HCV infection is characterized by its propensity to evolve into chronicity and by a wide clinical spectrum. About 85% of patients infected by HCV will develop chronic infection and resolution of acute hepatitis C is observed in only 15% (Palitzsch et al., 1999). The severity of the liver disease varies widely from asymptomatic chronic infection, with normal liver tests and nearly normal liver, to severe chronic hepatitis, leading rapidly to cirrhosis and hepatocellular carcinoma. The mechanisms responsible for the persistence of HCV infection and for the liver lesions are not well understood. The lack of an efficient in vitro replication system or an animal model (the chimpanzee model is limited) has greatly hampered the study of these mechanisms
This research paper is going to review today’s silent killer, the Hepatitis C virus. This paper will talk about the description of the disease, the signs and symptoms, the etiology and risk factors, diagnostic studies, treatments and prognosis of this disease. I had lived with this disease for over ten years before diagnosed so it is important to understand the signs and symptoms so the disease can be identified and a treatment plan can be identified as the sooner it is treated the more likely it will eradicate the disease.
Hepatitis C is an inflammation of the liver’s cells and tissues caused by the hepatitis C virus (HCV).
Hepatitis C virus (HCV) is from the virus family Flaviviridae with an RNA envelope serving as it's genetic material. The genetic material (RNA) is HCV's pathogenic structure. The genome is positive sense single stranded RNA, which is very similar to mRNA and can be translated quickly to the host cell (Bauman 2012). Hepatitis C is an enveloped virus, and the RNA also lacks a proofreading ability after replication, which results in mutations coding for many genotypes within the host. This genetic variability makes it difficult for the host immune system to clear all the HCV infections. As one infection clears, another strain is being produced (Bauman 2012). The HCV antibody detected by ELISA(Wilkinson
Hepatitis C typically has a slower and more insidious onset. The preicteric phase, the first of three phases, precedes jaundice that last from 1 - 21 days. When symptom do occur they can be so vague that people often don't realize what is truly going on. People actually may mistake these symptoms as a mild case of the influenza virus as the symptoms of this phase often mimic the symptoms of the flu. The interic phase is characterized by the onset of jaundice that last 2 - 4 weeks. Urine often becomes dark and stool may be a abnormally light color, this is cause by the absence of bile in the stool. Bile pigment deposits in the skin can cause pruritus to occur. The liver often becomes enlarged and tender. During the third phase, the posticteric
Although we are well aware of the mode of transmission, the hepatitis C virus itself remains a mystery. The genome of HCV is extremely mutable. Because HCV is an RNA virus and does not have adequate proofreading ability as it replicates, virions infecting humans undergo evolution with time, giving rise to the notion that HCV persists as a collection of virus quasispecies. Because it is constantly mutating, HCV is able to escape detection and elimination its human host. HCV undergoes quick mutation in a hypervariable region of the genome coding for the envelope proteins and escapes immune surveillance by the host. As a result, most HCV-infected people develop chronic infection. HCV also knocks out the host’s innate immunity.
Hepatitis C affects millions worldwide. Hepatitis C causes infection leading to chronic liver disease. Human hepatocyte chimeric mice were made by transplantation of the human hepatocyte to mice. Reverse genetic hepatitis C viruses of two different genotypes were made from infectious clones and human hepatocyte chimeric mice. Chimeric mice were injected with both genotypes of hepatitis C. There after treatment by interferon was administered. A control of human serum from a donor with chronic hepatitis C was used. The results obtained showed that mice injected with both genotypes of hepatitis C virus had a quantifiable level of virus present in the blood. It was observed that genotype 1 did not response to interferon therapy as compared to genotype 2. Results showed a decreased level of genotype 2 of hepatitis C virus after
There are four risk factors associated with HPV infection. Their factors are sexual activity, contraceptive use, pregnancy, and immune status. (Koutsky et al. 1988). The risk of acquiring the infection is greatly influenced by the number of sex partners, frequency of sexual intercourse, and the presence of genital warts on sex partners.
Hepatocellular carcinoma (HCC) is introduced as the fifth most common tumor and also the third most common cause of cancer-related deaths all around the world. Carcinogenesis of HCC is a multistep and complex process; it is known that multiple risk factors, such as chronic hepatitis B virus (HBV)or hepatitis C virus (HCV) infections, carcinogen exposure, cirrhosis and a group of single nucleotide polymorphisms, subscribe to hepatocarcinogenesis.Chronic HCV patients are susceptible to hepatic inflammation, developing liver fibrosis, cirrhosis and HCC. Such a case does not depend on virus genotype or viral load
According to the National Notifiable Diseases Surveillance System, there are 140 new cases and 2203 existing cases (Australian Health Department, 2016). This information has been accessed from their website and carries data from 1991 to 2015.
HPV (Human Papillomavirus) is a sexually transmitted infection. HPV is transmitted through vaginal, anal, and oral sex with someone who has the virus. There are many ways to be sure that you could be safe against HPV such as abstinence, get one or both of the vaccinations (Cervarix or Gardasil), and use condoms. Although condoms are not 100% guaranteed, it is still safe to take the precaution.
Nwakamma stated, “Routes of infection include organ transplantation, IV drug use, sexual contact, exposure to blood, perinatal transmission or occupational exposure” (Nwakamma). Organ transplantation was one of the first ways scientists were able to determine the cause of Hepatitis C. Another more common way Hepatitis C is still being spread is by IV drug use. If a IV needle is contaminated with infected blood, that can cause the person using it to get hepatitis C. When people are injecting drugs into their bodies using someone else’s needle, they are putting themselves at high risk to contract any infectious virus. Infectious viruses are not visible on objects but they are visible once they enter in your bloodstream. The formation of the virus is identified as a positive stranded RNA. Nwakamma makes a similar point about the description of the virus by stating, “The Hepatitis C virus is a small, enveloped, single-stranded RNA virus of the family Flaviviridae, and has a genome of approximately ten-thousand nucleotides coding for structural proteins” (Nwakamma). Once the Hepatitis C virus binds to a cell surface receptor that leads to viral entry into the host cell. Due to Flaviviridae being an RNA virus, it cannot replicate in the nucleus. Patients whose condition with Hepatitis C becomes chronic often have a hard time producing insulin. In accordance with the previous
Hepatitis C viral (HCV) infection is one of the many chronic illnesses that disproportionately affect the 2 million persons currently incarcerated in US jails and prisons. (ACA, 2015). HCV is most frequently acquired through exposure to infected blood in persons who injected drugs any time in their lifetime. Offenders are statistically at increased risk for bloodborne pathogen infections such as HCV because of the strong association of chronic addiction and criminal behavior. Correctional health care systems have more patients with HCV infection, on a percentage basis, than any other major health care system in the United States.
HCMV is capable of infecting an extensive range of cell types in vivo. According to Compton (2004), the infection of a fibroblast begins with an initial tethering of a virion to cell surface - heparan sulfate proteoglycans. Then the HCMV glycoprotein, gB, is directly fused to cellular receptors such as epidermal growth factor receptor (EGFR) and cellular integrins occurs at neutral pH (Compton, 1992). The fusion with the envelope is followed by attachment of the virion and release into the cytoplasm (Roizman & Pellet, 2001). HCMV entry into epithelial and endothelial cells occurs through endocytosis in a low-pH condition (Ryckman et al., 2006) using the viral glycoproteins UL131-128 (Hahn et al., 2004). Infected cells show several
HCV entry is the first step of interactions between virus and the target cell that is required for initiation of infection. Several host cell surface molecules including glycosaminoglycans, CD81, scavenger receptor class B type I (SRBI), members of the claudin family (CLDN1, 6 and 9) and mannose-binding lectins DC-SIGN and L-SIGN have been identified as putative HCV receptors orcoreceptorsas shown in Figure 2(Barth et al., 2006).
The hepatitis C virus (HCV) is the most widespread blood borne infection throughout the United States. It is estimated that nearly 3.2 million Americans are chronically infected (Centers for Disease Control and Prevention, 2014). HCV is a leading cause of cirrhosis, hepatocellular carcinoma, and is an indication for liver transplant (Medscape, 2012). As a result, HCV poses a significant economic burden on the American health care system.