Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes

The host-directed cleavage of measles virus fusion protein on infected lymphoid cells was studied to understand the mechanism of viral persistence in lymphoid cells in vivo. Several lymphoblastoid cell lines were infected with measles virus, and the viral glycoproteins expressed on the cell’s surfac...

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Main Authors:	Fujinami, RS, Oldstone, MBA
Format:	Online
Language:	English
Published:	The Rockefeller University Press 1981
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186533/

id	pubmed-2186533
recordtype	oai_dc
spelling	pubmed-21865332008-04-17 Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes Fujinami, RS Oldstone, MBA Articles The host-directed cleavage of measles virus fusion protein on infected lymphoid cells was studied to understand the mechanism of viral persistence in lymphoid cells in vivo. Several lymphoblastoid cell lines were infected with measles virus, and the viral glycoproteins expressed on the cell’s surface were radiolabeled and analyzed for cleavage of fusion (F(0)) to F(1) by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Daudi and Ramos lymphoblastoid cells were deficient in their ability to cleave measles virus fusion protein and correspondingly produced low titers of infectious measles virus, Daudi cells being more defective than Ramos cells. In contrast, other lymphoblastoid cells studied, Victor, Raji, Wi-L2, RPMI 8866, and Seraphine, cleaved the fusion polypeptide and made significantly more infectious virus. Despite their defect in cleaving F protein, Daudi cells were able to assemble and release (noninfectious) measles virus particles into the fluid phase. The deficit in Daudi cells was corrected by fusing infected Daudi cells with cleavage-competent cells such as Victor or Raji. Furthermore, the cleavage event performed by competent cells could be mimicked at the plasma membrane by treating infected Daudi cells with trypsin, implicating the role of a plasma membrane enzyme in cleaving F(0) to F(1) during measles virus infection. Hence, lymphoid cells deficient in the plasma membrane enzyme required to cleave F protein are permissive for measles virus, maintain viral gene products, produce mostly noninfectious virus, and fail to place the biologic activity F(1) protein on their surfaces. The Rockefeller University Press 1981-11-01 /pmc/articles/PMC2186533/ /pubmed/6895382 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Fujinami, RS Oldstone, MBA
spellingShingle	Fujinami, RS Oldstone, MBA Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes
author_facet	Fujinami, RS Oldstone, MBA
author_sort	Fujinami, RS
title	Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes
title_short	Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes
title_full	Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes
title_fullStr	Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes
title_full_unstemmed	Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes
title_sort	failure to cleave measles virus fusion protein in lymphoid cells. a possible mechanism for viral persistence in lymphocytes
description	The host-directed cleavage of measles virus fusion protein on infected lymphoid cells was studied to understand the mechanism of viral persistence in lymphoid cells in vivo. Several lymphoblastoid cell lines were infected with measles virus, and the viral glycoproteins expressed on the cell’s surface were radiolabeled and analyzed for cleavage of fusion (F(0)) to F(1) by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Daudi and Ramos lymphoblastoid cells were deficient in their ability to cleave measles virus fusion protein and correspondingly produced low titers of infectious measles virus, Daudi cells being more defective than Ramos cells. In contrast, other lymphoblastoid cells studied, Victor, Raji, Wi-L2, RPMI 8866, and Seraphine, cleaved the fusion polypeptide and made significantly more infectious virus. Despite their defect in cleaving F protein, Daudi cells were able to assemble and release (noninfectious) measles virus particles into the fluid phase. The deficit in Daudi cells was corrected by fusing infected Daudi cells with cleavage-competent cells such as Victor or Raji. Furthermore, the cleavage event performed by competent cells could be mimicked at the plasma membrane by treating infected Daudi cells with trypsin, implicating the role of a plasma membrane enzyme in cleaving F(0) to F(1) during measles virus infection. Hence, lymphoid cells deficient in the plasma membrane enzyme required to cleave F protein are permissive for measles virus, maintain viral gene products, produce mostly noninfectious virus, and fail to place the biologic activity F(1) protein on their surfaces.
publisher	The Rockefeller University Press
publishDate	1981
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186533/
_version_	1611427205811798016

Failure to cleave measles virus fusion protein in lymphoid cells. A possible mechanism for viral persistence in lymphocytes

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