Immunity to Bovine Herpesvirus 1: I. Viral lifecycle and innate immunity

AbstractBovine herpesvirus 1 (BHV-1) causes a variety of diseases and is globally distributed. It infects via mucosal epithelium, leading to rapid lytic replication and latent infection, primarily in sensory ganglia. Large amounts of virus can be excreted by the host on primary infection or upon recrudescence of latent infection, resulting in disease spread. The bovine immune response to BHV-1 is rapid, robust, balanced, and long-lasting. The innate immune system is the first to respond to the infection, with type I interferons (IFNs), inflammatory cytokines, killing of infected host cells, and priming of a balanced adaptive immune response. The virus possesses a variety of immune evasion strategies, including inhibition of type I IFN production, chemokine and complement binding, infection of macrophages and neutrophils, and latency. BHV-1 immune suppression contributes to the severity of its disease manifestations and to the bovine respiratory disease complex, the leading cause of cattle death loss in the USA.

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Bacterial Cyclic Dinucleotides and the cGAS–cGAMP–STING Pathway: A Role in Periodontitis?

Pathogens ◽

10.3390/pathogens10060675 ◽

2021 ◽

Vol 10 (6) ◽

pp. 675

Author(s):

Samira Elmanfi ◽

Mustafa Yilmaz ◽

Wilson W. S. Ong ◽

Kofi S. Yeboah ◽

Herman O. Sintim ◽

...

Keyword(s):

Immune Response ◽

Periodontal Disease ◽

Innate Immune ◽

Host Cells ◽

Type I Interferons ◽

Type I ◽

Vaccine Adjuvants ◽

Cyclic Dinucleotides ◽

Sting Pathway

Host cells can recognize cytosolic double-stranded DNAs and endogenous second messengers as cyclic dinucleotides—including c-di-GMP, c-di-AMP, and cGAMP—of invading microbes via the critical and essential innate immune signaling adaptor molecule known as STING. This recognition activates the innate immune system and leads to the production of Type I interferons and proinflammatory cytokines. In this review, we (1) focus on the possible role of bacterial cyclic dinucleotides and the STING/TBK1/IRF3 pathway in the pathogenesis of periodontal disease and the regulation of periodontal immune response, and (2) review and discuss activators and inhibitors of the STING pathway as immune response regulators and their potential utility in the treatment of periodontitis. PubMed/Medline, Scopus, and Web of Science were searched with the terms “STING”, “TBK 1”, “IRF3”, and “cGAS”—alone, or together with “periodontitis”. Current studies produced evidence for using STING-pathway-targeting molecules as part of anticancer therapy, and as vaccine adjuvants against microbial infections; however, the role of the STING/TBK1/IRF3 pathway in periodontal disease pathogenesis is still undiscovered. Understanding the stimulation of the innate immune response by cyclic dinucleotides opens a new approach to host modulation therapies in periodontology.

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TLR activation, immune response and viral protection elicited in cattle by a commercial vaccine against Bovine Herpesvirus-1

Virology ◽

10.1016/j.virol.2021.11.014 ◽

2021 ◽

Author(s):

Kornuta Claudia Alejandra ◽

Cheuquepán Felipe ◽

Bidart Juan Esteban ◽

Soria Ivana ◽

Gammella Mariela ◽

...

Keyword(s):

Immune Response ◽

Bovine Herpesvirus ◽

Bovine Herpesvirus 1 ◽

Commercial Vaccine ◽

Herpesvirus 1

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miR-26a Inhibits Feline Herpesvirus 1 Replication by Targeting SOCS5 and Promoting Type I Interferon Signaling

Viruses ◽

10.3390/v12010002 ◽

2019 ◽

Vol 12 (1) ◽

pp. 2 ◽

Cited By ~ 3

Author(s):

Jikai Zhang ◽

Zhijie Li ◽

Jiapei Huang ◽

Hang Yin ◽

Jin Tian ◽

...

Keyword(s):

Immune Response ◽

Viral Infection ◽

Innate Immune Response ◽

Antiviral Response ◽

Innate Immune ◽

Host Cells ◽

Type I ◽

Type I Ifn ◽

Feline Herpesvirus ◽

Herpesvirus 1

In response to viral infection, host cells activate various antiviral responses to inhibit virus replication. While feline herpesvirus 1 (FHV-1) manipulates the host early innate immune response in many different ways, the host could activate the antiviral response to counteract it through some unknown mechanisms. MicroRNAs (miRNAs) which serve as a class of regulatory factors in the host, participate in the regulation of the host innate immune response against virus infection. In this study, we found that the expression levels of miR-26a were significantly upregulated upon FHV-1 infection. Furthermore, FHV-1 infection induced the expression of miR-26a via a cGAS-dependent pathway, and knockdown of cellular cGAS significantly blocked the expression of miR-26a induced by poly (dA:dT) or FHV-1 infection. Next, we investigated the biological function of miR-26a during viral infection. miR-26a was able to increase the phosphorylation of STAT1 and promote type I IFN signaling, thus inhibiting viral replication. The mechanism study showed that miR-26a directly targeted host SOCS5. Knockdown of SOCS5 increased the phosphorylation of STAT1 and enhanced the type I IFN-mediated antiviral response, and overexpression of suppressor of the cytokine signalling 5 (SOCS5) decreased the phosphorylation of STAT1 and inhibited the type I IFN-mediated antiviral response. Meanwhile, with the knockdown of SOCS5, the upregulated expression of phosphorylated STAT1 and the anti-virus effect induced by miR-26a were significantly inhibited. Taken together, our data demonstrated a new strategy of host miRNAs against FHV-1 infection by enhancing IFN antiviral signaling.

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Induction of Immune Response to Bovine Herpesvirus-1 with Anti-idiotypic Antibodies

Viral Immunology ◽

10.1089/vim.1991.4.111 ◽

1991 ◽

Vol 4 (2) ◽

pp. 111-122 ◽

Cited By ~ 5

Author(s):

D.J. ORTEN ◽

P.O. REDDY ◽

D.N. REDDY ◽

W. XUE ◽

O.Y. ABDELMAGID ◽

...

Keyword(s):

Immune Response ◽

Bovine Herpesvirus ◽

Bovine Herpesvirus 1 ◽

Herpesvirus 1

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Immunity to bovine herpesvirus 1: II. Adaptive immunity and vaccinology

Animal Health Research Reviews ◽

10.1017/s1466252313000054 ◽

2013 ◽

Vol 14 (1) ◽

pp. 103-123 ◽

Cited By ~ 17

Author(s):

Randall L. Levings ◽

James A. Roth

Keyword(s):

Immune Response ◽

Immune System ◽

Cytotoxic T Lymphocyte ◽

Clinical Signs ◽

Human Herpesvirus ◽

Bovine Herpesvirus ◽

Genetically Engineered ◽

Cell Mediated Immunity ◽

Bovine Herpesvirus 1 ◽

Herpesvirus 1

AbstractBovine herpesvirus 1 (BHV-1) infection is widespread and causes a variety of diseases. Although similar in many respects to the human immune response to human herpesvirus 1, the differences in the bovine virus proteins, immune system components and strategies, physiology, and lifestyle mean the bovine immune response to BHV-1 is unique. The innate immune system initially responds to infection, and primes a balanced adaptive immune response. Cell-mediated immunity, including cytotoxic T lymphocyte killing of infected cells, is critical to recovery from infection. Humoral immunity, including neutralizing antibody and antibody-dependent cell-mediated cytotoxicity, is important to prevention or control of (re-)infection. BHV-1 immune evasion strategies include suppression of major histocompatibility complex presentation of viral antigen, helper T-cell killing, and latency. Immune suppression caused by the virus potentiates secondary infections and contributes to the costly bovine respiratory disease complex. Vaccination against BHV-1 is widely practiced. The many vaccines reported include replicating and non-replicating, conventional and genetically engineered, as well as marker and non-marker preparations. Current development focuses on delivery of major BHV-1 glycoproteins to elicit a balanced, protective immune response, while excluding serologic markers and virulence or other undesirable factors. In North America, vaccines are used to prevent or reduce clinical signs, whereas in some European Union countries marker vaccines have been employed in the eradication of BHV-1 disease.

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The cell-mediated immune response induced by plasmid encoding bovine herpesvirus 1 glycoprotein B is enhanced by plasmid encoding IL-12 when delivered intramuscularly or by gene gun, but not after intradermal injection

Vaccine ◽

10.1016/j.vaccine.2006.04.026 ◽

2006 ◽

Vol 24 (25) ◽

pp. 5349-5359 ◽

Cited By ~ 6

Author(s):

Y. Huang ◽

L.A. Babiuk ◽

S. van Drunen Littel-van den Hurk

Keyword(s):

Immune Response ◽

Bovine Herpesvirus ◽

Intradermal Injection ◽

Glycoprotein B ◽

Gene Gun ◽

Bovine Herpesvirus 1 ◽

Cell Mediated Immune Response ◽

Herpesvirus 1

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The Immunogenicity and Protective Efficacy of Bovine Herpesvirus 1 Glycoprotein D plus Emulsigen Are Increased by Formulation with CpG Oligodeoxynucleotides

Journal of Virology ◽

10.1128/jvi.76.18.9002-9010.2002 ◽

2002 ◽

Vol 76 (18) ◽

pp. 9002-9010 ◽

Cited By ~ 88

Author(s):

X. P. Ioannou ◽

P. Griebel ◽

R. Hecker ◽

L. A. Babiuk ◽

S. van Drunen Littel-van den Hurk

Keyword(s):

Immune Response ◽

Neutralizing Antibodies ◽

Protective Efficacy ◽

Bovine Herpesvirus ◽

Ammonium Bromide ◽

Cpg Odn ◽

Glycoprotein D ◽

Bovine Herpesvirus 1 ◽

Cpg Oligodeoxynucleotides ◽

Herpesvirus 1

ABSTRACT The immunogenicity and protective efficacy of a bovine herpesvirus 1 (BHV-1) subunit vaccine formulated with Emulsigen (Em) and a synthetic oligodeoxynucleotide containing unmethylated CpG dinucleotides (CpG ODN) was determined in cattle. A truncated, secreted version of BHV-1 glycoprotein D (tgD) formulated with Em and CpG ODN at concentrations of 25, 2.5, or 0.25 mg/dose produced a more balanced immune response, higher levels of virus neutralizing antibodies, and greater protection after BHV-1 challenge compared to tgD adjuvanted with either Em or CpG ODN alone. In contrast, tgD formulated with Em and either 25 mg of a non-CpG ODN or another immunostimulatory compound, dimethyl dioctadecyl ammonium bromide, induced similar immunity and protection compared to tgD formulated with Em alone, a finding which confirms the immunostimulatory effect of ODN to be CpG motif mediated. Our results demonstrate the ability of CpG ODN to induce a strong and balanced immune response in a target species.

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Truncated bovine herpesvirus-1 glycoprotein I (gpI) initiates a protective local immune response in its natural host

Vaccine ◽

10.1016/0264-410x(94)90053-1 ◽

1994 ◽

Vol 12 (2) ◽

pp. 145-152 ◽

Cited By ~ 15

Author(s):

Yi Gao ◽

Thomas P. Leary ◽

Linda Eskra ◽

Gary A. Splitter

Keyword(s):

Immune Response ◽

Bovine Herpesvirus ◽

Natural Host ◽

Local Immune Response ◽

Bovine Herpesvirus 1 ◽

Glycoprotein I ◽

Herpesvirus 1

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The in vivo effects of recombinant bovine herpesvirus-1 expressing bovine interferon-γ

Journal of General Virology ◽

10.1099/0022-1317-81-11-2665 ◽

2000 ◽

Vol 81 (11) ◽

pp. 2665-2673 ◽

Cited By ~ 44

Author(s):

Camilo Raggo ◽

Monique Habermehl ◽

Lorne A. Babiuk ◽

Philip Griebel

Keyword(s):

Primary Infection ◽

Latent Infection ◽

Bovine Herpesvirus ◽

Interferon Γ ◽

Bovine Herpesvirus 1 ◽

Recombinant Interferon ◽

Virus Shedding ◽

Ifn Γ ◽

Herpesvirus 1

To study the biological relevance of using bovine herpesvirus-1 (BHV-1) as a vector for expressing cytokines, a BHV-1 virus that expressed bovine interferon-γ (IFN-γ) was constructed. This recombinant virus (BHV-1/IFNγ) was then used to infect the natural host in a respiratory disease model. In vitro characterization of the recombinant interferon-γ confirmed that the cytokine expressed in BHV-1-infected cells was biologically active. The in vivo effects of the recombinant IFN-γ were then analysed during a primary infection and after reactivation of a latent infection. During the primary infection, similar body temperature, clinical responses and virus shedding were observed for calves infected with either recombinant BHV-1/IFNγ or parental gC−/LacZ+ virus. An analysis of cellular and humoral responses did not reveal any significant immunomodulation by BHV-1/IFNγ during the primary infection. The stability and activity of recombinant IFN-γ was also analysed following the establishment of a latent infection. The presence of recombinant IFN-γ did not significantly alter virus shedding following reactivation. The isolation of reactivated BHV-1/IFNγ virus confirmed that a functional IFN-γ gene was retained during latency. Thus, herpesviruses may provide virus vectors that retain functional genes during latency and recrudescence.

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