Differential Effects on Cell Fusion Activity of Mutations in Herpes Simplex Virus 1 Glycoprotein B (gB) Dependent on Whether a gD Receptor or a gB Receptor Is Overexpressed

作者：Fan Qing; Lin Erick; Satoh Takeshi; Arase Hisashi; Spear Patricia G^*

来源：Journal of Virology, 2009, 83(15): 7384-7390.

DOI：10.1128/JVI.00087-09

Glycoprotein B (gB) of herpes simplex virus (HSV) is one of four glycoproteins essential for viral entry and cell fusion. Recently, paired immunoglobulin-like type 2 receptor (PILR alpha) was identified as a receptor for HSV type 1 (HSV-1) gB. Both PILR alpha and a gD receptor were shown to participate in HSV-1 entry into certain cell types. The purpose of this study was to determine whether insertional mutations in gB had differential effects on its function with PILR alpha and the gD receptor, nectin-1. Previously described gB mutants and additional newly characterized mutants were used in this study. We found that insertional mutations near the N terminus and C terminus of gB and especially in the central region of the ectodomain reduced cell fusion activity when PILR alpha was overexpressed much more than when nectin-1 was overexpressed. Most of the insertions reduced the binding of gB to PILR alpha, for at least some forms of gB, but this reduction did not necessarily correlate with the selective reduction in cell fusion activity with PILR alpha. These results suggest that the regions targeted by the relevant mutations are critical for functional activity with PILR alpha. They also suggest that, although both the binding of gB to a gB receptor and the binding of gD to a gD receptor may be required for HSV-induced cell fusion, the two receptor-binding activities may have unequal weights in triggering fusogenic activity, depending on the ratios of gB and gD receptors or other factors.

• 出版日期2009-8-1
• 单位西北大学