Post-hemifusion stages of Lassa virus GPC-mediated fusion with endosomes are augmented by a late endosome-resident lipid

Abstract

Lassa fever virus (LASV) enters cells by endocytosis and fusion with late endosomes. The mechanisms of LASV glycoprotein complex (GPC) mediated membrane fusion and of virus targeting to late endosomes are not well understood. To gain insights into LASV fusion, we employed a cell-cell fusion model. We find that LASV GPC-mediated cell fusion is more efficient and occurs at higher pH with target cells expressing human LAMP1 compared to cells lacking this cognate receptor and that LASV fusion progresses through the same lipid intermediates, including hemifusion, as fusion induced by other viral glycoproteins.