- Title Information
- Title
- Characterizing the Impact of 5’ PreS1 Deletion Hepatitis B Virus Mutants on Endoplasmic Reticulum Stress
- Type of Resource (primo)
- dissertations
- Name:
Personal
- Name Part
- Luong, Selena
- Role
- Role Term:
Text
- creator
- Name:
Personal
- Name Part
- Tong, Shuping
- Role
- Role Term:
Text
- Reader
- Name:
Personal
- Name Part
- Li, Jisu
- Role
- Role Term:
Text
- Advisor
- Name:
Personal
- Name Part
- Dugan, Aisling
- Role
- Role Term:
Text
- Advisor
- Name:
Corporate
- Name Part
- Brown University. Biology and Medicine: Biotechnology
- Role
- Role Term:
Text
- sponsor
- Origin Information
- Copyright Date
- 2025
- Physical Description
- Extent
- , None p.
- digitalOrigin
- born digital
- Note:
thesis
- Thesis (Sc. M.)--Brown University, 2025
- Genre (aat)
- theses
- Abstract
- Hepatitis B Virus (HBV) remains a significant global health burden, chronically infecting
over 350 million individuals worldwide and increasing the risk of severe liver complications,
including hepatocellular carcinoma (HCC) and liver cirrhosis. Additionally, chronic infection of
HBV can lead to an accumulation of mutations within the viral genome, some of which have
been implicated in disease progression. Notably, in-frame deletions in the preS1 region of the
envelope gene have been associated with increased viral infectivity and pathogenicity.
In this study, we investigated the effects of a 5’ preS1 deletion mutant of genotype C
origin on ER stress in hepatocytes, which is a common feature prior to cancer development. We
specifically examined the expression levels of key ER stress responsible genes, including
GRP78, GADD153, and ATF6, to determine whether the mutant HBV DNA induces a more
pronounced ER stress response compared to the wild-type virus. Furthermore, we assessed
HBsAg production as an indicator of viral infectivity of the mutant, providing insight into how
preS1 mutations may contribute to HBV persistence and pathogenicity. Lastly, the clinical
relevance of the 5’ preS1 mutant was assessed by measuring the ER stress levels in chronically
infected liver cells.
By elucidating the mechanisms by which preS1 deletions contribute to liver injury, this
study provides new insights into the molecular underpinnings of HBV-induced liver disease. A
deeper understanding of these processes is crucial for developing targeted therapeutic
interventions, ultimately reducing the public health burden associated with chronic HBV
infection.
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00832729")
- Topic
- Biotechnology
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/01167670")
- Topic
- Virology
- Subject
- Topic
- HBV infection
- Subject (fast)
(authorityURI="http://id.worldcat.org/fast", valueURI="http://id.worldcat.org/fast/00909799")
- Topic
- Endoplasmic reticulum
- Language
- Language Term (ISO639-2B)
- English
- Record Information
- Record Content Source (marcorg)
- RPB
- Record Creation Date
(encoding="iso8601")
- 20250707