LDR | | 00000nam u2200205 4500 |
001 | | 000000431570 |
005 | | 20200224102812 |
008 | | 200131s2017 ||||||||||||||||| ||eng d |
020 | |
▼a 9781392335680 |
035 | |
▼a (MiAaPQ)AAI13918163 |
040 | |
▼a MiAaPQ
▼c MiAaPQ
▼d 247004 |
082 | 0 |
▼a 576.6 |
100 | 1 |
▼a Yetming, Kristen Dominique. |
245 | 10 |
▼a BHLF1, a Lytic-Cycle Gene Encoding a Long Non-Coding RNA Contributes to Epstein-Barr Virus Latency. |
260 | |
▼a [S.l.]:
▼b The Pennsylvania State University.,
▼c 2017. |
260 | 1 |
▼a Ann Arbor:
▼b ProQuest Dissertations & Theses,
▼c 2017. |
300 | |
▼a 199 p. |
500 | |
▼a Source: Dissertations Abstracts International, Volume: 81-01, Section: B. |
500 | |
▼a Publisher info.: Dissertation/Thesis. |
500 | |
▼a Advisor: Sample, Jeffery T. |
502 | 1 |
▼a Thesis (Ph.D.)--The Pennsylvania State University, 2017. |
520 | |
▼a Epstein-Barr virus (EBV) is a lymphotropic, gammaherpesvirus which efficiently establishes a persistent, lifelong infection in humans. As is common with other herpesviruses, EBV has both replicative (lytic) and latent cycles of infection. EBV latency, in which there is no virus production, can be subdivided into several distinct latency programs which are characterized by differential expression patterns of the viral latency-associated proteins: EBNA1, -2, -3A, -3B, -3C, -LP and LMP1, -2A, -2B. The major long-term reservoir of EBV is the memory B cell, and as latently-infected B cells progress from an initial state of EBV-driven cell proliferation to a state of long-term viral latency within the memory B-cell pool, there is a restriction in the expression of the viral latency proteins, due to the epigenetic silencing of the EBNA promoters Wp and Cp. This restriction in latency is essential for the persistence of EBV infection as cytotoxic T lymphocytes can remove infected B cells that continue to express several of the latencyassociated proteins.Historically, it has been thought that latency-associated EBV gene products only contribute to the latent cycle, and lytic-cycle genes only function during lytic infection. However, it has recently been found that there is a subset of "lytic" genes that are expressed upon the initiation of latency, one of which is BHLF1. This, along with several other lines of evidence, suggests that BHLF1 may have a latency-associated function. Thus, the goal of the work presented in this dissertation was to elucidate whether BHLF1 has a role in the establishment or maintenance of EBV latency. Using recombinant EBV (rEBV), we observed that infection of an EBV-negative cell line, BL2, with a wild-type (WT) rEBV is capable of sustaining latency III, whereas infection with mutant rEBVs, in which BHLF1 has been deleted, results in a transition from latency III to latency I within 3 months post-infection at both the protein and mRNA levels. Disruption of BHLF1 did not significantly influence the expression of other genes near the locus |
590 | |
▼a School code: 0176. |
650 | 4 |
▼a Molecular biology. |
650 | 4 |
▼a Microbiology. |
650 | 4 |
▼a Virology. |
690 | |
▼a 0307 |
690 | |
▼a 0410 |
690 | |
▼a 0720 |
710 | 20 |
▼a The Pennsylvania State University. |
773 | 0 |
▼t Dissertations Abstracts International
▼g 81-01B. |
773 | |
▼t Dissertation Abstract International |
790 | |
▼a 0176 |
791 | |
▼a Ph.D. |
792 | |
▼a 2017 |
793 | |
▼a English |
856 | 40 |
▼u http://www.riss.kr/pdu/ddodLink.do?id=T15492710
▼n KERIS
▼z 이 자료의 원문은 한국교육학술정보원에서 제공합니다. |
980 | |
▼a 202002
▼f 2020 |
990 | |
▼a ***1008102 |
991 | |
▼a E-BOOK |