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Analysis of the pseudorabies virus U...

Schwartz, Jennifer Ann.

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Analysis of the pseudorabies virus UL54 protein.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Analysis of the pseudorabies virus UL54 protein./
作者:	Schwartz, Jennifer Ann.
面頁冊數:	183 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-10, Section: B, page: 4979.
Contained By:	Dissertation Abstracts International65-10B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3151283
ISBN:	9780496112241

Analysis of the pseudorabies virus UL54 protein.
Schwartz, Jennifer Ann.

Analysis of the pseudorabies virus UL54 protein. - 183 p.

Source: Dissertation Abstracts International, Volume: 65-10, Section: B, page: 4979.

Thesis (Ph.D.)--Columbia University, 2005.

This dissertation studies several aspects of HSV, VZV and PrV biology. First, I extend and clarify previous findings regarding the role of the acidic NH2 terminus of ICP0 in the growth and replication of HSV-1. I demonstrate that mutant HSVs which synthesize low levels of ICP0 are nevertheless able to produce wild-type levels of progeny. This observation, in conjunction with my finding that ICP0 accumulates at nearly undetectable levels in dl1403 infected L7 cells, an ICP0 complementing cell line, supports the conclusion that ICP0 accumulates to levels in excess of those required for the initiation and maintenance of wild-type virus growth kinetics in tissue culture.

ISBN: 9780496112241Subjects--Topical Terms:

1017734
Biology, Microbiology.

Analysis of the pseudorabies virus UL54 protein.
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245 1 0 $a Analysis of the pseudorabies virus UL54 protein.
300 $a 183 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-10, Section: B, page: 4979.
500 $a Adviser: Saul Silverstein.
502 $a Thesis (Ph.D.)--Columbia University, 2005.
520 $a This dissertation studies several aspects of HSV, VZV and PrV biology. First, I extend and clarify previous findings regarding the role of the acidic NH2 terminus of ICP0 in the growth and replication of HSV-1. I demonstrate that mutant HSVs which synthesize low levels of ICP0 are nevertheless able to produce wild-type levels of progeny. This observation, in conjunction with my finding that ICP0 accumulates at nearly undetectable levels in dl1403 infected L7 cells, an ICP0 complementing cell line, supports the conclusion that ICP0 accumulates to levels in excess of those required for the initiation and maintenance of wild-type virus growth kinetics in tissue culture.
520 $a Second, by analyzing the HSV-1 life cycle in the presence of the cobalt chelate compound, CTC-96, I demonstrate that CTC-96 inhibits HSV-1 infection at the point of entry. The implications of this inhibition on the use of CTC-96 as a tool for analyzing the biology of HSV-1 entry and as an antiviral therapy are discussed.
520 $a Third, to further elucidate the functions of the VZV ORF4 protein, protein-protein interactions between ORF4 and host cellular proteins were examined. ORF4 and its homolog in HSV, ICP27, are closely related based on sequence homology and their ability to transactivate viral promoters. ICP27 has previously been shown to interact with a number of cellular factors. Of the ICP27 host protein partners I examined, all were capable of interacting with ORF4 in vitro. I performed a yeast two-hybrid screen to identify novel ORF4 binding proteins. Several host factors were identified and their ability to bind ICP27 was also analyzed.
520 $a Fourth, due to difficulties in studying VZV proteins in the context of a VZV infection, I have established a complementation system using the closely related alphaherpesvirus, PrV. The ORF4 homolog, UL54, was deleted, in part and in full, from PrV using bacterial artificial chromosomes and various allele exchange technologies in E. coli. To date all of the ICP27/ORF4 homologs in other herpesviruses have been shown to be essential. However, I show that unlike these other proteins, UL54 is non-essential. While not essential for virus growth in tissue culture, UL54 mutants have several phenotypes, including small plaque size in tissue culture and are highly attenuated in a mouse flank scarification model of PrV infection. Additionally, both ORF4 and ICP27 are capable of complementing the slow growth phenotype of the UL54 mutants. The use of the UL54 mutants as a tool to study the biology of ORF4 in the context of an alphaherpesvirus infection is discussed.
590 $a School code: 0054.
650 4 $a Biology, Microbiology. $3 1017734
690 $a 0410
710 2 0 $a Columbia University. $3 571054
773 0 $t Dissertation Abstracts International $g 65-10B.
790 1 0 $a Silverstein, Saul, $e advisor
790 $a 0054
791 $a Ph.D.
792 $a 2005
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