Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus détente

C A Benedict; T A Banks; L Senderowicz; M Ko; W J Britt; A Angulo; P Ghazal; C F Ware

doi:10.1016/S1074-7613(01)00222-9

Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus détente

C A Benedict, T A Banks, L Senderowicz, M Ko, W J Britt, A Angulo, P Ghazal, C F Ware

Deanery of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

Abstract

Tumor necrosis factor (TNF)-related cytokines regulate cell death and survival and provide strong selective pressures for viruses, such as cytomegalovirus (CMV), to evolve counterstrategies in order to persist in immune-competent hosts. Signaling by the lymphotoxin (LT)-beta receptor or TNF receptor-1, but not Fas or TRAIL receptors, inhibits the cytopathicity and replication of human CMV by a nonapoptotic, reversible process that requires nuclear factor kappa B (NF-kappa B)-dependent induction of interferon-beta (IFN-beta). Efficient induction of IFN-beta requires virus infection and LT signaling, demonstrating the need for both host and viral factors in the curtailment of viral replication without cellular elimination. LT alpha-deficient mice and LT beta R-Fc transgenic mice were profoundly susceptible to murine CMV infection. Together, these results reveal an essential and conserved role for LTs in establishing host defense to CMV.

Original language	English
Pages (from-to)	617-26
Number of pages	10
Journal	Infection and Immunity
Volume	15
Issue number	4
DOIs	https://doi.org/10.1016/S1074-7613(01)00222-9
Publication status	Published - 2001

Keywords

Adaptor Proteins, Signal Transducing
Animals
Carrier Proteins
Cells, Cultured
Cytomegalovirus
Fas-Associated Death Domain Protein
Herpesviridae Infections
Host-Parasite Interactions
Humans
Interferon-beta
Lymphotoxin beta Receptor
Lymphotoxin-alpha
Membrane Proteins
Mice
Mice, Transgenic
Muromegalovirus
NF-kappa B
Proteins
RNA, Messenger
Receptors, Tumor Necrosis Factor
Survival Rate
TNF Receptor-Associated Factor 3
Transcriptional Activation
Tumor Necrosis Factor Ligand Superfamily Member 14
Tumor Necrosis Factor-alpha
Virus Replication

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10.1016/S1074-7613(01)00222-9

Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta
Copyright 2001 by Cell Press
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title = "Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus d{\'e}tente",

abstract = "Tumor necrosis factor (TNF)-related cytokines regulate cell death and survival and provide strong selective pressures for viruses, such as cytomegalovirus (CMV), to evolve counterstrategies in order to persist in immune-competent hosts. Signaling by the lymphotoxin (LT)-beta receptor or TNF receptor-1, but not Fas or TRAIL receptors, inhibits the cytopathicity and replication of human CMV by a nonapoptotic, reversible process that requires nuclear factor kappa B (NF-kappa B)-dependent induction of interferon-beta (IFN-beta). Efficient induction of IFN-beta requires virus infection and LT signaling, demonstrating the need for both host and viral factors in the curtailment of viral replication without cellular elimination. LT alpha-deficient mice and LT beta R-Fc transgenic mice were profoundly susceptible to murine CMV infection. Together, these results reveal an essential and conserved role for LTs in establishing host defense to CMV.",

keywords = "Adaptor Proteins, Signal Transducing, Animals, Carrier Proteins, Cells, Cultured, Cytomegalovirus, Fas-Associated Death Domain Protein, Herpesviridae Infections, Host-Parasite Interactions, Humans, Interferon-beta, Lymphotoxin beta Receptor, Lymphotoxin-alpha, Membrane Proteins, Mice, Mice, Transgenic, Muromegalovirus, NF-kappa B, Proteins, RNA, Messenger, Receptors, Tumor Necrosis Factor, Survival Rate, TNF Receptor-Associated Factor 3, Transcriptional Activation, Tumor Necrosis Factor Ligand Superfamily Member 14, Tumor Necrosis Factor-alpha, Virus Replication",

author = "Benedict, {C A} and Banks, {T A} and L Senderowicz and M Ko and Britt, {W J} and A Angulo and P Ghazal and Ware, {C F}",

year = "2001",

doi = "10.1016/S1074-7613(01)00222-9",

language = "English",

volume = "15",

pages = "617--26",

journal = "Infection and Immunity",

issn = "0019-9567",

publisher = "American Society for Microbiology",

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T1 - Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus détente

AU - Benedict, C A

AU - Banks, T A

AU - Senderowicz, L

AU - Ko, M

AU - Britt, W J

AU - Angulo, A

AU - Ghazal, P

AU - Ware, C F

PY - 2001

Y1 - 2001

N2 - Tumor necrosis factor (TNF)-related cytokines regulate cell death and survival and provide strong selective pressures for viruses, such as cytomegalovirus (CMV), to evolve counterstrategies in order to persist in immune-competent hosts. Signaling by the lymphotoxin (LT)-beta receptor or TNF receptor-1, but not Fas or TRAIL receptors, inhibits the cytopathicity and replication of human CMV by a nonapoptotic, reversible process that requires nuclear factor kappa B (NF-kappa B)-dependent induction of interferon-beta (IFN-beta). Efficient induction of IFN-beta requires virus infection and LT signaling, demonstrating the need for both host and viral factors in the curtailment of viral replication without cellular elimination. LT alpha-deficient mice and LT beta R-Fc transgenic mice were profoundly susceptible to murine CMV infection. Together, these results reveal an essential and conserved role for LTs in establishing host defense to CMV.

AB - Tumor necrosis factor (TNF)-related cytokines regulate cell death and survival and provide strong selective pressures for viruses, such as cytomegalovirus (CMV), to evolve counterstrategies in order to persist in immune-competent hosts. Signaling by the lymphotoxin (LT)-beta receptor or TNF receptor-1, but not Fas or TRAIL receptors, inhibits the cytopathicity and replication of human CMV by a nonapoptotic, reversible process that requires nuclear factor kappa B (NF-kappa B)-dependent induction of interferon-beta (IFN-beta). Efficient induction of IFN-beta requires virus infection and LT signaling, demonstrating the need for both host and viral factors in the curtailment of viral replication without cellular elimination. LT alpha-deficient mice and LT beta R-Fc transgenic mice were profoundly susceptible to murine CMV infection. Together, these results reveal an essential and conserved role for LTs in establishing host defense to CMV.

KW - Adaptor Proteins, Signal Transducing

KW - Animals

KW - Carrier Proteins

KW - Cells, Cultured

KW - Cytomegalovirus

KW - Fas-Associated Death Domain Protein

KW - Herpesviridae Infections

KW - Host-Parasite Interactions

KW - Humans

KW - Interferon-beta

KW - Lymphotoxin beta Receptor

KW - Lymphotoxin-alpha

KW - Membrane Proteins

KW - Mice

KW - Mice, Transgenic

KW - Muromegalovirus

KW - NF-kappa B

KW - Proteins

KW - RNA, Messenger

KW - Receptors, Tumor Necrosis Factor

KW - Survival Rate

KW - TNF Receptor-Associated Factor 3

KW - Transcriptional Activation

KW - Tumor Necrosis Factor Ligand Superfamily Member 14

KW - Tumor Necrosis Factor-alpha

KW - Virus Replication

U2 - 10.1016/S1074-7613(01)00222-9

DO - 10.1016/S1074-7613(01)00222-9

M3 - Article

C2 - 11672543

VL - 15

SP - 617

EP - 626

JO - Infection and Immunity

JF - Infection and Immunity

SN - 0019-9567

IS - 4

ER -

Lymphotoxins and cytomegalovirus cooperatively induce interferon-beta, establishing host-virus détente

Abstract

Keywords

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