Co-administration of CVB3 with anti-CVB2 antibody in mice resulted in viral titres 1-2 logs higher than CVB3 alone, accompanied by greater histopathological damage in the heart.
Does anti-CVB2 antibody enhance CVB3 infection and myocardial damage in murine models?
Antibody enhancement of infectivity by cross-reactive antibodies may exacerbate coxsackievirus pathogenesis and myocardial damage.
Group B coxsackieviruses (CVBs) are a major cause of viral myocarditis and pancreatitis in humans and produce a similar pattern of disease in inbred strains of mice. As there are six strains of CVBs, individuals can be infected with multiple serotypes. This raises the possibility of antibody enhancement of infectivity (AEI) by cross-reactive but non-neutralizing antibody to a different strain from a prior infection. To determine whether AEI plays a role in coxsackievirus pathogenesis, an in vitro system using the murine macrophage cell line J774.1 was tested for enhanced infection when incubated with CVB3 plus anti-CVB2 antibody. Yields of virus were found to increase by 10-50-fold and the percentage of infected cells increased proportionately. The effect was Fc-mediated as F(ab')2 fragments of the antibody could not mediate the effect. To determine whether AEI could also be demonstrated in vivo CVB3 was injected into 5-week-old mice together with mouse polyclonal anti-CVB2. Controls included mice injected with PBS or CVB3 alone. Results showed that the titres of virus in tissues of animals injected with virus plus antibody were 1-2 logs higher than when virus was injected alone. This was accompanied by greater histopathological damage, particularly in the heart. These results have implications for human disease as infection with multiple strains likely occurs during the lifetime of an individual.
Girn et al. (Fri,) conducted a other in Coxsackievirus B3 infection. CVB3 plus anti-CVB2 antibody vs. PBS or CVB3 alone was evaluated on Viral yield/titres and histopathological damage. Co-administration of CVB3 with anti-CVB2 antibody in mice resulted in viral titres 1-2 logs higher than CVB3 alone, accompanied by greater histopathological damage in the heart.