Abstract
Vaccination is one of the most important tools to protect pigs against infection with porcine reproductive and respiratory syndrome virus 1 (PRRSV-1). Although neutralizing antibodies are considered to represent an important mechanism of protective immunity, anti-PRRSV antibodies, in particular at subneutralizing concentrations, have also been reported to exacerbate PRRSV infection, probably through FcγR-mediated uptake of antibody-opsonized PRRSV, resulting in enhanced infection of, and replication in, target cells. Therefore, we investigated this pathway using sera from an animal experiment in which vaccine-mediated enhancement of clinical symptoms was observed. Three groups of six pigs were vaccinated with an inactivated PRRSV vaccine based on the PRRSV-1 subtype 3 strain Lena and challenged after a single or a prime-boost immunization protocol, or injected with PBS. We specifically tested if sera obtained from these animals can enhance macrophage infections, viral shedding, or cytokine release at different dilutions. Neither the presence of neutralizing antibodies nor general anti-PRRSV antibodies, mediated an enhanced infection, increased viral release or cytokine production by macrophages. Taken together, our data indicate that the exacerbated disease was not caused by antibodies.
Highlights
Antibody-dependent enhancement (ADE) of infection is a phenomenon that has been associated with many different viruses, such as lactate dehydrogenase elevating virus [1], HIV-1 [2,3], dengue virus [4,5], Japanese encephalitis virus (JEV) [6], and FMDV [7,8,9]
We have recently developed a novel inactivated vaccine against porcine reproductive and respiratory syndrome virus 1 (PRRSV-1), subtype 1 strains, that showed promising protective results [31]
In the sera from the randomly selected control animal #1445, we occasionally found evidence of ADE, but this was observed before challenge and was not consistently found at particular dilutions nor did it appear to be titratable (Figure 5)
Summary
Antibody-dependent enhancement (ADE) of infection is a phenomenon that has been associated with many different viruses, such as lactate dehydrogenase elevating virus [1], HIV-1 [2,3], dengue virus [4,5], Japanese encephalitis virus (JEV) [6], and FMDV [7,8,9]. For some of these infections, this in vitro phenomenon has been associated with immunity-enhanced disease. ADE was found at subneutralizing concentrations, at which antibodies are binding to the virus but are not sufficiently numerous to mediate neutralization. If the virus can replicate in Viruses 2019, 11, 829; doi:10.3390/v11090829 www.mdpi.com/journal/viruses
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