Two mutations in gB-1 and gD-1 of herpes simplex virus type 1 are involved in the ?fusion from without? phenotype in different cell types

Abstract

Previous studies have shown that certain strains of herpes simplex viruses type 1 (HSV-1) are able to induce "fusion from without" (FFWO) which means no transcription or translation of the viral genome happens. The main determinants for FFWO in BHK cells are mutations in the C-terminal part of gB-1. But single mutations in this part of the genome are not sufficient to transfer the FFWO phenotype also to Vero cells. Here, we report that FFWO of HSV strains indeed need additional mutations in the N-terminal part of gD in order to produce the FFWO phenotype in BHK and Vero cells. By marker transfer we are able to show that loss of mutations in the N-terminal part of gD influences the ability to induce FFWO in Vero cells but not in BHK cells. We assume that a mutated gD allows the entrance of a multiple number of virus particles into the cell and enhances therefore the fusion activity of the mutated gB. Mutations in gD alone are not sufficient for fusion activity of HSV.

Nectin-2-mediated entry of a syncytial strain of herpes simplex virus via pH-independent fusion with the plasma membrane of Chinese hamster ovary cells

“…Compared to the wild type HSV-1 KOS strain, the gB [47] and gD [42] of ANG path have 10 and 7 amino acid differences, respectively. Alterations in gD at positions 25 and 27 [52] as well as ectodomain and cytoplasmic tail mutations in gB [47,48] have been proposed to be important for FFWO activity. The role of these residues in the selection of entry route is currently being evaluated.…”

The human autoantigen La/SS-B accelerates herpes simplex virus type 1 replication in transfected mouse 3T3 cells

“…A series of cell lines expressing either the human exon 1, exon 1 0 or the human La gene had been recently prepared and shown to express different levels of human La protein ( [31], see also The cells were infected with herpes simplex virus type 1. We used the four different strains including ANG, HSZP, HFEM, and 17synþ [36][37][38]. The cells were infected using different plaqueforming unit (PFU) ranges from 1 to 20 PFU per cell.…”