Antibody-dependent enhancement of coxsackievirus b4 infectivity of human peripheral blood mononuclear cells results in increased interferon-alpha synthesis

IgG devoid of neutralizing activity and isolated from donor plasma by chrom atography formed immune complexes with coxsackievirus B4 (CVB4) and signifi cantly increased the infection of peripheral blood mononuclear cells with C VB4. The major host cells for CVB4 infection enhanced with IgG are monocyti c CD14(+) cells. The roles of CVB and adenovirus receptor and Fc receptor I I and III have been shown. Increased viral replication and the release of i nfectious particles were demonstrated when interferon (IFN)-alpha produced by infected cells was first neutralized by use of antibodies. The CVB4 IgG- induced synthesis of IFN-alpha by monocytes reflected entry and uncoating o f CVB4 but not of viral replication and required the presence of CVB4 RNA i nside the cells. Thus, CVB4 can infect monocytes by an antibody-dependent m echanism through interactions between the virus, antiviral antibodies, and specific receptors that result in IFN-alpha production.