000-fold for M'CD2 and M-PCD2 viruses (log 2.6). In addition, anti-Pr4 convalescent serum mediated M-II for M-PCD2 (log 3.8) but not for Malawi or M'CD2 (log 1.3). These data indicate that the ASFV CD2-like protein is sufficient for mediating M-II. The correlation of an M-II response with protective immunity suggests that ASFV CD2 may be a significant protective antigen.