Search

Your search keyword '"Zsak L"' showing total 177 results
Start Over Author "Zsak L"
177 results on '"Zsak L"'

5. Comparative full genome analysis of four infectious laryngotracheitis virus (Gallid herpesvirus-1) virulent isolates from the United States

Author

Spatz, S. J., primary, Volkening, J. D., additional, Keeler, C. L., additional, Kutish, G. F., additional, Riblet, S. M., additional, Boettger, C. M., additional, Clark, K. F., additional, Zsak, L., additional, Afonso, C. L., additional, Mundt, E. S., additional, Rock, D. L., additional, and Garcia, M., additional

Published
2011
Full Text
View/download PDF

9. Genome of Horsepox Virus

Author

Tulman, E. R., primary, Delhon, G., additional, Afonso, C. L., additional, Lu, Z., additional, Zsak, L., additional, Sandybaev, N. T., additional, Kerembekova, U. Z., additional, Zaitsev, V. L., additional, Kutish, G. F., additional, and Rock, D. L., additional

Published
2006
Full Text
View/download PDF

10. Genome of Deerpox Virus

Author

Afonso, C. L., primary, Delhon, G., additional, Tulman, E. R., additional, Lu, Z., additional, Zsak, A., additional, Becerra, V. M., additional, Zsak, L., additional, Kutish, G. F., additional, and Rock, D. L., additional

Published
2005
Full Text
View/download PDF

15. The Genome of Canarypox Virus

Author

Tulman, E. R., primary, Afonso, C. L., additional, Lu, Z., additional, Zsak, L., additional, Kutish, G. F., additional, and Rock, D. L., additional

Published
2004
Full Text
View/download PDF

16. The Genomes of Sheeppox and Goatpox Viruses

Author

Tulman, E. R., primary, Afonso, C. L., additional, Lu, Z., additional, Zsak, L., additional, Sur, J.-H., additional, Sandybaev, N. T., additional, Kerembekova, U. Z., additional, Zaitsev, V. L., additional, Kutish, G. F., additional, and Rock, D. L., additional

Published
2002
Full Text
View/download PDF

18. The Genome of Camelpox Virus

Author

Afonso, C.L, primary, Tulman, E.R, additional, Lu, Z, additional, Zsak, L, additional, Sandybaev, N.T, additional, Kerembekova, U.Z, additional, Zaitsev, V.L, additional, Kutish, G.F, additional, and Rock, D.L, additional

Published
2002
Full Text
View/download PDF

19. The Genome of Swinepox Virus

Author

Afonso, C. L., primary, Tulman, E. R., additional, Lu, Z., additional, Zsak, L., additional, Osorio, F. A., additional, Balinsky, C., additional, Kutish, G. F., additional, and Rock, D. L., additional

Published
2002
Full Text
View/download PDF

26. The Genome of Fowlpox Virus

Author

Afonso, C. L., primary, Tulman, E. R., additional, Lu, Z., additional, Zsak, L., additional, Kutish, G. F., additional, and Rock, D. L., additional

Published
2000
Full Text
View/download PDF

43. An African Swine Fever Virus ERV1-ALRHomologue, 9GL, Affects Virion Maturation and Viral Growth in Macrophages and Viral Virulence in Swine

Author

Lewis, T., Zsak, L., Burrage, T. G., Lu, Z., Kutish, G. F., Neilan, J. G., and Rock, D. L.

Abstract

ABSTRACTThe African swine fever virus (ASFV) genome contains a gene,9GL, with similarity to yeast ERV1andALRgenes. ERV1has been shown to function in oxidative phosphorylation and in cell growth, while ALRhas hepatotrophic activity. 9GLencodes a protein of 119 amino acids and was highly conserved at both nucleotide and amino acid levels among all ASFV field isolates examined. Monospecific rabbit polyclonal antibody produced to a glutathione S-transferase–9GL fusion protein specifically immunoprecipitated a 14-kDa protein from macrophage cell cultures infected with the ASFV isolate Malawi Lil-20/1 (MAL). Time course analysis and viral DNA synthesis inhibitor experiments indicated that p14 was a late viral protein. A9GLgene deletion mutant of MAL (?9GL), exhibited a growth defect in macrophages of approximately 2 log10units and had a small-plaque phenotype compared to either a revertant (9GL-R) or the parental virus. 9GL affected normal virion maturation; virions containing acentric nucleoid structures comprised 90 to 99% of all virions observed in ?9GL-infected macrophages. The ?9GL virus was markedly attenuated in swine. In contrast to 9GL-R infection, where mortality was 100%, all ?9GL-infected animals survived infection. With the exception of a transient fever response in some animals, ?9GL-infected animals remained clinically normal and exhibited significant 100- to 10,000-fold reductions in viremia titers. All pigs previously infected with ?9GL survived infection when subsequently challenged with a lethal dose of virulent parental MAL. Thus, ASFV9GLgene deletion mutants may prove useful as live-attenuated ASF vaccines.

Published
2000
Full Text
View/download PDF

44. A Nonessential African Swine Fever Virus Gene UKIs a Significant Virulence Determinant in Domestic Swine

Author

Zsak, L., Caler, E., Lu, Z., Kutish, G. F., Neilan, J. G., and Rock, D. L.

Abstract

ABSTRACTSequence analysis of the right variable genomic region of the pathogenic African swine fever virus (ASFV) isolate E70 revealed a novel gene, UK, that is immediately upstream from the previously described ASFV virulence-associated gene NL-S(L. Zsak, Z. Lu, G. F. Kutish, J. G. Neilan, and D. L. Rock, J. Virol. 70:8865–8871, 1996). UK, transcriptionally oriented toward the right end of the genome, predicts a protein of 96 amino acids with a molecular mass of 10.7 kDa. Searches of genetic databases did not find significant similarity betweenUKand other known genes. Sequence analysis of theUKgenes from several pathogenic ASFVs from Europe, the Caribbean, and Africa demonstrated that this gene was highly conserved among diverse pathogenic isolates, including those from both tick and pig sources. Polyclonal antibodies raised against the UK protein specifically precipitated a 15-kDa protein from ASFV-infected macrophage cell cultures as early as 2 h postinfection. A recombinant UKgene deletion mutant, ?UK, and its revertant, UK-R, were constructed from the E70 isolate to study gene function. Although deletion of UKdid not affect the growth characteristics of the virus in macrophage cell cultures, ?UK exhibited reduced virulence in infected pigs. While mortality among parental E70- or UK-R-infected animals was 100%, all ?UK-infected pigs survived infection. Fever responses were comparable in E70-, UK-R-, and ?UK-infected groups; however, ?UK-infected animals exhibited significant, 100- to 1,000-fold, reductions in viremia titers. These data indicate that the highly conserved UKgene of ASFV, while being nonessential for growth in macrophages in vitro, is an important viral virulence determinant for domestic pigs.

Published
1998
Full Text
View/download PDF

45. Early interactions of pseudorabies virus with host cells: functions of glycoprotein gIII

Author

Zuckermann, F, Zsak, L, Reilly, L, Sugg, N, and Ben-Porat, T

Abstract

Adsorption of mutants of pseudorabies virus (PrV) lacking glycoprotein gIII is slower and less efficient than is that of wild-type virus (C. Schreurs, T. C. Mettenleiter, F. Zuckermann, N. Snugg, and T. Ben-Porat, J. Virol. 62:2251-2257, 1988). To ascertain the functions of gIII in the early interactions of PrV with its host cells, we compared the effect on wild-type virus and gIII- mutants of antibodies specific for various PrV proteins. Although adsorption of wild-type virus was inhibited by polyvalent antisera against PrV as well as by sera against gIII and gp50 (but not sera against gII), adsorption of the gIII- mutants was not inhibited by any of these antisera. These results suggest that, in contrast to adsorption of wild-type PrV, the initial interactions of the gIII- mutants with their host cells are not mediated by specific viral proteins. Furthermore, competition experiments showed that wild-type Prv and the gIII- mutants do not compete for attachment to the same cellular components. These findings show that the initial attachment of PrV to its host cells can occur by a least two different modes--one mediated by glycoprotein gIII and the other unspecific. gIII- mutants not only did not adsorb as readily to cells as did wild-type virus but also did not penetrate cells as rapidly as did wild-type virus after having adsorbed. Antibodies against gIII did not inhibit the penetration of adsorbed virus (wild type or gIII-), whereas antibodies against gII and gp50 did. It is unlikely, therefore, that gIII functions directly in virus penetration. Our results support the premises that efficient adsorption of PrV to host cell components is mediated either directly or indirectly by gIII (or a complex of viral proteins for which the presence of gIII is functionally essential) and that this pathway of adsorption promotes the interactions of other viral membrane proteins with the appropriate cellular proteins, leading to the rapid penetration of the virus into the cells. The slower penetration of the gIII- mutants than of wild-type PrV appears to be related to the slower and less efficient alternative mode of adsorption of PrV that occurs in the absence of glycoprotein gIII.

Published
1989
Full Text
View/download PDF

49. The pathogenicity of avian metapneumovirus subtype C wild bird isolates in domestic turkeys

Author

Cha Ra Mi, Yu Qingzhong, and Zsak Laszlo

Subjects
Avian metapneumovirus, Wild bird, Pathogenicity, Turkeys, Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background Avian metapneumovirus subtype C (aMPV/C) causes severe upper respiratory disease in turkeys. Previous report revealed the presence of aMPV/C in wild birds in the southeast regions of the U.S. Methods In this study, aMPV/C positive oral swabs from American coots (AC) and Canada geese (CG) were passaged three times in the respiratory tract of specific pathogen free (SPF) turkeys and used as aMPV/C P3 virus isolates in subsequent studies. Results Wild bird P3 isolates showed similar growth characteristics when compared to virulent aMPV/C in chicken embryo fibroblast ( CEF) cell cultures and their glycoprotein G gene sequence was closely related to the G gene of aMPV/C Colorado reference virus. Three-day-old commercial or SPF turkeys were inoculated oculonasally with wild bird aMPV/C P3 isolates. At 5 and 7 days post-inoculation (DPI), severe clinical signs were observed in both of the AC and CG virus-exposed groups. Viral RNA was detected in tracheal swabs by reverse transcriptase polymerase chain reaction (RT-PCR). In addition, immunohistochemistry showed virus replication in the nasal turbinate and trachea. All virus-exposed turkeys developed positive antibody response by 14 DPI. Conclusions Our data demonstrate that aMPV/C wild bird isolates induced typical aMPV/C disease in the domestic turkeys.

Published
2013
Full Text
View/download PDF

50. The complete genome sequence and genetic analysis of ΦCA82 a novel uncultured microphage from the turkey gastrointestinal system

Author

Seal Bruce S, Oakley Brian B, Day J Michael, and Zsak Laszlo

Subjects
microphage, microviridae, turkey, enteric, metagenomics, Infectious and parasitic diseases, RC109-216
Abstract

Abstract The genomic DNA sequence of a novel enteric uncultured microphage, ΦCA82 from a turkey gastrointestinal system was determined utilizing metagenomics techniques. The entire circular, single-stranded nucleotide sequence of the genome was 5,514 nucleotides. The ΦCA82 genome is quite different from other microviruses as indicated by comparisons of nucleotide similarity, predicted protein similarity, and functional classifications. Only three genes showed significant similarity to microviral proteins as determined by local alignments using BLAST analysis. ORF1 encoded a predicted phage F capsid protein that was phylogenetically most similar to the Microviridae ΦMH2K member's major coat protein. The ΦCA82 genome also encoded a predicted minor capsid protein (ORF2) and putative replication initiation protein (ORF3) most similar to the microviral bacteriophage SpV4. The distant evolutionary relationship of ΦCA82 suggests that the divergence of this novel turkey microvirus from other microviruses may reflect unique evolutionary pressures encountered within the turkey gastrointestinal system.

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results