Interferon treatment inhibits onset of herpes simplex virus immediate-early transcription

Mittnacht, Sibylle; Straub, Petra; Kirchner, Holger; Jacobsen, Helmut

doi:10.1016/0042-6822(88)90637-x

Cited by 93 publications

(63 citation statements)

References 45 publications

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“…EBV latency can be disrupted into lytic replication by some chemical or physiological factors, including viral superinfection (30). It is well known that IFNs inhibit viral replications, including herpesviruses (61)(62)(63)(64)(65)(66)(67)(68). Thus, the inhibition of EBV lytic replication by IFNs is anticipated, and we did find that IFN-␣ was capable of inhibiting lytic replication of EBV (data not shown).…”

Section: Discussionmentioning

confidence: 44%

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

Brumm

Zhang

2006

Journal of Biological Chemistry

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Epstein-Barr virus (EBV)3 is a human ␥ herpesvirus and is an important cause of lymphomas in patients with advanced human immunodeficiency virus infection or AIDS and in severely immunocompromised people, especially organ transplant recipients. Also, EBV infection is associated with the development of nasopharyngeal carcinoma and Burkitt's lymphoma (BL) (1, 2).The biologic hallmark of EBV-cell interaction is latency. Three types of latency have been described, each having its own distinct pattern of gene expression. Type I latency is exemplified by BL tumors in vivo. EBV nuclear antigen 1 (EBNA-1) protein is expressed in this form of latency. Type II latency is exemplified by nasopharyngeal carcinoma and Hodgkin disease. EBNA-1, latent membrane protein 1 (LMP-1), and LMP2A and LMP2B proteins are expressed in type II latency. Type III latency is represented by lymphoblastoid cell lines. Nine viral proteins are expressed, including six nuclear proteins (EBNA-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, and EBNA-LP) and three integral membrane proteins (LMP-1, LMP-2A, and LMP-2B) (reviewed in Refs. 1 and 2).EBV LMP-1 is the principal oncoprotein required for EBV transformation of human B cells and establishment of latency in vitro. LMP-1 is an integral membrane protein with six transmembrane-spanning domains with a long C-terminal domain, which is located in the cytoplasm (2, 3). Two C-terminal activator regions (CTARs) have been identified to initiate signal transduction. LMP-1 acts as a constitutively active receptor-like molecule that does not need the binding of a ligand (4). LMP-1 appears to be a central effector of altered cell growth, survival, adhesive, invasive, and antiviral potential (5-9).Type I interferons (IFNs) are cytokines with many functions including antiviral and anti-proliferation (10, 11). IFNs are produced upon the infection of cells by viruses. There are a large number of type I IFN genes in the human: 13 IFN-␣ genes, 1 IFN-␤ gene, and 1 IFN-gene (12). It is not known now why there are so many type I IFN genes. However, a unique role for IFN-␤ for a fully effective antiviral response, which cannot be compensated by IFN-␣, has been documented (13).The amount of IFNs produced by viruses or double-stranded RNA can be increased robustly by treating cells with IFN before infection, a phenomenon known as IFN priming (14 -16). The stimulation of IFN production observed upon priming results from an increase in the rate of IFN gene transcription and requires an IFN-inducible factor(s) (17,18).The mechanism of the transcriptional activation of IFNs has been under intensive investigation. One of the major players in the IFN production is IFN regulatory factor 7 (IRF-7). IRF-7 was cloned in the context of EBV latency and has an intimate relation with EBV (19 -25). IRF-7 is inducible by type I IFNs and can be further activated by phosphorylation and nuclear translocation upon viral infection, and activated IRF-7 is partially responsible for the robust transcriptional activation of IFNs (23,[26][27][28][29].Prev...

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Section: Discussionmentioning

confidence: 44%

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

Brumm

Zhang

2006

Journal of Biological Chemistry

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“…5). Furthermore, the investigations of Mittnacht et al (1988) indicated that IFN-~ inhibited the transcription of HSV-1 immediate early genes. If rBoIFN-cql has a similar action this would suggest that BHV-l-induced lymphocytolysis involves a mechanism independent of viral gene transcription or protein synthesis.…”

Section: Discussionmentioning

confidence: 99%

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes

Griebel

Ohmann²,

Lawman³

et al. 1990

Journal of General Virology

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The interaction between activated bovine T lymphocytes (BTLs) and bovine herpesvirus type 1 (BHV-1) was investigated. BHV-1 infection of BTLs reduced the amplitude of recombinant bovine interleukin 2-induced proliferative responses. This decreased proliferation was caused by a virus-induced lymphocytolysis which was dependent on viable virus and was not inhibited by recombinant bovine interferon-~xl. Furthermore, lymphocytolysis was not associated with virus replication or with the synthesis of detectable levels of viral proteins. Electron microscopic examination of virusinfected cells revealed that lymphocytolysis was characterized by early nuclear disintegration resembling apoptosis. These observations suggest that activated T cells, localized at the site of BHV-1 infection, may be susceptible to virus-induced cytolysis.

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“…A number of investigators have concluded that IFN blocks HSV replication at the onset of IE viral gene transcription (Mittnacht et al, 1988;Oberman & Panet, 1988;Feduchi et al, 1989;De Stasio & Taylor, 1989). To initiate virus replication the virion-associated protein VP16 forms a complex with cellular components, and this complex activates transcription of IE genes (Preston et al, 1988;Kristie et al, 1989;LaMarco & McKnight, 1989).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, it has the potential to interfere with the early steps of virus invasion and replication (Gaines et al, 1987;Gresser et al, 1976;Domke-Opitz et al, 1986). The mechanism of action of IFN-induced antiviral proteins on HSV replication has been intensively studied (Domke-Opitz et al, 1986;Mittnacht et al, 1988;Mufioz & Carrasco, 1984;Oberman & Panet, 1988;Feduchi et al, 1989;Straub et al, 1986). The currently available data suggest that HSV multiplication is blocked by IFN-induced antiviral proteins at an early step in virus synthesis, possibly an event between the uncoating of the infecting virion and the onset of immediate early (IE) viral gene transcription.…”

Section: Introductionmentioning

confidence: 99%

Mapping the genetic region coding for herpes simplex virus resistance to mouse interferon /beta

Oakes

Lausch

1993

Journal of General Virology

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Herpes simplex virus (HSV) ocular virulence has been associated with strain sensitivity to mouse interferon (IFN)-ct/fl. To identifiy the region of the virus genome associated with heightened resistance to this cytokine, intertypic recombinants were constructed using the intact genome of avirulent, IFN-sensitive HSV type 1 (strain 35) and XbaI-digested DNA from virulent, IFNresistant HSV type 2 (strain 186). An intertypic recombinant, designated HSV-R4, was isolated which grew to titres 10-to 100-fold higher than HSV-l(35) in mouse ocular tissue in vivo, and induced stromal keratitis. The recombinant which was several orders of magnitude more resistant to mouse IFN-ct/fl than HSV-l(35) had a genome composed of HSV-l(35) DNA except for a 12 kb fragment (0.15 to 0.23 map units) derived from HSV-2(186). To define the IFN resistance locus further, three overlapping subclones of this 12 kb fragment were constructed from the HSV-2(186) genome and subjected to marker rescue experiments. The cloned BamHI D fragment was the only subclone that promoted HSV-1 (35) ocular growth in vivo. An intertypic recombinant, designated HSV-R(BD), was isolated from the 35 x 186 BamHI D transfection progeny pool. This recombinant, in contrast to HSV-l(35), was several orders of magnitude more resistant to mouse IFN-ct/fl inhibition in vitro, grew 10-to 100-fold better in mouse ocular tissue in vivo, and caused severe necrotizing stromal keratitis in BALB/c mice. Analysis of the recombinant genome indicated that the HSV-2 genetic information responsible for IFN resistance of HSV-R(BD) was located within the BamHI D fragment, most likely mapping to that region containing three partial open reading frames designated UL14, UL15 and UL16. The products encoded by this region remain to be identified.

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Interferon treatment inhibits onset of herpes simplex virus immediate-early transcription

Cited by 93 publications

References 45 publications

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes

Mapping the genetic region coding for herpes simplex virus resistance to mouse interferon /beta

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