Topic > The Zika Virus and Its Potential in the Treatment of Brain Cancer

IntroductionUntil now, viruses have only been seen as harmful, dangerous and detrimental to our health. Since their discovery in 1892 they have been perceived as a threat to global health; it is not a remedy or a possible treatment for one of the leading causes of mortality in the world. However, recent scientific studies have shown that a specific strain, known as the Zika virus, could potentially treat aggressive brain tumors such as glioblastomas. Due to the teratogenic characteristics of the virus, it has been linked to an increase in fetuses developing neural abnormalities as it infects and ultimately kills cells vital in neurodevelopment. Its correct redesign could lead the pathogen to selectively target the cancer stem cells in the brain responsible for the tumors; If successful, this breakthrough could completely reform brain cancer treatment and consequently transform oncology. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an Original Essay The following essay will discuss a number of factors that will help explain whether the virus could be used as a drug. The opening paragraphs will explain what Zika is; it is history, structure, pathogenesis and symptoms. Next, the essay will explore Zika as a teratogen by explaining exactly how it affects the developing brain and generates various abnormalities. Third, the essay will investigate brain cancer and how the Zika virus can challenge aggressive tumors. Finally, we will conclude by evaluating whether the use of the virus as a cure would be more successful than the treatments already available and whether its production as a drug would be feasible from both a financial and ethical point of view. HistoryTo reach a conclusion on whether or not Although While the Zika virus cannot potentially be re-engineered and used as a treatment for brain cancer, it is crucial to first understand what it actually is. The characteristics need to be understood to decipher its pathogenesis and to come to an informed decision on whether harnessing the ability to infect the developing brain could revolutionize modern medicine. Zika's name is inherited from where it was first isolated; the Ziika forest of Uganda in 1947. The initial identification occurred in the sentinel rhesus macaque and the virus was first diagnosed in a human in 1952. Although it was discovered 70 years ago; the first outbreak of the disease occurred only ten years ago on the island of Yap. Since then, there have been several countries that have experienced epidemics, which has sparked the scientific community's interest in the pathogen. Zika is classified as a flavivirus and is therefore part of the ssRNA (+) taxonomic group. The structure of the virus is important to understand how it behaves. The genome is organized linearly, which means that, unlike circular RNA, it has a beginning and an end. This is coupled with monopartite genomic segmentation; Zika's genetic material consists of only a single strand of positive RNA, which is very similar to our human mRNA. This characteristic is essential in the replication of the virus in our body. The capsid has an icosahedral-like structure T = pseudo3, like all other flaviviruses, composed of 12 pentameric capsomers and 20 hexametric capsomers surrounding the genetic material of the virus. It is then further surrounded by an E dimer and an M protein that constitute the envelope and attachment protein. The structure of the virus is crucial for scientists to understand how exactly it uses its components to cause damage to the human body. The infection is caused by somearthropods, particularly mosquitoes, which make Zika an arbovirus. Additionally, other methods of transmission include sexual contact and blood transfusions. The strains involved in the infection and transmission of the Zika virus belong to the Aedes group; usually Aedes A Egypti or Aedes Albopictus. When the Aedes mosquito lands on the skin, it pierces the outermost layer, the epidermis, using its proboscis. This then continues to penetrate through the skin and into the second layer, the dermis, which has its own blood supply and consequently the nutrients that female mosquitoes need to feed on to produce and mature their eggs. As the proboscis passes through the epidermal and dermal layers, cells in both layers become susceptible to the Zika virus. Due to this, the permissive cells become infected; For a cell to be permissive to Zika it must have receptors that bind to the virus' attachment protein. This then leads to the fusion of the virus and the host cell, initiating replication. Once the virus enters the host cell, the process of replication begins, which is how the virus causes damage to our bodies and leads to harmful effects on unborn children. This is probably the most important part of the process that scientists need to understand in order to observe what the virus would do if it targeted cancerous tumors. When the pathogen gets close enough to a human cell that is permissive to the virus, its attachment proteins bind to receptors on the host cell. The bond that occurs between the host cell and the virus triggers a process called "clathrin-mediated endocytosis"; the virus is absorbed by budding towards the inside of the vesicles of the plasma membrane. These vesicles contain proteins with specific receptor sites for absorbed molecules. Once endocytosis occurs, the virus successfully infiltrates the cell and begins to replicate. It does this by hijacking the cell's "protein production system" and thus leads to the synthesis of the viral's own proteins. This happens successfully because the virus's genome greatly mimics the human one, which means it can exploit the host's cellular machinery. The cell continues to produce viral proteins until it dies, releasing the virus which then proceeds to infect other cells. This process will continue as the infection spreads.2 However, regardless of the virus's ability to destroy our cells, the effect and symptoms in adults are usually minimal and in most cases cause mild fever and skin rashes and more rarely headache and conjunctivitis. the danger of Zika is exposed if contracted by pregnant women as this can consequently lead to the birth of children with congenital Zika syndrome; a unique pattern of birth defects found among fetuses and children infected with the Zika virus during pregnancy. Congenital Zika virus has five main characteristics, one of which is related specifically to the brain and has inspired scientists to consider the possibility of redesigning the virus as a medicinal drug; microcephaly. In addition to this specific condition, the virus has also been linked to brain-related complications in children; these abnormalities include brain atrophy and asymmetry, abnormally formed or absent brain structures, hydrocephalus, and neuronal migration disorders. There is general consensus in the scientific community that Zika is responsible for these diseases; but how? How does the virus, practically harmless to adults, cause dangerous deformities in the fetus? Since the fetus is in the womb, it cannot be bitten by an infected mosquito and therefore contracts the virus through infectiontransplacental: the virus is transmitted from mother to fetus through the placenta. This organ plays a vital role in the healthy growth and development of the fetus as it provides it with essential nutrients. Once infected, the virus replicates in its cells, destroying the placental barrier, allowing the pathogen to easily access the fetal brain. Overcoming the barrier is the first step towards the death of the fetus; hence the virus was shown to efficiently target human cortical neural progenitor cells (NPCs); these resemble stem cells as they have the ability to differentiate into other cell types but are already more specific. The death of these infected cells leads to a reduction in the thickness of both the NPC and neuronal layers and therefore to an overall reduction in the size of the organoids; the inevitable increase in destroyed cells accelerates the flattening of the neuronal layers, ultimately causing microcephaly. It is this ability to efficiently target and destroy neuronal cells that has inspired scientists to consider the possible benefits the virus' disease process could have regarding brain cancer. Applying a single, universal definition to brain cancer is difficult due to its variety and complexity, however, in short, cancer can be defined as "a class of diseases characterized by uncontrolled cell growth." Because it is caused by rapid and unmanageable cell division, cancer is essentially a disease of mitosis; but how can a vital process in the growth and development of all multicellular organisms malfunction and become a major cause of death worldwide? The lethal process of cancer development begins when a cell changes from normal to cancerous; this occurs when the cell ignores or ignores "checkpoints" that control the rate of mitosis. Often this is due to a DNA mutation that occurs in one of the genes that code for control proteins that regulate growth, for example the p53 gene. This gene is also called the “guardian of the genome” and usually functions to control the cell cycle. It is therefore not particularly surprising that this gene has been found to be mutated in over 50% of all human tumors. Once crucial cell cycle genes begin to behave abnormally, cancer cells begin to proliferate violently through uncontrolled mitosis, eventually forming a mass of cancerous cells more commonly known as a tumor. Not all tumors, however, are cancer; Benign tumors remain in their original location and do not spread to infect other parts of the body. They are usually fatal only if they press on vital organs; as for the brain, those located in critical areas can be life-threatening. The most worrying effects of tumors come from malignant ones; these metastatic cells spread and infect other areas of the body through angiogenesis. The development of new blood vessels is triggered by chemical signals from tumors, giving them access to their own supply of oxygen and "food", as well as an escape route to travel to various areas of the body. Metastases are particularly abundant throughout the brain; this is mainly due to the dense blood supply needed for the organ to function effectively, which is particularly attractive to cancer cells. As a result, studies have concluded that about a quarter of all malignant tumors will spread to the brain, and that metastatic tumors are more commonly found in the brain than tumors that originated there, so most cases of brain cancer I am the result of this.?