Hepatitis C VirusA virus is an infectious agent that is only able to reproduce inside a host celland consist of a protein coat, hereditary material, and often a membranous envelope. Hepatitis C, also known as HCV is a viral infection that attacks the liver. HCV belongs to the “genus Hepacivirus”, and is a member of the Flaviviridae virus family (Chevaliez and Pawlotsky, 2006, P.1). The Hepatitis C virus is the direct cause of the contagious liver disease Hepatitis C. This virus is transmitted when one individual comes in contact with the contaminated blood of an individual with HCV. The most common way one can contract this virus, is through unsterile needles and syringes. Hepatitis C can also be spread through hygiene products, such as razors. HCV may be contracted through sexual interactions, however it is very unlikely. Mothers who are carriers of the Hepatitis C virus have a “1 in 25 chance” of passing the virus to their children (Holland and Nall, 2017). Since HCV is a blood-borne virus, there are no animal or insect vectors present. Prior to June, 1992 individuals who received blood transfusions or organ transplants might have acquired the Hepatitis C virus (Holland and Nall , 2017). This was due to the lack of sensitivity in blood testings during that time period (Holland and Nall , 2017). Hepatitis C enters the cells of the host by attaching itself to a liver cell, then utilizes proteins on the lipid coat in order to attach to a receptor cite (Trustees of Dartmouth College, 2018). To enter the cell, the HCV protein core must go through the plasma membrane. In order for the Hepatitis C virus to enter the cell it must fuse it’s lipid layer to the plasma membrane. After the membrane consumes the virus, viral RNA is released as a result of the protein coat dissolving; this takes place during the penetration step of the Lytic Cycle. The viral RNA then synthesizes the RNA transcriptase. In order for new viral RNA to be made, the viral RNA must create an opposite of itself or an “antisense version” (Trustees of Dartmouth College, 2018). This will result in several copies of the viral RNA, some of which will contain mutations. Following the reproduction of viral RNA, it then directs the construction of capsomeres, which are the “building blocks for the virus’s protective protein coat” (Trustees of Dartmouth College, 2018). After the capsomeres are produced, they assemble to form the capsid. The virus then attaches to the plasma membrane, which results in the creation of a bud. The plasma membrane later releases the virus, allowing them to attach to other liver cells. This process is referred to as “budding and release”. (Trustees of Dartmouth College, 2018, P.1) Hepatitis C attacks the liver, which is an internal organ that “produces bile, maintains blood glucose levels, and detoxifies poisonous chemicals in the blood” (Campbell Biology AP, Ninth Edition, P.G-37). HCV causes inflammation of the liver, which prevents it from carrying out these essential functions. Hepatitis C henders the liver’s production of bile, which can make it very difficult to digest foods that are high in fat. HCV has two different stages, which include acute and chronic. During the acute stage of HCV, most patients are non-symptomatic, however some can experience mild symptoms, such as fatigue and vomiting. Gallbladder inflammation can also occur during the acute stage of Hepatitis C, although it is rare (Pietrangelo and Cherney, 2017, P.2). Although acute HCV is minor, chronic Hepatitis C can be detrimental and can lead to severe liver issues, such as cirrhosis and liver cancer. Individuals with chronic Hepatitis C will most likely experience symptoms related to cirrhosis, which is scarring of the liver. Some of the symptoms include dark yellow urine, weight loss, vomiting blood and jaundice. HCV can disrupt the central nervous system, by preventing the liver from filtering toxins found in the blood. In addition, Hepatitis C also prevents the liver from regulating blood clotting. This can increase the pressure in the main vein that leads to the liver (portal vein), ultimately causing “portal hypertension” and “variceal bleeding” (Pietrangelo and Cherney, 2017, P.1). Overall, Hepatitis C can cause a variety of conditions that have a wide range of severity, that are a direct correlation to the stage of HCV (acute or chronic). Hepatitis C is considered curable if the virus goes undetected for six months following treatment. If the patient still has trace of the virus in their system after 6 months of treatment, this indicates that the virus has become chronic. HCV can be treated with antiviral medication, such as Pegylated interferon and Ribavirin. These antivirals work by attacking the virus and disrupting stages of their life cycle, preventing the reproduction of viral cells (Davis, 2017, P.1).Hepatitis C can be prevented by avoiding direct exposure to blood.Since there is no vaccine to prevent HCV, one must take precautions in order to reduce the chance of catching the virus. Individuals that use intravenous drugs are at a higher risk of getting Hepatitis C, due to the commonality of sharing needles. Another way to prevent the virus, is being extra precautious when getting tattoos. If one receives a tattoo from unsterile equipment, that is a prime way to contract the virus. Individuals that work in the medical field need to be cautious when dealing with equipment that draws blood. Needles and other tools need to be discarded and safely disposed of. Hepatitis C is the most prevalent blood-borne virus in the United States (Chou, 2012, P.1) There are around 150 million individuals that carry the HCV virus worldwide (Pietrangelo, 2014). This growing epidemic can be reduced with the proper education and prevention methods.