Deletions in vaccine strains of pseudorabies virus and their effect on synthesis of glycoprotein gp63

Petrovskis, Erik; Timmins, J G; Gierman, Todd; Post, Leonard

doi:10.1128/jvi.60.3.1166-1169.1986

Cited by 123 publications

(55 citation statements)

References 17 publications

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“…Effect of gp63 and gI on virus replication. Neither gI nor gp63 is essential for replication in vitro (2,12,13,18). Indeed, the yields of infectious virus and of viral particles obtained from RK and PK cells infected with gIor gp63deletion-M13 insertion mutants, with glor gp63-deletion mutants, or with wild-type virus are approximately the same (3, 13).…”

Section: Resultsmentioning

confidence: 99%

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Complex between glycoproteins gI and gp63 of pseudorabies virus: its effect on virus replication

Zuckermann

Mettenleiter

Schreurs

et al. 1988

J Virol

114

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To ascertain the biological functions of different glycoproteins that are nonessential for pseudorabies virus growth in vitro, we have constructed mutants defective in one (or a combination) of these glycoproteins and have examined various aspects of their role in the infective process. We made the following two observations. (i) Glycoproteins gI and gp63 are noncovalently complexed to each other. They are coprecipitated by antisera against either one of these glycoproteins but do not share antigenic determinants: monoclonal antibodies against gp63 do not immunoprecipitate gI from extracts of gp63mutant-infected cells, and monoclonal antibodies against gI do not immunoprecipitate gp63 from extracts of glmutant-infected cells. (ii) Mutants unable to synthesize either gI or gp63 have some common biological characteristics; they have a growth advantage in primary chicken embryo fibroblasts. Furthermore, we have shown previously that in conjunction with glycoprotein gIII, gI and gp63 are necessary for the expression of virulence (T. C. Mettenleiter, C.

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Section: Resultsmentioning

confidence: 99%

“…Pseudorabies virus (PrV), a herpesvirus of swine, encodes at least four glycoproteins that are not essential for growth in cell culture (2,12,18,21,22,26). Primary isolates of PrV, however, do express these glycoproteins; consequently, they must play a role in virus replication, at least in vivo.…”

mentioning

confidence: 99%

Complex between glycoproteins gI and gp63 of pseudorabies virus: its effect on virus replication

Zuckermann

Mettenleiter

Schreurs

et al. 1988

J Virol

114

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“…Most of the Us region has been sequenced, and detailed restriction maps of that region of the genome are available (27,28). The availability of these restriction maps allowed us to map the deletions in some of the vaccine strains in detail.…”

Section: Mapping Deletions In the S Component Of Attenuated Strainsmentioning

confidence: 99%

“…Deletions in the short unique (Us) component of the genome are present in the genomes of several viable variants of PrV (7,17,22,27). Interestingly, several attenuated strains of PrV consist of homogeneous populations of virions with genomes that carry such deletions.…”

mentioning

confidence: 99%

Host cell-specific growth advantage of pseudorabies virus with a deletion in the genome sequences encoding a structural glycoprotein

Mettenleiter

Lomniczi

Sugg

et al. 1988

J Virol

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Several attenuated strains of pseudorabies virus contain genomes that carry a deletion in their short unique (Us) component. The sizes of the deletions are different in the various attenuated strains; the deletions may include part of one of the inverted repeats as well as part of the Us region of the genome. In most cases, the deletion includes the gene encoding the glycoprotein gI. The attenuated strains with a deletion in their S component have a common history of having been cultivated in chicken embryo fibroblasts (CEF). We show here that passage of wild-type virus in CEF promotes the emergence of populations of virions with a deletion in their S component. The emergence of these mutants is the result of their growth advantage over the wild type and is related to the lack of expression of gI, as shown by the following. (i) The Norden strain (which has a deletion in the Us) was marker rescued to restore an intact Us. The nonrescued Norden strain had a growth advantage over the rescued Norden strain in CEF. (ii) Passage of wild-type (gI+) virus in CEF but not in rabbit kidney or pig kidney cells resulted invariably in the emergence of virions whose genomes had a deletion in the S component. (iii) Passage of a glmutant in CEF did not result in the emergence of such virions. The emergence of virions with a deletion in their S component thus appears to be linked to gI expression. We conclude that gI is deleterious to the growth of pseudorabies virus in CEF and that this effect is cell type specific.

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“…Functional studies indicate that gp63 and gl play major roles in the release of progeny virions from PRV infected cells (62,66,68,74), The host immune response to gp63 has not been described to date.…”

Section: Structural Prv Alvcooroteinsmentioning

confidence: 99%

Studies on the immunoreactivity of native and recombinant pseudorabies virus nucleocapsid proteins

McGinley

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Deletions in vaccine strains of pseudorabies virus and their effect on synthesis of glycoprotein gp63

Cited by 123 publications

References 17 publications

Complex between glycoproteins gI and gp63 of pseudorabies virus: its effect on virus replication

Complex between glycoproteins gI and gp63 of pseudorabies virus: its effect on virus replication

Host cell-specific growth advantage of pseudorabies virus with a deletion in the genome sequences encoding a structural glycoprotein

Studies on the immunoreactivity of native and recombinant pseudorabies virus nucleocapsid proteins

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