DNA Viruses Cause Cancer

The function is determined by its structure. Basically, if the structure changes, then the function also changes or could even no longer work at all. There are multiple examples of structure and function in a cell. In a eukaryotic cell, the function of a nucleus is to regulate gene expression and DNA replication during the cell cycle. The main structure in the nucleus include a nucleolus, in which it has a sphere-like shape and contains Rrna that is bound to proteins. The cell wall is another organelle that is a protective layer next to the cell membrane. Its function is to protect the cell, regulate growth and store carbohydrates for the plant to use when it is growing. When all this information is put together, it proves that cells are alive. Viruses on the other hand, do not have any of this to prove that they are alive.

A virus is an infecting agent. Viruses are non-living they need a living host, a living organism to replicate themselves. When it invades a cell it will implant their code that is capable of copying itself. This will cause a detrimental effect, corrupting the system ti its advantage or complete destruction.

A virus is a capsule containing genetic material, even smaller than bacteria. The main task of virus is to reproduce. However, viruses need a suitable host to

There are two important type of genes responsible for the development or cancer namely tumor suppressor because their normal function is

A lot of the time when a virus come into contact with the host or as we may know it, the cell, it can insert its genetic material into its host, literally taking over the host's functions. Some viruses may remain dormant inside host cells for long periods, causing no obvious change in their host cells, but once stimulated new viruses are formed, self-assemble, and burst out of the host cell, killing the cell and going on to infect other cells. All this is just a constant battle between the host and cell. Without a host cell, viruses cannot carry out their life-sustaining functions or reproduce. They cannot synthesize proteins, because they lack ribosomes and must use the ribosomes of their host cells to translate viral messenger RNA into viral proteins. Viruses cannot generate or store energy, but have to derive their energy, and all other metabolic functions, from the host cell. Sometimes the virus will not be in the cell but outside functioning as coat for the protein. Viruses cause a number of diseases in humans most commonly heard of ones are, smallpox, the common cold, chickenpox, influenza, shingles, herpes, polio, rabies, ebola, hanta fever, and AIDS are examples of the diseases caused by viruses. Even some types of cancer but not all. As Sun Tzu wrote in The Art of War, “All warfare is based on deception”. He could have easily been describing the ancient battle between virus and host

Signs and symptoms of oropharyngeal cancer include a lump in the neck and a sore throat.

Oncogenes were discovered in the 1960s, when it was discovered that some animal cancers such as lymphomas were caused by viruses. Some of these viruses were notable due to the simplicity of their RNA genome. These viruses only had three distinct transcription units, involved in the replication of the virus (coat proteins and reverse transcriptase etc.), and an extra gene. This was an oncogene. When oncogenes are properly functioning they are termed proto-oncogenes (Todd R, 1999). Their normal function is to control cell proliferation. These function in growth signalling pathways, and conversely to tumour suppressing cells are activated through a gain in function rather than a loss of it. This occurs in two ways, by producing more of a product, or producing a subtly different product, as a result of a mutation similar to tumour suppressor genes (Croce, 2008). Oncogenes play a particularly strong role in the development of breast cancers. Often the normal ERBB2 and other related genes are amplified in late stage neuroblastomas and rhabdomyosarcomas. ERBB2 encodes HER2 which is a member of the epidermal growth factor

Human papilloma virus will cause almost all cases of cervical cancer, and therefore is the highest risk factor. There are many factors that will determine if HPV will lead to cervical cancer, HPV directly affects and transforms either or both the deepest layer of the mucous epithelial cells and more superficial layers. Targeting the receptors found in the layers of the stratified squamous epithelium. This is where the virus will proliferate into more differentiated cells to spawn offspring virus. The virus replication is what causes the skin characteristics of a wart. With the help of a pap smear, we are able to investigate if cervical epithelial cells are healthy and normal or determine which point in dysplasia they are at in transforming to cancerous cells. The HPV virus does not need a host to survive, and can survive in low and high temperatures.

Virus-induced neoplasia may also be subjected to additional host and environmental factors that may modify the transformation process. Studies have shown that there are Cellular genes that are homologous to the transforming genes of the retroviruses, a family of RNA viruses that can induce oncogenic transformation

Tumour suppressor genes: In health this family of genes usually act as a counter balance for oncogenesis. It is thought that they may be responsible for repairing gene damage in cells, or are growth inhibitor genes. In Hodgkin’s disease, there are often evidences of mutation in tumour suppressor genes as well as other genes.

Genetic engineering allows biologists to manipulate an organism's genomes by utilizing biotechnology (Moulton, 2004 ). The Talimogene Laherparepvec virus, otherwise known as T-vec, is an oncolytic virus. A oncolytic virus, is a virus that destroys cancerous cells. The T-vec virus has recently had successful results for treating melanoma cancer. The virus originated from the herpes simplex virus 1 and has been genetically altered to help destroy cancer cells.The virus gets injected into the lesions, lesions are areas on or in the body that have been damaged . Not only does the virus destroy cancer cells, it also activities the immune system to attack the cancer cells. Many changes were done to diminish the virus, expand the selective for the cancer cells, and release the cytokine. The modifications that were implanted in the virus were, HSV-1 strain (JS1) which is the DNA set of the herpes virus, that increases the death of the tumour cells. To delete ICP34.5, that stops the HSV infection in the cells that are not tumorous, and will provide selective tumour duplication. As Well as the deletion of ICP47 that allows antigen presentation, an antigen is a substance that helps enable an immune response. Placing in the US11 will

Cancer is one of the leading causes of death worldwide as it can develop in almost any organ or tissue. Significant advances in understanding the cellular basis of cancer and the underlying biological mechanisms of tumour has been vastly improved in the recent years (Jiang et al. 1994). Cancer is a genetic disease which requires a series of mutation during mitosis to develop, its characteristics can be associated with their ability to grow and divide abnormal cells uncontrollable while in the mean time invade and cause nearby blood vessels to serve its need. Even though many people are affected by cancer today, the abilities which cancer cells have make it hard to find a single effective treatment for cancer. The focus of research now lies

Inside the body, they encounter two situations, one where they meet healthy cells, and the other when they meet cancer cells. The interaction between the oncolytic virus and healthy cells is depicted in Figure 3.A and 3.B. The OV interacts with the normal cell; however, because of the modifications made to it, it is unable to infect the healthy cell, resulting in it eventually floating away in the bloodstream to find new cells. The oncolytic virus and a cancer cells’ interaction however is much more interesting and is depicted in Figure 2.C, 2.D and 2.E. When the oncolytic virus encounters a cancer cell, it immediately recognizes it and proceeds to infect it. The infection results in the genetic material of the virus being injected into the cancer cell. Thus, the cancer cell now has a new ‘information manual’ it can follow. The new information manual instructs the cancer cell to stop carrying out its own functions, and instead only make more copies of the oncolytic virus. Thus, as shown in Figure 2.I, the cancer cell gets filled with more and more of the oncolytic virus particles, until finally the cell does not have more space. At this point, like a balloon with too much air in it, the cell bursts, releasing the oncolytic virus particles into its surroundings. The oncolytic virus, now even larger in number flows through the bloodstream looking for more cancer cells to infect and repeats this process. The oncolytic virus is thus able to travel throughout the patient’s body, eliminating any cancer cells it encounters along the way. This article compares TCI to the use of OVs and discusses which one might be a better alternative. Although the patient’s body has less chance of rejecting T-cell therapy, oncolytic viruses can be delivered using vaccines, due to which they can travel via the bloodstream eliminating tumors anywhere in the

HPVs are divided into two different categories low-risk and high-risk depending how they behave overtime. ‘High-risk’ mucosal HPVs are the causative agents of cervical cancers, with HPV16 and HPV18 being the most common oncogenic types associated with 50% and 20% of the carcinomas respectively (Bosch et al., 1995). There are two viral protein that causes the degradation of the tumor suppressor genes; E6 and E7. These two protein work together to cause the tumor by destroying the host machinery. E6 oncoprotein has the capacity to block apoptosis, changes the function of several proteins and thereby modifying the signals of the cells. One of the major function of the E6 protein is to target the p53 (a tumor suppressor protein), it inactivates and recruit the E3 ubiquitin ligase E6AP (Huibregtse et al., 1991; Scheffner et al., 1993) by binding to a conserved

Whereas, In cervical cancer, HPV play a role in encoded genes in tumor cell growth. In addition to the stimulation of proliferation of cell the inactivation of tumor suppressor genes, such as p53 may be a pathway leading to malignancy in HPV and hepatitis B virus.