Abstract
BackgroundHerpesviruses can be neutralized in vitro but remain infectious in immune hosts. One difference between these settings is the availability of immunoglobulin Fc receptors. The question therefore arises whether a herpesvirus exposed to apparently neutralizing antibody can still infect Fc receptor+ cells.Principal FindingsImmune sera blocked murine gamma-herpesvirus-68 (MHV-68) infection of fibroblasts, but failed to block and even enhanced its infection of macrophages and dendritic cells. Viral glycoprotein-specific monoclonal antibodies also enhanced infection. MHV-68 appeared to be predominantly latent in macrophages regardless of whether Fc receptors were engaged, but the infection was not abortive and new virus production soon overwhelmed infected cultures. Lytically infected macrophages down-regulated MHC class I-restricted antigen presentation, endocytosis and their response to LPS.ConclusionsIgG Fc receptors limit the neutralization of gamma-herpesviruses such as MHV-68.
Highlights
Persistent viruses typically transmit infection by reactivating in immune hosts
In order to test whether this neutralization applied to Fc receptors (FcRs)+ cells, we incubated murine gammaherpesvirus-68 (MHV-68) virions with sera from immune mice and added the antibody-coated virions to either BHK-21 fibroblasts or RAW264.7 macrophages (Fig. 1)
The virus used (BAC+) expresses eGFP from a human cytomegalovirus (HCMV) IE1 promoter, so eGFP expression provides a convenient marker of infection [35]
Summary
Persistent viruses typically transmit infection by reactivating in immune hosts. They differ fundamentally from epidemic viruses, whose replication and transmission are blocked by established immunity. The chief defence against epidemic viruses is neutralizing antibody [1], which mainly blocks receptor binding [2]. Herpesviruses can be neutralized in vitro but remain infectious in immune hosts. One difference between these settings is the availability of immunoglobulin Fc receptors. The question arises whether a herpesvirus exposed to apparently neutralizing antibody can still infect Fc receptor+ cells. Immune sera blocked murine gammaherpesvirus-68 (MHV-68) infection of fibroblasts, but failed to block and even enhanced its infection of macrophages and dendritic cells. IgG Fc receptors limit the neutralization of gamma-herpesviruses such as MHV-68
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