A genetically improved Aujeszky's disease vaccine strain derived from K/61 displays enhanced antigenicity in pigs

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Abstract

Aujeszky's disease vaccine strain Bartha K/61 carries two genetic defects that can be deleterious in a vaccine strain. It is deficient in the expression of glycoprotein gC, a protective antigen of the Aujeszky's disease virus and its gM lacks carbohydrates side chains. Both glycoproteins are necessary for the optimal growth as well, therefore the antigenicity of a live vaccine that is deficient in these functions, must be impaired in vivo. Optimal growth of a vaccine strain in vivo is a prerequisite of the accumulation of viral antigens necessary for immunstimulation. In order to correct these defects, a mixed infection of K/61 and a virulent strain was performed to generate recombinants. From the offsprings, a recombinant (designated MNC+/10a) was selected in which the essential properties of vaccine K/61, such as the defects of its major virulence gene and the lack of gE gene were retained, while the function of gC was restored (Fig. 2). Probably, gM was also rescued because MNC+/10a forms larger plaques than K/61 (Fig. 4). 3 weeks old piglets inoculated intranasally with 107 plaque forming units of MNC+/10a remained healthy and it proved aviailent in day-old chikens injected intracerebrally (Table 1). A restriction site marker (BamHI 2a+2b) was also transferred from the virulent parent to the avirulent MNC+/10a strain (Fig. 1, 3). MNC+/10a showed ten-fold higher growth capacity in the nose of piglets as compared to K/61 (with 75×104 and 6×104 total PFU produced, respectively) (Table 2). On intramuscular injection MNC+/10a induced significantly higher antibody level than K/61 (ADV-ELISA titres were 1:300-500 and 1:100-300, respectively) (Table 2, Fig. 5). There was a positive correlation between the ability of the vaccine strain to replicate in the nasal mucosa and the primary antibody response (Table 2). This is the first report demonstrating that the restoration of a protective protein function has indeed resulted in an improved antigenicity as measured by an elevated level of antibody production.

Translated title of the contributionA genetically improved Aujeszky's disease vaccine strain derived from K/61 displays enhanced antigenicity in pigs
Original languageHungarian
Pages (from-to)195-203
Number of pages9
JournalMagyar Allatorvosok Lapja
Volume120
Issue number4
Publication statusPublished - 1998

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Pseudorabies
Aujeszky disease
Swine
Vaccines
vaccines
swine
piglets
glycoproteins
Antibody Formation
Glycoproteins
nasal mucosa
Growth
antibodies
Suid herpesvirus 1
viral antigens
Suid Herpesvirus 1
genetic disorders
live vaccines
antibody formation
intramuscular injection

ASJC Scopus subject areas

  • veterinary(all)

Cite this

@article{e1612320bd03483d80cee5b1989e4c5a,
title = "Az Aujeszky-f{\'e}le betegs{\'e}g elleni, fokozott antigenit{\'a}s{\'u}, genetikailag jav{\'i}tott vakcinat{\"o}rzs elo{\'a}ll{\'i}t{\'a}sa a K/61 jelu t{\"o}rzsbol",
abstract = "Aujeszky's disease vaccine strain Bartha K/61 carries two genetic defects that can be deleterious in a vaccine strain. It is deficient in the expression of glycoprotein gC, a protective antigen of the Aujeszky's disease virus and its gM lacks carbohydrates side chains. Both glycoproteins are necessary for the optimal growth as well, therefore the antigenicity of a live vaccine that is deficient in these functions, must be impaired in vivo. Optimal growth of a vaccine strain in vivo is a prerequisite of the accumulation of viral antigens necessary for immunstimulation. In order to correct these defects, a mixed infection of K/61 and a virulent strain was performed to generate recombinants. From the offsprings, a recombinant (designated MNC+/10a) was selected in which the essential properties of vaccine K/61, such as the defects of its major virulence gene and the lack of gE gene were retained, while the function of gC was restored (Fig. 2). Probably, gM was also rescued because MNC+/10a forms larger plaques than K/61 (Fig. 4). 3 weeks old piglets inoculated intranasally with 107 plaque forming units of MNC+/10a remained healthy and it proved aviailent in day-old chikens injected intracerebrally (Table 1). A restriction site marker (BamHI 2a+2b) was also transferred from the virulent parent to the avirulent MNC+/10a strain (Fig. 1, 3). MNC+/10a showed ten-fold higher growth capacity in the nose of piglets as compared to K/61 (with 75×104 and 6×104 total PFU produced, respectively) (Table 2). On intramuscular injection MNC+/10a induced significantly higher antibody level than K/61 (ADV-ELISA titres were 1:300-500 and 1:100-300, respectively) (Table 2, Fig. 5). There was a positive correlation between the ability of the vaccine strain to replicate in the nasal mucosa and the primary antibody response (Table 2). This is the first report demonstrating that the restoration of a protective protein function has indeed resulted in an improved antigenicity as measured by an elevated level of antibody production.",
author = "B. Lomniczi and E. Wehmann",
year = "1998",
language = "Hungarian",
volume = "120",
pages = "195--203",
journal = "Magyar Allatorvosok Lapja",
issn = "0025-004X",
publisher = "Magyar Mezogazdasag Ltd",
number = "4",

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TY - JOUR

T1 - Az Aujeszky-féle betegség elleni, fokozott antigenitású, genetikailag javított vakcinatörzs eloállítása a K/61 jelu törzsbol

AU - Lomniczi, B.

AU - Wehmann, E.

PY - 1998

Y1 - 1998

N2 - Aujeszky's disease vaccine strain Bartha K/61 carries two genetic defects that can be deleterious in a vaccine strain. It is deficient in the expression of glycoprotein gC, a protective antigen of the Aujeszky's disease virus and its gM lacks carbohydrates side chains. Both glycoproteins are necessary for the optimal growth as well, therefore the antigenicity of a live vaccine that is deficient in these functions, must be impaired in vivo. Optimal growth of a vaccine strain in vivo is a prerequisite of the accumulation of viral antigens necessary for immunstimulation. In order to correct these defects, a mixed infection of K/61 and a virulent strain was performed to generate recombinants. From the offsprings, a recombinant (designated MNC+/10a) was selected in which the essential properties of vaccine K/61, such as the defects of its major virulence gene and the lack of gE gene were retained, while the function of gC was restored (Fig. 2). Probably, gM was also rescued because MNC+/10a forms larger plaques than K/61 (Fig. 4). 3 weeks old piglets inoculated intranasally with 107 plaque forming units of MNC+/10a remained healthy and it proved aviailent in day-old chikens injected intracerebrally (Table 1). A restriction site marker (BamHI 2a+2b) was also transferred from the virulent parent to the avirulent MNC+/10a strain (Fig. 1, 3). MNC+/10a showed ten-fold higher growth capacity in the nose of piglets as compared to K/61 (with 75×104 and 6×104 total PFU produced, respectively) (Table 2). On intramuscular injection MNC+/10a induced significantly higher antibody level than K/61 (ADV-ELISA titres were 1:300-500 and 1:100-300, respectively) (Table 2, Fig. 5). There was a positive correlation between the ability of the vaccine strain to replicate in the nasal mucosa and the primary antibody response (Table 2). This is the first report demonstrating that the restoration of a protective protein function has indeed resulted in an improved antigenicity as measured by an elevated level of antibody production.

AB - Aujeszky's disease vaccine strain Bartha K/61 carries two genetic defects that can be deleterious in a vaccine strain. It is deficient in the expression of glycoprotein gC, a protective antigen of the Aujeszky's disease virus and its gM lacks carbohydrates side chains. Both glycoproteins are necessary for the optimal growth as well, therefore the antigenicity of a live vaccine that is deficient in these functions, must be impaired in vivo. Optimal growth of a vaccine strain in vivo is a prerequisite of the accumulation of viral antigens necessary for immunstimulation. In order to correct these defects, a mixed infection of K/61 and a virulent strain was performed to generate recombinants. From the offsprings, a recombinant (designated MNC+/10a) was selected in which the essential properties of vaccine K/61, such as the defects of its major virulence gene and the lack of gE gene were retained, while the function of gC was restored (Fig. 2). Probably, gM was also rescued because MNC+/10a forms larger plaques than K/61 (Fig. 4). 3 weeks old piglets inoculated intranasally with 107 plaque forming units of MNC+/10a remained healthy and it proved aviailent in day-old chikens injected intracerebrally (Table 1). A restriction site marker (BamHI 2a+2b) was also transferred from the virulent parent to the avirulent MNC+/10a strain (Fig. 1, 3). MNC+/10a showed ten-fold higher growth capacity in the nose of piglets as compared to K/61 (with 75×104 and 6×104 total PFU produced, respectively) (Table 2). On intramuscular injection MNC+/10a induced significantly higher antibody level than K/61 (ADV-ELISA titres were 1:300-500 and 1:100-300, respectively) (Table 2, Fig. 5). There was a positive correlation between the ability of the vaccine strain to replicate in the nasal mucosa and the primary antibody response (Table 2). This is the first report demonstrating that the restoration of a protective protein function has indeed resulted in an improved antigenicity as measured by an elevated level of antibody production.

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