東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Murine host factors involved in susc...

Thach, Dzung Chi.

FindBook

Google Book

Amazon

博客來

Murine host factors involved in susceptibility and resistance to neuroadapted Sindbis virus.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Murine host factors involved in susceptibility and resistance to neuroadapted Sindbis virus./
作者:	Thach, Dzung Chi.
面頁冊數:	127 p.
附註:	Adviser: Diane E. Griffin.
Contained By:	Dissertation Abstracts International62-10B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3028339
ISBN:	0493405089

Murine host factors involved in susceptibility and resistance to neuroadapted Sindbis virus.
Thach, Dzung Chi.

Murine host factors involved in susceptibility and resistance to neuroadapted Sindbis virus. - 127 p.

Adviser: Diane E. Griffin.

Thesis (Ph.D.)--The Johns Hopkins University, 2002.

Infectious diseases can be conceptualized as the interaction of the pathogen, host, and environment. In these studies, we used the paradigm of neuroadapted Sindbis virus (NSV), the pathogen, which infects neurons of the central nervous system of mice, the host, causing hind-limb paralysis and fatal encephalomyelitis in most mouse strains in a controlled environment. To elucidate the role of host contributions to disease outcomes, we screened a panel of inbred mouse strains looking for genetic variation in percent mortality of mice after NSV infection. From this screen, we picked two mouse strains for further study: the C57BL/6 mouse strain showing 100% mortality, and the BALB/cBy mouse strain showing 0% mortality. We compared NSV pathogenesis in these two mouse strains, showing that C57BL/6 mice have more severe signs, higher virus replication, more extensive virus spread, faster infectious virus clearance, slower viral RNA clearance, and higher type I interferon and neutralizing antibody production than BALB/cBy mice. These studies generated phenotypic variations, at different steps in the viral pathogenesis pathways, for subsequent genetics studies; of which, we focused on differences in viral RNA levels in the brain, percent paralysis, and percent mortality. Our genetic analysis of these traits in reciprocal F1 crosses, congenics, recombinant inbreds, and F2 mice showed that a major quantitative trait locus (QTL), <italic>Nsv1 </italic>, at the distal end of chromosome two controlled early viral RNA replication and determined the likelihood of paralysis and mortality. We also characterized Sindbis virus infection of neuronal cell lines; of which, the CSM14.1 cell-line showed the most potential for studies involving innate mechanisms of clearance, reactivation, and persistance of virus in neurons.

ISBN: 0493405089Subjects--Topical Terms:

1017730
Biology, Genetics.

Murine host factors involved in susceptibility and resistance to neuroadapted Sindbis virus.
LDR:03074nam 2200313 a 45 001 927654
005 20110425
008 110425s2002 eng d
020 $a 0493405089
035 $a (UnM)AAI3028339
035 $a AAI3028339
040 $a UnM $c UnM
100 1 $a Thach, Dzung Chi. $3 1251218
245 1 0 $a Murine host factors involved in susceptibility and resistance to neuroadapted Sindbis virus.
300 $a 127 p.
500 $a Adviser: Diane E. Griffin.
500 $a Source: Dissertation Abstracts International, Volume: 62-10, Section: B, page: 4364.
502 $a Thesis (Ph.D.)--The Johns Hopkins University, 2002.
520 $a Infectious diseases can be conceptualized as the interaction of the pathogen, host, and environment. In these studies, we used the paradigm of neuroadapted Sindbis virus (NSV), the pathogen, which infects neurons of the central nervous system of mice, the host, causing hind-limb paralysis and fatal encephalomyelitis in most mouse strains in a controlled environment. To elucidate the role of host contributions to disease outcomes, we screened a panel of inbred mouse strains looking for genetic variation in percent mortality of mice after NSV infection. From this screen, we picked two mouse strains for further study: the C57BL/6 mouse strain showing 100% mortality, and the BALB/cBy mouse strain showing 0% mortality. We compared NSV pathogenesis in these two mouse strains, showing that C57BL/6 mice have more severe signs, higher virus replication, more extensive virus spread, faster infectious virus clearance, slower viral RNA clearance, and higher type I interferon and neutralizing antibody production than BALB/cBy mice. These studies generated phenotypic variations, at different steps in the viral pathogenesis pathways, for subsequent genetics studies; of which, we focused on differences in viral RNA levels in the brain, percent paralysis, and percent mortality. Our genetic analysis of these traits in reciprocal F1 crosses, congenics, recombinant inbreds, and F2 mice showed that a major quantitative trait locus (QTL), <italic>Nsv1 </italic>, at the distal end of chromosome two controlled early viral RNA replication and determined the likelihood of paralysis and mortality. We also characterized Sindbis virus infection of neuronal cell lines; of which, the CSM14.1 cell-line showed the most potential for studies involving innate mechanisms of clearance, reactivation, and persistance of virus in neurons.
520 $a Finally, some thoughts are offered on future directions towards identifying genes involved in susceptibility and resistance of mice to NSV infection and their functions. These studies add to our understanding of the host's genetic contribution to NSV-induced fatal encephalomyelitis.
590 $a School code: 0098.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Health Sciences, Pathology. $3 1017854
690 $a 0317
690 $a 0369
690 $a 0410
690 $a 0571
710 2 0 $a The Johns Hopkins University. $3 1017431
773 0 $t Dissertation Abstracts International $g 62-10B.
790 $a 0098
790 1 0 $a Griffin, Diane E., $e advisor
791 $a Ph.D.
792 $a 2002
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3028339