Control of virus-induced cell fusion by host cell lipid composition

David S. Roos, Cynthia S. Duchala, Charles B. Stephensen, Kathryn V. Holivies, Purnell W. Choppin

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Virus-induced cell fusion has been examined in a series of stable cell lines which were originally selected for resistance to the fusogenic effects of polyethylene glycol (PEG). For a wide variety of viruses, including murine hepatitis virus (a coronavirus), vesicular stomatitis virus (a rhabdovirus), and two paramyxoviruses (Sendai virus and SV5), susceptibility to virus-induced fusion was found to be inversely correlated with susceptibility to PEG-induced fusion. This phenomenon was observed both for cell fusion occurring in the course of viral infection and for fusion induced "from without" by the addition of high titers of noninfectious or inactivated virus. The fusion-altered cell lines (fusible by virus but not by PEG) are characterized by their unusual lipid composition, including marked elevation of saturated fatty acids and the presence of an unusual ether-linked neutral lipid. To test the association between lipid composition and fusion, acyl chain saturation was manipulated by supplementing the culture medium with exogenous fatty acids. In such experiments, it was possible to control the responses of these cells to both viral and chemical fusogens. Increasing the cellular content of saturated fatty acyl chains increased the susceptibility of cells to viral fusion and decreased susceptibility to PEG-induced fusion, whereas lowering fatty acid saturation had the opposite effect. Thus, parallel cultures of cells can be either driven toward the PEG-fusible/virus-fusion-resistant phenotype of the parental cells or rendered susceptible to viral fusion but resistant to PEG-induced fusion, solely by the alteration of cellular lipids. The ability of cellular lipid composition to regulate virus-induced membrane fusion suggests a possible role for lipids in viral infection and pathogenesis.

Original languageEnglish (US)
Pages (from-to)345-357
Number of pages13
JournalVirology
Volume175
Issue number2
DOIs
StatePublished - 1990
Externally publishedYes

Fingerprint

Cell Fusion
Viruses
Lipids
Fatty Acids
Virus Diseases
Rhabdoviridae
Murine hepatitis virus
Sendai virus
Cell Line
Virus Internalization
Coronavirus
Vesicular Stomatitis
Ether
Culture Media
Cell Culture Techniques
Phenotype

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

Cite this

Roos, D. S., Duchala, C. S., Stephensen, C. B., Holivies, K. V., & Choppin, P. W. (1990). Control of virus-induced cell fusion by host cell lipid composition. Virology, 175(2), 345-357. https://doi.org/10.1016/0042-6822(90)90419-R

Control of virus-induced cell fusion by host cell lipid composition. / Roos, David S.; Duchala, Cynthia S.; Stephensen, Charles B.; Holivies, Kathryn V.; Choppin, Purnell W.

In: Virology, Vol. 175, No. 2, 1990, p. 345-357.

Research output: Contribution to journalArticle

Roos, DS, Duchala, CS, Stephensen, CB, Holivies, KV & Choppin, PW 1990, 'Control of virus-induced cell fusion by host cell lipid composition', Virology, vol. 175, no. 2, pp. 345-357. https://doi.org/10.1016/0042-6822(90)90419-R
Roos DS, Duchala CS, Stephensen CB, Holivies KV, Choppin PW. Control of virus-induced cell fusion by host cell lipid composition. Virology. 1990;175(2):345-357. https://doi.org/10.1016/0042-6822(90)90419-R
Roos, David S. ; Duchala, Cynthia S. ; Stephensen, Charles B. ; Holivies, Kathryn V. ; Choppin, Purnell W. / Control of virus-induced cell fusion by host cell lipid composition. In: Virology. 1990 ; Vol. 175, No. 2. pp. 345-357.
@article{175ab8bd0a7e4a6183f10442f64df7e6,
title = "Control of virus-induced cell fusion by host cell lipid composition",
abstract = "Virus-induced cell fusion has been examined in a series of stable cell lines which were originally selected for resistance to the fusogenic effects of polyethylene glycol (PEG). For a wide variety of viruses, including murine hepatitis virus (a coronavirus), vesicular stomatitis virus (a rhabdovirus), and two paramyxoviruses (Sendai virus and SV5), susceptibility to virus-induced fusion was found to be inversely correlated with susceptibility to PEG-induced fusion. This phenomenon was observed both for cell fusion occurring in the course of viral infection and for fusion induced {"}from without{"} by the addition of high titers of noninfectious or inactivated virus. The fusion-altered cell lines (fusible by virus but not by PEG) are characterized by their unusual lipid composition, including marked elevation of saturated fatty acids and the presence of an unusual ether-linked neutral lipid. To test the association between lipid composition and fusion, acyl chain saturation was manipulated by supplementing the culture medium with exogenous fatty acids. In such experiments, it was possible to control the responses of these cells to both viral and chemical fusogens. Increasing the cellular content of saturated fatty acyl chains increased the susceptibility of cells to viral fusion and decreased susceptibility to PEG-induced fusion, whereas lowering fatty acid saturation had the opposite effect. Thus, parallel cultures of cells can be either driven toward the PEG-fusible/virus-fusion-resistant phenotype of the parental cells or rendered susceptible to viral fusion but resistant to PEG-induced fusion, solely by the alteration of cellular lipids. The ability of cellular lipid composition to regulate virus-induced membrane fusion suggests a possible role for lipids in viral infection and pathogenesis.",
author = "Roos, {David S.} and Duchala, {Cynthia S.} and Stephensen, {Charles B.} and Holivies, {Kathryn V.} and Choppin, {Purnell W.}",
year = "1990",
doi = "10.1016/0042-6822(90)90419-R",
language = "English (US)",
volume = "175",
pages = "345--357",
journal = "Virology",
issn = "0042-6822",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Control of virus-induced cell fusion by host cell lipid composition

AU - Roos, David S.

AU - Duchala, Cynthia S.

AU - Stephensen, Charles B.

AU - Holivies, Kathryn V.

AU - Choppin, Purnell W.

PY - 1990

Y1 - 1990

N2 - Virus-induced cell fusion has been examined in a series of stable cell lines which were originally selected for resistance to the fusogenic effects of polyethylene glycol (PEG). For a wide variety of viruses, including murine hepatitis virus (a coronavirus), vesicular stomatitis virus (a rhabdovirus), and two paramyxoviruses (Sendai virus and SV5), susceptibility to virus-induced fusion was found to be inversely correlated with susceptibility to PEG-induced fusion. This phenomenon was observed both for cell fusion occurring in the course of viral infection and for fusion induced "from without" by the addition of high titers of noninfectious or inactivated virus. The fusion-altered cell lines (fusible by virus but not by PEG) are characterized by their unusual lipid composition, including marked elevation of saturated fatty acids and the presence of an unusual ether-linked neutral lipid. To test the association between lipid composition and fusion, acyl chain saturation was manipulated by supplementing the culture medium with exogenous fatty acids. In such experiments, it was possible to control the responses of these cells to both viral and chemical fusogens. Increasing the cellular content of saturated fatty acyl chains increased the susceptibility of cells to viral fusion and decreased susceptibility to PEG-induced fusion, whereas lowering fatty acid saturation had the opposite effect. Thus, parallel cultures of cells can be either driven toward the PEG-fusible/virus-fusion-resistant phenotype of the parental cells or rendered susceptible to viral fusion but resistant to PEG-induced fusion, solely by the alteration of cellular lipids. The ability of cellular lipid composition to regulate virus-induced membrane fusion suggests a possible role for lipids in viral infection and pathogenesis.

AB - Virus-induced cell fusion has been examined in a series of stable cell lines which were originally selected for resistance to the fusogenic effects of polyethylene glycol (PEG). For a wide variety of viruses, including murine hepatitis virus (a coronavirus), vesicular stomatitis virus (a rhabdovirus), and two paramyxoviruses (Sendai virus and SV5), susceptibility to virus-induced fusion was found to be inversely correlated with susceptibility to PEG-induced fusion. This phenomenon was observed both for cell fusion occurring in the course of viral infection and for fusion induced "from without" by the addition of high titers of noninfectious or inactivated virus. The fusion-altered cell lines (fusible by virus but not by PEG) are characterized by their unusual lipid composition, including marked elevation of saturated fatty acids and the presence of an unusual ether-linked neutral lipid. To test the association between lipid composition and fusion, acyl chain saturation was manipulated by supplementing the culture medium with exogenous fatty acids. In such experiments, it was possible to control the responses of these cells to both viral and chemical fusogens. Increasing the cellular content of saturated fatty acyl chains increased the susceptibility of cells to viral fusion and decreased susceptibility to PEG-induced fusion, whereas lowering fatty acid saturation had the opposite effect. Thus, parallel cultures of cells can be either driven toward the PEG-fusible/virus-fusion-resistant phenotype of the parental cells or rendered susceptible to viral fusion but resistant to PEG-induced fusion, solely by the alteration of cellular lipids. The ability of cellular lipid composition to regulate virus-induced membrane fusion suggests a possible role for lipids in viral infection and pathogenesis.

UR - http://www.scopus.com/inward/record.url?scp=0025348217&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025348217&partnerID=8YFLogxK

U2 - 10.1016/0042-6822(90)90419-R

DO - 10.1016/0042-6822(90)90419-R

M3 - Article

VL - 175

SP - 345

EP - 357

JO - Virology

JF - Virology

SN - 0042-6822

IS - 2

ER -