Since the avian cancer virus experiment in 2011, scientists have confirmed seven different viruses that cause about ten to fifteen percent of human cancer globally. Notably, these distinct viruses have revealed unprecedented links between innate immunities as well as sensors and tumour suppressors, implying that they control both cancer and viral infections.
Apparently, these varied cancers remain to be a substantial health challenge, especially in developing economies, alongside the underserved and immuno-suppressed individuals in developed economies.
Among the several human tumour viruses evidenced by several scientists and scholars, this paper will explore the Epstein-Barr virus (EBV), the Hepatitis B virus (HBV) and the Human papilloma virus (HPV) along with their distinct ways by which they cause tumours.
Introduction
The burden associated with viral infections in cancer remains to be high, although it has been overlooked by a number of cancer researchers. However, several studies on viruses have cropped up from the cancer field, providing significant insights into both non-infectious and infectious causes of cancer. Since the avian cancer virus experiment of the year 2011, scientists have confirmed seven different viruses that cause about ten to fifteen percent of human cancer globally. Notably, these distinct viruses have revealed unprecedented links between innate immunities as well as sensors, and tumour suppressor, implying that they control both cancer and viral infections.
Apparently, these varied cancers remain to be a substantial health challenge, especially in developing economies, alongside the underserved and immuno-suppressed individuals in developed economies (Cancer Research UK, 2014). Again, these cancers are comprised of readily identifiable diagnosis, prevention and therapy targets. Among the several human tumour viruses evidenced by several scientists and scholars, this paper will explore the Epstein - Barr virus (EBV), Hepatitis B virus (HBV) and Human papilloma virus (HPV) along with their distinct ways by which they cause tumours.
Epstein-Barr virus (EBV)
EBV Microbe Description
The EBV, which is also termed as the human herpes virus 4 (HHV4) was described fifty-three years after the initial experiments of Rous; in 1964 in the identification of the EBV particles in cell lines from Burkitt’s lymphoma African patients (Moore & Chang, 2010). The EBV is a herpes virus that contains a large double-stranded DNA genome, and just like all other herpesviruses, it encodes enzymes that are involved in DNA replication as well as repair and nucleotide biosynthesis. It also possesses the ability to establish latency in B lymphocytes, reactivating into a lytic cycle (Liao, 2006). In other words, EBV infects and stays in certain WBCs (white blood cells) in the body known as B lymphocytes (B cells), and it is renowned in causing infectious mononucleosis or naturally occurring human tumours.
EBV Disease Explanation
According to scientists, EBV remains to be an ever-present virus, which is often common recognized as the principal agent for infectious mononucleosis, mostly termed as ‘mono’ or the ‘kissing disease.’ Research demonstrates that about ninety-five percent of all adults have been estimated to be seropositive, with most of the EBV infections being subclinical (Chiras, 2013). In addition, EBV has been linked with several malignancies including B and T cell lymphomas, leiomyosarcomas, Hodgkin’s disease, post-transplant lymphoproliferative disease alongside nasopharyngeal carcinomas. Among these cancers, Burkitt’s lymphoma, leiomyosarcomas and post-transplant lymphoproliferative diseases have been noted to demonstrate an increased frequency in patients who have immunodeficiency; hence, suggesting immunosurveillance role in the malignant transformation suppression (Moore & Chang, 2010).
Course of the EBV Infection
The oropharyngeal cavity remains to be the primary site of the EBV, and the virus has the ability of infecting the B cells and the epithelial cells, alongside switching between these two cells. Apparently, the major surface glycoprotein-gp 350/220, attaches itself to the cd21 receptor cells on the B cells (Llovet et al. 2003). The B cells’ transformation remains to be a highly efficient process that requires a large portion of the genome of the EBV, which develops into circular for both replication and latency (Liao, 2006). As a result, the virus will directly enter the latent gene expression state with the lytic cycle suppression.
Current Research and Future Research/Directions
Significantly, immune therapy of tumours linked with EBV has currently been the focus of research because the standard therapy has commonly involved the utilization of radiation therapy, multi-agent chemotherapy and together with surgery (Lavanchy, 2004). It is a phenomenon that has concentrated on adoptive transfer of specific cytotoxic T-cells of EBV and exhibited significant success, though it has to overcome some obstacles including potential graft versus host disease and resistance because of selected EBV epitopes’ mutation (Moore & Chang, 2010).
Currently, vaccines that have the ability of preventing primary infection of the EBV or that can boost immune responses against tumours related with EBV remain under investigation. So far, much of the development has focused mainly on gp 350/220 subunit vaccines because it represents one of the most abundant proteins on the coat of the virus, on top of being the protein against which the neutralizing antibody response of the human EBV is directed (Moore & Chang, 2010). Another direction entails the use of a recombinant vaccinia viral vector in expressing the membrane antigen of an EVB since a successful vaccine is supposed to have the highest impact in global regions that have high incidences of certain malignancies (Liao, 2006).
World Relevance
As aforementioned, since a successful vaccine has to possess the highest impact in global regions that have high incidences of certain malignancies, directions that involve the use of a recombinant vaccinia viral vector so as to express an EVB antigen have to be stressed. For instance, Burkitt’s lymphoma has been observed to be the highest common childhood malignancy in the African continent, especially in central Africa where EBV and malaria are measured as cofactors in its carcinogenesis (Chiras, 2013). Recent researches have demonstrated that about ninety-five percent of children in these regions are affected by the age of three, unlike in the United States and other places where infection is normally delayed till adolescence. Again, nasopharyngeal carcinoma has been observed to be rather rare, although it has an unusually high frequency in southern China, close to more than twenty times higher compared to that of the most populations (Moore & Chang, 2010).
Hepatitis B virus (HBV)
HBV Microbe Description
Hepatitis B virus, unlike Hepatitis C virus, is a DNA virus of the hepadnaviridae family, although the features of the resulting diseases of the two share several similarities. The HBV virion is a 42-nm particle that has an electron-dense core (nucleocapsid) of a diameter of 27 nm, enveloped by the surface protein (HBsAg) that is entrenched in a membranous lipid copied from the cell of the host. The virion genome of the HBV is circular and has about 3.2 kb in size, consisting of DNA that is mostly double-stranded (Barreto et al. 2014). Moreover, it has a compact organization containing four overlapping reading frames in the same direction and has no noncoding regions. The minus strand is unit length and consists of a protein that is covalently joined to the 5’ end while the other strand (plus strand) is variable in length, although it contains not more than unit length, besides having an RNA oligonucleotide at its 5’ end (Moore & Chang, 2010). Therefore, there is no strand that is closed, and circularity is usually maintained by cohesive ends. The HBV’s four overlapping open reading frames in the genome aid the transcription and expression of varied hepatitis B proteins, a process that takes place through the use of the manifold in-frame start codons (Chiras, 2013). Again, the HBV genome contains parts responsible for the regulation of the transcription, determination of the polyadenylation site and regulation of a specific transcript nucleocapsid encapsidation.
HBV Disease Explanation
Remarkably, hepatitis B is a blood-borne pathogen, which can cause acute and chronic hepatitis. In this sense, chronic hepatitis; infections lasting for more than three months, have the potential of causing cirrhosis and liver failure (Liao, 2006). Most importantly, chronic infections can result in the establishment of hepatocellular carcinoma. Scientists affirm that the hepatocellular carcinoma is an insistent tumour that may occur in the liver disease setting, arising from infections with HBV, though the exact oncogenesis mechanism with this virus remains uncertain (Chiras, 2013). Acute HBV infection only causes mild symptoms, with a significant number of infected adults successfully clearing the virus and acquiring a lasting immunity.
HBV Disease Course
The surface antigen appears in most patients’ sera in the time of incubation, two to eight weeks before the onset of jaundice or the biochemical liver damage evidence. The antigen persists in the acute illness, normally clearing from the circulation in times of convalescence. The DNA polymerase activity, which is linked with the virus, appears in the circulation, correlating in time with liver cells damage, facilitated by increased serum transaminases (Moore & Chang, 2010). The polymerase activity will last for some days or weeks in acute situations, and for several months or years in certain persistent carriers (Barreto et al. 2014). The antibody to the core antigen remains in the serum two to ten weeks after the appearance of the surface antigen, and it is often noticeable for several years after recovery. Afterward, the core antibody titer appears so as to correlate with the virus replication amount and duration, as eventually, the antibody to the surface antigen component materializes (Liao, 2006).
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- Quote paper
- Business Administrator Mutinda Jackson (Author), 2018, The different ways in which viruses cause tumors, Munich, GRIN Verlag, https://www.hausarbeiten.de/document/429538
