Study on Caenorhabditis elegans Growth Retardation Induced by Small Hepatitis Delta Antigen Expression in Pharynx

• Main Authors: Tsui-yun Chang, 張翠芸
• Other Authors: Szecheng J. Lo
• Format: Others
• Language: zh-TW
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/49138295848563102432

碩士 === 國立陽明大學 === 微生物及免疫學研究所 === 97 === It is known that hepatitis delta virus (HDV) requires hepatitis B virus (HBV) to complete its life cycle. When patients are coinfected or superinfected with HBV and HDV, it causes fulminant hepatitis and progressive chronic liver cirrhosis, indicating HDV plays an important role that makes the symptoms become more seriously. The mechanism by which HDV infection contributes to clinical hepatitis is poorly understood. HDV has two different size of proteins, small and large delta antigens (SDAg and LDAg), they might interact with hosts’ molecules and make some symptoms. Our lab has established Caenorhabditis elegans (C.elegans) as a platform to study whether HDV antigens will affect worm growth. In previous studies, transgenic worms expressing SDAg in pharynx caused growth retard. In my thesis, I used different length of SDAgs named SD441, SD327, SD267, and SD201 to dissect the domain of delta antigens, which leads to growth retard, as well the effect of different genotypes (genotype I, genotype II, genotype III) and expression at different stages. I found that (1) the influence are distinct in all different length of SDAgs, except SD441, the SDAg without nuclear-localization signal ( NLS ), (2) SDAg expression at L4 stage has the most serious effect, and (3) the degree of effect is genotype II > genotype I > genotype III. These results show that the entrance of SDAg into hosts’ nucleus is very important to result in growth retardation and egg-laying activity. SDAg might interfere with unknown molecules in the nucleus. Therefore, if these molecules would be identified, we could search for the homologous genes in human, and possible to delineate the molecular mechanisms involved in the pathogenesis of HDV.