It is estimated that viral infections contribute to 15 20 of all human cancers (McLaughlin-Drubin et al, 2008, p127). Over the past 30 years it has become much more evident that there are several viruses that keep showing up in cancerous tissues and it is becoming more evident that these viruses play significant roles in the multistage development of this 15-20% of human cancers (McLaughlin-Drubin et al, 2008, p127). Some of the foremost cancer causing viruses in humans are oncogenic (promotes the cause of cancers) viruses which can contribute to different steps of the carcinogenic process(McLaughlin-Drubin et al, 2008,p127). These viruses include papillomavirus, hepatitis B virus, hepatitis C virus and Epstein-Barr virus which appear to be related to certain human cancers such as cervical carcinoma, primary liver cell carcinoma (Hepatocellular carcinoma), Burkitt's lymphoma and nasopharyngeal carcinoma and many others. (Fey et al 1998, p1). One of the main pieces of evidence that shows viruses cause, or at least contribute to cancer includes the presence of viral DNA, RNA and proteins in tumours (Fey et al 1998, p1).
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The ability to fuse cells is shared by many enveloped viruses. Some of these viruses include common human pathogens and most of the known oncogenic viruses. These viruses enter cells with the help of viral proteins that fuse cell membranes (Marsh et al,2006, p729). A well-known consequence of this mechanism is the ability of viruses, including common human pathogens and several viruses to fuse cells, both in vitro and in vivo (D.M. Duelli,2007, p431). Viruses that can fuse cells are nearly anywhere within humans suggesting that accidental fusion in the body is not uncommon (Duelli et al,2007, p431). Normally this is not harmful but cells made by accidental fusion are likely to be abnormal. This could potentially lead to chromosomal instability which underlies most malignant properties of many cancers and their ability to escape therapy, a virus causes cancer by inducing massive chromosomal instability through cell fusion ( Duelli and Lazebnik ,2007, p968). In other words, when the enveloped virus enters a cell one of the mechanisms it can use is cell membrane fusion. The virus does this by attaching it's envelope to the surface membrane of the cell with external glycoproteins. Once attached the envelope then unfolds and releases its genetic material into the cell and the envelope itself becomes part of the cell membrane, as seen in Figure 1. The genetic material then “chops and changes” the host cell's genome to help suit its requirements for replication (Eckert et al, 2001, p778), this is not the only way a virus can gain entry to a cell. As previously stated, this change in genetic information can lead to chromosomal instability and can then potentially lead to carcinogenesis.
Hepatitis C is an example of a single-stranded RNA virus that has a link with carcinogenesis. According to the World Health Organization (WHO), cirrhosis and primary liver cancer caused 783,000 and 619,000 deaths in 2002 (Perz et al,2006, p519).” Hepatocellular carcinoma (HCC) is one of the most common cancers in the world , perhaps even the most common” according to Beasley et al ( 2006, p1942). Hepatocellular carcinoma contributes to 70% to 85% of all cases of liver cancer (Perz et al,2006). Chronic infection of hepatitis B virus (HBV) or hepatitis C virus (HCV) is associated with a higher risk of developing HCC. A recent study of this in 2002 has shown that HBV- and HCV are accountable for 54% and 31% of HCC (Perz et al,2006, p534). In the majority of infected individuals, HCV establishes a persistent and life-long infection by evading the immune system by mutation, preventing its host cells from apoptosis and interfering with cellular functions (Gale et al,(2005. p940). Infection with HCV causes inflammation and fibrosis of the liver, which can progress to cirrhosis and ultimately lead to tumour development (McLaughlin-Drubin et al, 2008, p132). While it is currently thought that chronic inflammation and cirrhosis play key roles in HCV-induced carcinogenesis, the exact underlying mechanisms are not fully understood (Fattovich et al,2004, p35). However this does not mean the mechanisms are not understood at all. It has been found that proteins encoded by HCV have also been shown to activate cellular oncoproteins and deactivate tumor suppressors, such as p53 ,CREB2/LZIP and the retinoblastoma protein (pRB). Finally, HCV causes genome instability, suggesting that certain HCV proteins may have a cause mutation by manipulating the host cells genetic information (McLaughlin-Drubin et al, 2008, p132). So even though the underlying mechanisms are not fully understood there is still research to be done on these HCV proteins which could reveal the accurate role of HCV in carcinogenesis.
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Unlike hepatitis C, hepatitis B is an example of a small DNA virus with circular, partially double-stranded, DNA genome which also has a link with carcinogenesis. Also like hepatitis C, infection with HBV can enter a cell and can cause changes to the host cells genome such as chromosomal deletions and replacing the cells genetic material with its own viral sequences from one chromosome to another (McLaughlin-Drubin et al, 2008, p132), this may case genomic instability and could also activate proto-oncogenes [256-260] which could cause carcinogenesis. Upon examination of the DNA sequences present in HCC, proteins encoded by HBV can be seen that. These DNA sequences show the encoding of the HBV X protein (HBx) and truncated envelope PreS2/S viral proteins seem to be present in the majority of HCC tumor cells. Also viral hepatitis B spliced protein (HBSP) has been identified in HBV-infected patients (Soussan et al, 2000, p57)However, the presence of these proteins in tumors does not confirm their role in HCC development therefore further studies on these proteins are necessary to determine their potential contributions to HCC development.