Entry and egress of varicella virus blocked by same anti-gH monoclonal antibody

Abstract

Varicella virus is one of the most reclusive human herpesviruses. The virus is not released from infected cultured cells. Rather, infectivity is transferred by fusion of contiguous cells. To further investigate this process, infected cells were viewed by scanning electron microscopy. Thousands of viral particles were observed in elongated clusters overlying the virus-induced syncytia. When virus-infected cells were covered postinfection with medium supplemented with a monoclonal antibody to glycoprotein gpIII (gH homolog), syncytial formation was completely blocked and no progeny viral particles were observed on the surface of the monolayer. Removal of the antibody was followed by rapid progression of cytopathic effect. Addition of antibody to other viral proteins did not alter the infection. Thus, a monoclonal antibody to a single viral determinant on glycoprotein gpIII (gH) can prevent syncytial formation postinfection and block progression of infectivity. Since the same monoclonal antibody can inhibit entry, this study greatly expands the role of antibody in the modulation of herpesvirus infection.