Epstein–Barr Virus Entry

Abstract

Entry of Epstein-Barr virus into human lymphoblastoid cells (Daudi cells) was studied by electron microscopy. At the site of viral attachment, two distinct interactions conducive to penetration of the virus occurred between the viral envelope and cell membrane, namely, (i) simultaneous dissolution of both the envelope and cell membrane, presumably resulting in passage of viral capsids into the cytoplasm and (ii) dissolution confined to the cell membrane with resulting penetration of enveloped virus. In the latter case envelope dissolution appears to occur subsequently in the cytoplasm with release of capsids. Fusion of the viral envelope with the cell membrane was not observed. The capsids exhibited two distinct structural forms one dense, the other translucent or light in appearance. The former disrupted near the cell membrane with release of viral cores into the cytoplasm whereas the light capsids containing dense cores migrated toward the nucleus and accumulated in the perinuclear region. Apparently the process of releasing deoxyribonucleic acid (DNA) from the light capsid is slowed down or prevented in Daudi cells. A hypothesis is presented concerning the manner in which these two types of capsids initiate infection.

Comparative Mutagenesis of Pseudorabies Virus and Epstein-Barr Virus gH Identifies a Structural Determinant within Domain III of gH Required for Surface Expression and Entry Function

“…In contrast, the herpesvirus core fusion machinery consists of the heterodimeric complex gH/gL and the fusogen gB, with an additional receptorbinding protein such as gD in the alphaherpesvirus pseudorabies virus (PrV) or gp42 in the gammaherpesvirus Epstein-Barr virus (EBV) (1). For infectious entry, PrV requires gB and gH/gL as well as gD, which binds to specific host cell receptors such as nectin-1 and -2 and HveD (2), whereas EBV requires gB, gH/gL, and gp42 for B cell entry, with gp42 binding the receptor HLA class II (3). In contrast, for infection of epithelial cells, EBV uses gH/gL to bind to integrin receptors so that only gH/gL and gB are required for entry into these cells (3).…”

“…For infectious entry, PrV requires gB and gH/gL as well as gD, which binds to specific host cell receptors such as nectin-1 and -2 and HveD (2), whereas EBV requires gB, gH/gL, and gp42 for B cell entry, with gp42 binding the receptor HLA class II (3). In contrast, for infection of epithelial cells, EBV uses gH/gL to bind to integrin receptors so that only gH/gL and gB are required for entry into these cells (3).…”

HLA-DQ β1 alleles associated with Epstein-Barr virus (EBV) infectivity and EBV gp42 binding to cells

“…host cell proteins, which may contribute to virus infectivity at various steps including virus entry, replication, and immune control (3,31,32), the observation that the interaction of gp42 with HLA class II is essential for EBV infection (7,9,12,33) may explain the ability of a single genetic locus to influence infectivity with EBV.…”

Avaliação diagnóstica das infecções por vírus Epstein-Barr, parvovírus B19 e vírus linfotrópico de células T humanas em pacientes portadores de lúpus eritematoso sistêmico em hospital de referência do Estado do Pará, Brasil

“…Para infecções primárias agudas, nota-se uma produção de IgM mais eficiente em relação aos períodos de reativação do EBV 54 . Como as infecções primárias pelo vírus ocorrem, em sua grande maioria, em crianças e adultos jovens 18 , isso explicaria a associação dessa resposta humoral aguda com pacientes menos senis. Outra explicação seria o nível de estresse ao qual o paciente é submetido.…”

“…O vírus apresenta genoma de DNA de fita dupla (DNAfd) linear, composto por cerca de 87 genes codificantes 17 e envolvido por um capsídeo icosaédrico com 162 capsômeros, tegumento e envelope composto por glicoproteínas 18 . O vírus é altamente disseminado, infectando cerca de 90% da população mundial 19 .…”