THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES

THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES

A variety of lymphoid cell populations were examined in terms of their ability to replicate vesicular stomatitis virus (VSV), a lytic, RNA-containing virus maturing at the cell surface. The number of cells capable of producing VSV was estimated in terms of infectious centers by the virus plaque ass...

Full description

Bibliographic Details
Main Authors: Nowakowski, Maja, Feldman, Joseph D., Kano, Shogo, Bloom, Barry R.
Format: Online
Language:English
Published: The Rockefeller University Press 1973
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139232/
id pubmed-2139232
recordtype oai_dc
spelling pubmed-21392322008-04-17 THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES Nowakowski, Maja Feldman, Joseph D. Kano, Shogo Bloom, Barry R. Article A variety of lymphoid cell populations were examined in terms of their ability to replicate vesicular stomatitis virus (VSV), a lytic, RNA-containing virus maturing at the cell surface. The number of cells capable of producing VSV was estimated in terms of infectious centers by the virus plaque assay (VPA), and morphologically by electron microscopy (EM). The lymphoid cells examined in this study included: (a) lymph node cells from delayed hypersensitive guinea pigs stimulated by specific antigen, (b) mouse spleen cells activated by selective bone marrow-derived (B) cell and thymus derived (T) cell mitogens, and (c) cells of human and murine continuous lymphoblastoid or lymphoma lines. In unstimulated cultures of guinea pig lymph node cells there is a background of approximately 1 in 1,000 cells which produces VSV; in purified protein derivative (PPD)-stimulated cultures the number of cells producing virus was 1.6% in the VPA and 1.9% by EM. These cells were large lymphocytes with some morphological features of transformed lymphocytes but were not typical blast cells. A few macrophages were associated with virus in both stimulated and control cultures. These observations indicate that (a) cells responsive to antigens, as detected by a marker virus, were lymphocytes; (b) cells other than lymphocytes (macrophages) were capable of replicating VSV even without antigenic stimulation; and (c) the correlation of results obtained by VPA and morphologic examination was usually quite good. Of the total number of mouse spleen cells stimulated with concanavalin (Con A), a T cell mitogen, 4.5 (EM)–5.7% (VPA) were associated with VSV. These were characteristic transformed lymphocytes, similar to phytohemagglutinin (PHA)-stimulated human lymphocytes. In contrast Escherichia coli lipopolysaccharide (LPS)-treated mouse spleen cultures contained lower numbers of virus plaque-forming cells. The majority of such cells associated with virus displayed extensive rough endoplasmic reticulum. Two cultured murine lymphomas containing lymphocytes with the θ surface marker (L5178Y and EL-4) showed a 15–100-fold higher incidence of virus-producing cells than leukemias (L1210 and C57Bl/6) which did not carry this marker. Similarly, the L2C guinea pig leukemia, a known B cell leukemia, yielded a low percent of virus plaque-forming cells (<2%). However, MOPC-104, a plasma cell tumor presumed to be of B cell origin, was found to be an efficient virus producer. There was a wide variation in the efficiency of VSV replication among human lymphoblastoid lines. One line, Wil-2, produced 80% infectious centers after 24 h of exposure to VSV, and all cells were associated with virus at the EM level. The relationship between the virus-producing cells and different lymphocyte subpopulations as well as the efficiency of the two assays for studying virus-producing lymphocytes is discussed. The Rockefeller University Press 1973-03-31 /pmc/articles/PMC2139232/ /pubmed/4348276 Text en Copyright © 1973 by The Rockefeller University Press 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 Nowakowski, Maja
Feldman, Joseph D.
Kano, Shogo
Bloom, Barry R.
spellingShingle Nowakowski, Maja
Feldman, Joseph D.
Kano, Shogo
Bloom, Barry R.
THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES
author_facet Nowakowski, Maja
Feldman, Joseph D.
Kano, Shogo
Bloom, Barry R.
author_sort Nowakowski, Maja
title THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES
title_short THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES
title_full THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES
title_fullStr THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES
title_full_unstemmed THE PRODUCTION OF VESICULAR STOMATITIS VIRUS BY ANTIGEN- OR MITOGEN-STIMULATED LYMPHOCYTES AND CONTINUOUS LYMPHOBLASTOID LINES
title_sort production of vesicular stomatitis virus by antigen- or mitogen-stimulated lymphocytes and continuous lymphoblastoid lines
description A variety of lymphoid cell populations were examined in terms of their ability to replicate vesicular stomatitis virus (VSV), a lytic, RNA-containing virus maturing at the cell surface. The number of cells capable of producing VSV was estimated in terms of infectious centers by the virus plaque assay (VPA), and morphologically by electron microscopy (EM). The lymphoid cells examined in this study included: (a) lymph node cells from delayed hypersensitive guinea pigs stimulated by specific antigen, (b) mouse spleen cells activated by selective bone marrow-derived (B) cell and thymus derived (T) cell mitogens, and (c) cells of human and murine continuous lymphoblastoid or lymphoma lines. In unstimulated cultures of guinea pig lymph node cells there is a background of approximately 1 in 1,000 cells which produces VSV; in purified protein derivative (PPD)-stimulated cultures the number of cells producing virus was 1.6% in the VPA and 1.9% by EM. These cells were large lymphocytes with some morphological features of transformed lymphocytes but were not typical blast cells. A few macrophages were associated with virus in both stimulated and control cultures. These observations indicate that (a) cells responsive to antigens, as detected by a marker virus, were lymphocytes; (b) cells other than lymphocytes (macrophages) were capable of replicating VSV even without antigenic stimulation; and (c) the correlation of results obtained by VPA and morphologic examination was usually quite good. Of the total number of mouse spleen cells stimulated with concanavalin (Con A), a T cell mitogen, 4.5 (EM)–5.7% (VPA) were associated with VSV. These were characteristic transformed lymphocytes, similar to phytohemagglutinin (PHA)-stimulated human lymphocytes. In contrast Escherichia coli lipopolysaccharide (LPS)-treated mouse spleen cultures contained lower numbers of virus plaque-forming cells. The majority of such cells associated with virus displayed extensive rough endoplasmic reticulum. Two cultured murine lymphomas containing lymphocytes with the θ surface marker (L5178Y and EL-4) showed a 15–100-fold higher incidence of virus-producing cells than leukemias (L1210 and C57Bl/6) which did not carry this marker. Similarly, the L2C guinea pig leukemia, a known B cell leukemia, yielded a low percent of virus plaque-forming cells (<2%). However, MOPC-104, a plasma cell tumor presumed to be of B cell origin, was found to be an efficient virus producer. There was a wide variation in the efficiency of VSV replication among human lymphoblastoid lines. One line, Wil-2, produced 80% infectious centers after 24 h of exposure to VSV, and all cells were associated with virus at the EM level. The relationship between the virus-producing cells and different lymphocyte subpopulations as well as the efficiency of the two assays for studying virus-producing lymphocytes is discussed.
publisher The Rockefeller University Press
publishDate 1973
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139232/
_version_ 1611421620665057280

Similar Items