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

1991 ◽  
Vol 4 (2) ◽  
pp. 111-122 ◽  
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

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

Virology ◽  
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

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

2013 ◽  
Vol 14 (1) ◽  
pp. 88-102 ◽  
Author(s):  
Randall L. Levings ◽  
James A. Roth
Keyword(s):  
Immune Response ◽  
Latent Infection ◽  
Bovine Herpesvirus ◽  
Lytic Replication ◽  
Host Cells ◽  
Type I Interferons ◽  
Disease Spread ◽  
Type I ◽  
Bovine Herpesvirus 1 ◽  
Herpesvirus 1

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.

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

2013 ◽  
Vol 14 (1) ◽  
pp. 103-123 ◽  
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.

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

2002 ◽  
Vol 76 (18) ◽  
pp. 9002-9010 ◽  
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.

scholarly journals Bovine Herpesvirus-1 (BHV-1) Recombinant Expressing Pseudorabies Virus (PrV) Glycoproteins B and C Induces Type 1 Immune Response in BALB/c mice

2002 ◽  
Vol 64 (7) ◽  
pp. 589-596 ◽  
Author(s):  
Yasuhiro TAKASHIMA ◽  
Noriko NAGANE ◽  
Orkash HUSHUR ◽  
Yasunobu MATSUMOTO ◽  
Haruki OTSUKA
Keyword(s):  
Immune Response ◽  
Pseudorabies Virus ◽  
Bovine Herpesvirus ◽  
Bovine Herpesvirus 1 ◽  
Herpesvirus 1
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