Induction of protective immunity and neutralizing antibodies to pseudorabies virus by immunization of anti-idiotypic antibodies

Tsuda, Toshitaka; Onodera, Takashi; Sugimura, Takaaki; Murakami, Yosuke

doi:10.1007/bf01309810

Cited by 10 publications

(5 citation statements)

References 20 publications

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“…The most efficacious virus-neutralizing antibodies target PRV gC and gD (89, 115 164, 256, 293, 425). Subunit vaccines consisting of gC or gD, as well as anti-idiotypic anti-gD antibodies elicit some degree of protective immune responses (257,261,409). A large portion of the neutralizing activity in convalescent swine sera is directed against gC (27).…”

Section: Dna Vaccinesmentioning

confidence: 99%

Molecular Biology of Pseudorabies Virus: Impact on Neurovirology and Veterinary Medicine

Pomeranz

Reynolds

Hengartner

2005

Microbiol Mol Biol Rev

724

657

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Pseudorabies virus (PRV) is a herpesvirus of swine, a member of the Alphaherpesvirinae subfamily, and the etiological agent of Aujeszky's disease. This review describes the contributions of PRV research to herpesvirus biology, neurobiology, and viral pathogenesis by focusing on (i) the molecular biology of PRV, (ii) model systems to study PRV pathogenesis and neurovirulence, (iii) PRV transsynaptic tracing of neuronal circuits, and (iv) veterinary aspects of pseudorabies disease. The structure of the enveloped infectious particle, the content of the viral DNA genome, and a step-by-step overview of the viral replication cycle are presented. PRV infection is initiated by binding to cellular receptors to allow penetration into the cell. After reaching the nucleus, the viral genome directs a regulated gene expression cascade that culminates with viral DNA replication and production of new virion constituents. Finally, progeny virions self-assemble and exit the host cells. Animal models and neuronal culture systems developed for the study of PRV pathogenesis and neurovirulence are discussed. PRV serves as a self-perpetuating transsynaptic tracer of neuronal circuitry, and we detail the original studies of PRV circuitry mapping, the biology underlying this application, and the development of the next generation of tracer viruses. The basic veterinary aspects of pseudorabies management and disease in swine are discussed. PRV infection progresses from acute infection of the respiratory epithelium to latent infection in the peripheral nervous system. Sporadic reactivation from latency can transmit PRV to new hosts. The successful management of PRV disease has relied on vaccination, prevention, and testing

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Section: Dna Vaccinesmentioning

confidence: 99%

Molecular Biology of Pseudorabies Virus: Impact on Neurovirology and Veterinary Medicine

Pomeranz

Reynolds

Hengartner

2005

Microbiol Mol Biol Rev

724

657

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“…It was interesting to note that both RAb2-B1 and RAb2-B2 reacted strongly with M1877 ( Fig. 2, b response to the original antigen, which has been demonstrated in numerous antibody systems (5,7,8,14,15,17,21,22,24,25,28,29). Our observation that immunization of mice with RAb2-A induced an anti-VP7 antibody response further supports the conclusion that RAb2-A represents the internal image of VP7.…”

Section: Discussionmentioning

confidence: 75%

“…On the other hand, the absence of cross-reaction among the idiotypic regions of the three anti-VP7 mAbs should not be surprising since a low incidence of cross-reacting Ids was found among mAbs directed to the same antigenic site but derived from different fusions (26). It was interesting to note that both RAb2-B1 and RAb2-B2 reacted strongly with M1877 response to the original antigen, which has been demonstrated in numerous antibody systems (5,7,8,14,15,17,21,22,24,25,28,29). Our observation that immunization of mice with RAb2-A induced an anti-VP7 antibody response further supports the conclusion that RAb2-A represents the internal image of VP7.…”

Section: Discussionmentioning

confidence: 78%

Evidence That Two Distinct Populations of Rabbit Anti‐Idiotypic Antibodies Are Induced by Three Monoclonal Antibodies Specific for Bluetongue Virus Core Protein VP7

Lin¹,

Zhou²

1996

Microbiology and Immunology

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Three groups of anti‐idiotypic antibodies (anti‐Id or Ab2), designated RAb2‐A, RAb2‐B1, and RAb2‐B2, were isolated from rabbit antiserum raised against three monoclonal antibodies (mAbs) (M1875, M1877, and M1886) specific for the bluetongue virus core protein, VP7. RAb2‐A was specific for the idiotype of M1875. RAb2‐B1 and RAb2‐B2, isolated through the M1877 and M1886 affinity columns, respectively, were directed against the common idiotype that is shared by M1877 and M1886 and therefore classified in the same population (RAb2‐B). Further characterization revealed that the two anti‐Id populations, RAb2‐A and RAb2‐B, were significantly different. RAb2‐A was an Ab2β type of anti‐Id since (i) its reaction with M1875 was inhibited by the antigen; (ii) it inhibited the M1875‐VP7 interaction; and (iii) it elicited anti‐VP7 antibody response in Balb/c mice. In contrast, RAb2‐B may represent an Ab2α type of anti‐Id since its reactions with M1877 or M1886 were not inhibited by the antigen, even though it inhibited mAbs from binding to the antigen. These results indicated that RAb2‐A and RAb2‐B represent two distinct populations of anti‐Ids to anti‐VP7 mAbs with similar epitope specificity.

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“…Anti-idiotype (anti-Id or Ab2) immunizations for HV (Kennedy et al , 1984; Gurish et al , 1988; Tsuda et al , 1992; Zhou and Afshar, 1995), and BHV-1 in particular have been reported. Srikumaran et al (1990), Hariharan et al (1991), and Orten et al (1991) used neutralizing murine MAb as Ab1 to generate bovine polyclonal Ab (PAb), bovine MAb, or rabbit PAb Ab2 respectively, which in turn were used to elicit neutralizing Ab3 in mice.…”

Section: Vaccinationmentioning

confidence: 99%

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

Levings

Roth

2013

Anim. Health. Res. Rev.

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Bovine 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 antibodydependent 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. AbstractBovine herpesvirus 1 (BHV-1) infection is widespread and causes a variety of diseases.

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Induction of protective immunity and neutralizing antibodies to pseudorabies virus by immunization of anti-idiotypic antibodies

Cited by 10 publications

References 20 publications

Molecular Biology of Pseudorabies Virus: Impact on Neurovirology and Veterinary Medicine

Molecular Biology of Pseudorabies Virus: Impact on Neurovirology and Veterinary Medicine

Evidence That Two Distinct Populations of Rabbit Anti‐Idiotypic Antibodies Are Induced by Three Monoclonal Antibodies Specific for Bluetongue Virus Core Protein VP7

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

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