Introduction:
Hepatitis A virus (formerly known as Enterovirus 72) has a long history and it still has a big impact on human populations in the modern world. From time of the ancient Greek doctor Hippocrates, Hepatitis A virus (HAV) was noted for causing jaundice. By the 8th century, it was realized that icteric disease was caused by an infectious agent. Later in the history, in 1885, it was discovered by scientists that hepatitis could be spread through blood transfusions. Now, it is well- known that the virus is mainly transmitted via fecal-oral route which results from contamination of food and water by fecal matter and direct contact with infected individuals. Initially another icteric agent, Hepatitis B virus, was isolated in 1973
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However, later studies that tried to transmit viral hepatitis to non-human primates gave negative results. In the current time, humans are known to be the only host for hepatitis A virus. Up to date, single human serotype and 4 distinct genotypes of the virus are detected(2). HAV is noted as being a highly stable virus in high temperature and low pH conditions(3).
Replication of HAV: HAV targets hepatocytes which are cells of main tissue of liver. The virus is non-enveloped as it is released from the host cell via lysis of the host cell membrane without acquiring a lipid bilayer membrane from the host. Site of replication for HAV is cytoplasm of the host cell. Upon detection of hepatitis a virus cellular receptor on the target cell by viral capsid protein(s), the viral capsid undergoes conformational change releasing its genome into the host cell cytoplasm. Primary event followed by uncoating process is translation of ss (+) RNA of virus which serves as a, mRNA, translational template. Genome of HAV is a single stranded (+) RNA containing 5‘ nontranslated region (5‘ NTR), a single large open reading frame (ORF) , and a short 3’ NTR followed by a poly(A) tail(4). 5’ end of the RNA genome contains VPg protein bound to it. VPg acts as a primer during replication of viral genome. Host cell mRNA contains 5‘ cap which is
The virus fuses with the cell’s plasma membrane. The capsid proteins are removed, releasing the viral proteins and RNA. Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. Reverse transcriptase catalyzes the synthesis of a second DNA strand complementary to the first. The double-stranded DNA is incorporated as a provirus into the cell’s DNA. Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral proteins. The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). Vesicles transport the glycoproteins from the ER to the cell’s plasma membrane. Capsids are assembled around viral genomes and reverse transcriptase molecules. New viruses bud off from the host cell.
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
HSV is a human nuclear DNA virus that can replicate in many different species of animal as well as in many different types of cells. It can gain access to different types of cells due to its 12 envelope surface glycoproteins and uses the heparan moiety of the receptors to attach to cells
Houghton, M., n.d., Virtual Lab 9: Discovering the Virus Responsible for Hepatitis C, Chiron Corporation, http://www.mhhe.com/biosci/genbio/raven6/lab9/labs/lab9/exp1/index.html, June 28,
The Hepatitis B virus (HBV) is a species of the genus Orthohepadnavirus that is transmitted via blood and bodily fluids. It affects the liver by causing a wide range of diseases, “from acute hepatitis (including fulminant hepatic failure), to chronic hepatitis, cirrhosis and potentially hepatocellular carcinoma” (Liang, 2009).
Hepatitis A is a highly contagious infection. The infection affects mostly the liver and internal organs. Hepatitis A is caused by a virus. You can get this virus by eating or drinking food contaminated by fecal matter. Symptoms do not normally appear until after you have contracted the virus for a few weeks. People most at risk for contracting this virus are children, laboratory workers, and people who have liver problems.
Hepatitis B virus (HBV) is a major reason which contributes to liver disease and threatens health of human beings. (1) It has enveloped virion. The basic conformation is that a signal –stranded viral RNA packaged into the assembling capsid and reverse-transcribed into DNA in this compartment. (2, 3) HBV capsids are commonly in which they present two distinct icosahedral geometries, composed of 90 and 120 dimers with masses of ≈3 and ≈4 MDa, respectively, corresponding to triangulation numbers of T = 3 and T = 4 and nominally consisting of 180 and 240 subunits. (4, 5, 6) Capsid protein has a 140-resudue N-terminal core domain which is connected to a 34-residue protaimine domain via a 10-residue linker. (7)The protamine domain binds
The hepatitis C virus is a single-stranded RNA virus of the Flaviviridae family. The virus replicates within hepatocytes and is most notable for lacking a proofreading polymerase which enables copious amounts of viral mutations. There are 6 genotypes of HCV with the most widely distributed genotypes being types 1, the most common, and type 2.
Hepatitis A is a viral infection of the liver. The virus causes inflammation in your liver and is contagious. Most cases of hepatitis A are fairly mild and people recover fully.
In this case study, I believe that Thomas is experiencing hepatitis A (HAV). His symptoms includes mild jaundice of the sclera and skin, abdominal tenderness with hepatomegaly, as well as dark yellow urine. In hepatitis
Infection is first initialted by the attachment to the host cell glucosaminoglycans, usually heparin sulphate and chondroiton sulphate, with viral glycoprotein C (gC). This bond results in at least five glycoprtoeins, gB, gC, gD, gH and gL, binding to other cell surface receptors, such as Herpesvirus entry mediator or nectin 1α or β (4). Fusion of the viral envelope follows, and the de-enveloped tegument capsid is transported to the nuclear pores via the microtubular network, where DNA is released into the nucleus. Nuclear pore complex accepts the viral DNA from the capsid, minimizing the diffusion of DNA to the cytoplasm, and the transfer is completed by nuclear pore proteins (5). The viral genome circularizes upon entering the nucleus, and transcription of the five immediate early genes (IE) is done by the host RNA polymerase II. Among the IE genes are ICP0, ICP4, ICP22,
There is no difference in the pathogenicity between subtypes because cross immunity exists among them due to universal presence of the “a” determinant (Ganen, 1996). Antibody to “a” determinant is used in the diagnostic assay kit for HBsAg detection (Caan, 1996). The complete virus or Dane particles are the infectious viron of HBV (Ganen, 1996). Its outer shell is a lipoprotein envelope containing the viral surface glycoprotein. The inner core particle (hepatitis B core antigen) or nucleocapsid has a diameter of 25 – 27nm and its major structural protein is the C protein (Adabara et al., 2012) within the core is the viral DNA, a protein kinase and a polymerise known to be centrally involved in genomic replication. The core also contains non particulate soluble antigen (HBeAg) derived from HBcAg by proteoltic self-cleavage. The viral DNA is a double stranded circular molecule. This molecule has an unusual structure such that its two DNA are not perfectly symmetrical. Replication of HBV occurs predominantly in liver but also occurs in lymphocytes, spleen, kidney and pancreas. HBsAg is a product of S gene of the HBV genome and the prime constituent hepatitis B particle forms. It is manufactured in the cytoplasm of infected hepatocytes in high quantities, the excess that did not combine with DNA to produce viral
Hepatitis C is an inflammation of the liver’s cells and tissues caused by the hepatitis C virus (HCV).
There is no specific treatment for viral Hepatitis. Bed rest and preferably hospitalization is a necessary step in the early treatment. Even though Hepatitis A is a highly contagious virus, isolation of the patient to a single room is not necessary. However, proper prevention methods such as washing your hand after handling the patient, careful handling of the body fluids and feces and wearing gloves when drawing blood is important.
Hepatitis A is a liver disease caused by the Hepatitis A virus. It may cause fever, malaise, anorexia, nausea, and abdominal discomfort, followed within a few days by jaundice the disease ranges in clinical severity from a mild illness lasting 1–2 weeks to a severely disabling disease lasting several months. Good personal hygiene and proper sanitation can help prevent Hepatitis A. Transmission may occur by direct person-to-person contact; or from contaminated water, ice, or shellfish from contaminated water; or from fruits, vegetables, or other foods that are eaten uncooked, but which may become contaminated during handling. Hepatitis A can affect anyone