To cite this article:
Akram Nimrah, Imran Muhammad, Noreen Mamoona, Ahmed Fayyaz, Atif Muhammad, Fatima Zareen, and Bilal Waqar Ahmed. Viral Immunology. January 2017, 30 (1): 20-27. Doi: 10.1089 / vim.2016.0109.
Published in Volume: 30 Issue 1: January 1, 2017
Online Ahead of Print: November 10, 2016
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Author information
Nimrah Akram, 1 Muhammad Imran, 1 Mamoona Noreen, 2 Fayyaz Ahmed, 1 Muhammad Atif, 1 Zareen Fatima, 3 and Ahmed Bilal Waqar1
1Department of Medical Laboratory Sciences (DMLS), Faculty of Health and Allied Sciences (FHAS), Imperial College of Business Studies (ICBS), Lahore, Pakistan.
2Department of Zoology, The Women University Multan, Multan, Pakistan.
3Department of Radiological Sciences and Medical Imaging (DRSMI), FHAS, ICBS, Lahore, Pakistan.
Address correspondence to:
Dr. Muhammad Imran
Department of Medical Laboratory Sciences (DMLS)
Faculty of Health and Allied Sciences (FHAS)
Imperial College of Business Studies (ICBS)
Lahore 54000
Pakistan
E-mail: [email protected]
ABSTRACT
Viruses are the intracellular pathogens that reproduce only in the living cell and manipulate the cellular machinery to produce more viruses. Viral replications can affect cellular genes of the host in multiple cancerous ways. Approximately, 20% of all human oncogenesis is caused by cancer-causing As well as the major host cells are transformed into cancerous cells on the basis of host genetic variability. . Oncogenic viruses encode genes that cause viral replication and transformation of the host cells to produce viral proteins and protein complexes. From the basic viral infection to tumorigenesis is length of due to the involvement of factors like Fas complications, cellular mutations, and exposure to other (HCV), Epstein-Barr virus (EBV), Human papilloma virus (HPV), Kaposi's sarcoma herpes virus (KSHV), Hepatitis B virus (HBV), Hepatitis C virus (HCV) And Human T lymphotrophic virus 1 (HTLV-1). This review article summarizes advanced knowledge related to human oncogenic viruses and the molecular mechanisms that lead to tumorigenesis in humans. 作者: StephenW 时间: 2017-3-1 19:31
HBV is a partially double-stranded DNA virus. HBV was diagnosed as a serum-borne infective jaundice in 1940 (11). HBV is highly contagious and may be transmitted by exposure to HBV-infected blood and other body fluids through breaks in cutaneous and mucosal membrane. HBV infection is usually asymptomatic in adults, while it becomes chronic in young children or neonates (53). Chronicity with HBV has a major role in the development of hepatocellular carcinoma (HCC), and antiviral drugs are used to reduce HBV DNA levels to mitigate the possibility of HCC. HBV integrates its DNA into the host cellular genome causing mutations and accelerating liver inflammation (38). The precise pathologic mechanism of HBV infection is not completely understood. None of HBV proteins has been directly linked with acute oncogenic activity as the process of HCC development is a multistep complicated process that spans several decades (26). HBV encoded X antigen (HBx), a transcriptional activator of host cellular genes that is involved in HCC development. HBx activates specific cyclins, cyclin-dependent pathways, JAK/STAT pathway, and mitogen-activated protein kinase (MAPK) pathway leading to liver carcinogenesis due to interruption of tumor suppressor genes as shown in Figure 4 (17).
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FIG. 4. Role of HBx in HCC development: Hepatits B X-antigen induces host cell genome instability and altered expression of various cytokines leading to antiviral state. HCC, hepatocellular carcinoma.
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A recent report of mice studies has shown the oncogenic role of HBx protein in the induction of HCC. Only HBx does not cause the cancers, but c-myc involvement leads to the development of cancer. HBx protein only acts as a promoter in tumor induction (60).
HBx causes p53 suppression that promotes the inactivation of pRb and also downregulates various CDK inhibitors (70). The involvement of tumor-associated fetal protein (AFP) action in HBx generating oncogenesis is also reported. The study on 614 HCC patients revealed that AFP is an intracellular signaling molecule acting as a probable participator in HBx inducing carcinogenesis (71). It is reviewed that recurrence of tumors is a dominating obstacle for diagnostic improvement of HBV-related HCC. Major viral factors for hepatic carcinoma recurrence include HBsAg, HBeAg, HBV DNA levels, and HBcAg (48). 作者: StephenW 时间: 2017-3-1 19:35