Search In this Thesis
   Search In this Thesis  
العنوان
An Implication of EBV association with Hepatocellular Cancer Patients \
المؤلف
Atwa, Ahmed Atwa Abdel-Sammad.
هيئة الاعداد
باحث / Ahmed Atwa Abdel-Sammad Atwa
مشرف / Maha El-Bassuni
مشرف / Randa Mohamed Talaat
مناقش / Soheer Abdel-Rahman Abdel-Samee
مناقش / Olfat Mohammed Hendi
الموضوع
Oncogenic Viruses- Oncogenic Viruses. Antiviral Agents- therapeutic use. Neoplasms- virology.
تاريخ النشر
2013.
عدد الصفحات
1computer optical disc :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
Molecular Biology
تاريخ الإجازة
1/1/2013
مكان الإجازة
جامعة مدينة السادات - معهد بحوث الهندسة الوراثية - Molecular Biology Department
الفهرس
Only 14 pages are availabe for public view

from 130

from 130

Abstract

EBV was the first human virus directly implicated in
carcinogenesis. Since its discovery it has been considered as a major
player in the development of a wide range of cancers. Recent studies have
concluded EBV itself or infected cell clones might promote replication of
the HCV
Hepatitis C virus (HCV) is an enveloped virus belonging to the
Flaviviridae family, whose genome consists of a positive-stranded 9.5 kb
RNA molecule and encodes a large polyprotein precursor of 3000 amino
acids
EBNA1 is responsible for supporting HCV replication, suggesting
that EBV may be involved in the development of hepatocellular
carcinoma (HCC)
HCV replication was promoted by EBV and that EBNA1 was
responsible for supporting HCV replication. Furthermore, deletion
analysis of the EBNA1 gene showed good correlation between the
transactivational activity of the EBNA1 gene and its activity supporting
HCV replication. EBNA1 is a DNA-binding protein that binds to clusters
of specific sequences within the origin of latent viral DNA replication. The protein is required for maintenance and replication of EBV plasmids
in EBV-infected cells.
It is possible that EBNA1 promotes the transcription of foreign
genes when the genes have the cognate sequence for EBNA1 binding,
although no promoter of a cellular gene that has cognate sequences for
EBNA1 binding and is transactivated by EBNA1 has been found.
Therefore, it is conceivable that EBNA1 promotes HCV replication via
its transactivating function. Many research has revealed that EBNA1 can bind to HCV RNA,
at least in vitro, and might therefore be capable of controlling gene
expression at the post-transcriptional. The research assumes that EBNA1
influences HCV replication not directly but indirectly by inducing
transcription of the cellular gene.
Persistent HCV infection is frequently associated with liver
cirrhosis and hepatpocellular carcinoma.
Worldwide, chronic infection with the hepatitis C virus (HCV) is a
leading cause of morbidity and mortality, and a link seems to exist
between HCV and HCC. Early evidence linking HCC with HCV was the
sequential development of chronic liver disease and liver cancer in many
patients with either community-aquired or transfusion – related hepatitis.
The aim of the present study was to assess the value of estimation
of Epstein-Barr Virus (Ab) and HCV and to correlate them with the
Hepatocellular Carcinoma (HCC).
This study was carried out on ٤٥ cases divided into three groups:- Group 1: include 15 patients considered as control patient with a low conc.
of EBV (Ab) antibodies, negative for HCC , negative for HCV-RNA,
negative for anti-HIV antibodies, and negative for (HBs Ag).
Group 2: include 15 patients, positive for HCC, with a moderate conc. of
EBV (Ab) antibodies, negative for HCV RNA, negative for anti-HIV
antibodies, and negative for (HBsAg).
Group 3: include 15 patients, positive for HCC, with a high conc. of EBV
(Ab) antibodies, positive for HCV RNA, negative for anti-HIV antibodies,
and negative test for (HBsAg).