Essay, Research Paper: Hepatitis

Hepatitis
A B C D E

Hepatitis' target for each variation is the liver. Each virus differs greatly in its structure, mode of replication, course of disease, and mode of transmission. Of the hepatitis virus' most common are the A and B viruses. Each infects and damages the liver. Icteric symptoms are jaundice and release of liver enzymes, and is readily spread before even becoming symptomatic.
Some generalizations are of these viruses are as following: HAV is caused by a picornavirus that contains RNA. It is also known as the infectious hepatitis. This type is spread by the oral fecal route that incubates for approximately one month. This does not cause chronic liver disease and rarely causes fatal disease.
HBV is known as the serum hepatitis. It is produced by a DNA virus. The HBV is spread paternally through blood, needles, sexual contact and as well perinatally. The median for its incubation is about three months and is followed by chronic hepatitis in 5% to 10% of patients. The virus is associated with hepatocellular carcinoma.
Non-A, non-B hepatitis viruses, or NANBHV viruses include HCV and HEV. These are possible undefined hepatitis viruses. The HCV virus' mode of transmission is the same as HBV but differs in replication and general course, as well, it can cause chronic liver disease. It is a flavivirus.
HDV, or the delta virus is unique because it only occurs in patients that have a HBV infection. HBV is a "helper" for HDV. It provides an envelope for the HDV and its antigen.
Hepatitis A
This virus is often spread by the consumption of contaminated water, shellfish and other foods.
The structure of the HAV is characteristic to a picovirus. The naked isohedral capsid is 27 NM and is surrounding a positive single strand RNA genome of about 7470 nucleotides. This virus has a VPg protein attached to the 5' end and polyadenosine attached to the 3' end. The capsid for this virus is extremely stable.
The HAV has not been studied extensively but it specifically interacts with the receptor sites of the liver cells. The virus establishes a slow, steady state of infection with little or no cytopathology.
Near 40% of acute hepatitis cases are caused by HAV. IT is spread by person to person contact usually via fecal oral route, or exposure to contaminated food and or water. It is found transiently found in the blood and high concentrations are found in the feces after several weeks (especially two weeks before onset of jaundice. The virus, although , is not found in the urine or and other body fluids. HAV is readily spread because it is contagious before it is symptomatic.
HAV is resistant to detergents, acids (like gastric acid), and are able to survive in temperatures like 60 degrees C. It can survive for many months in fresh and salt water. Raw and improperly treated sewage can taint the water and shellfish.
HAV outbreaks usually come from a single source eg. Water supply, restaurant, daycare centers.
Daycare centers are most major of settings. Unhygienic conditions are directly related to infection. The seropositivty rate varies from 13% in Sweden, 88% in Taiwan, 97% in Yugoslavia, and 44% in the U.S.
The spread of the HAV is reduced by interrupting the fecal oral route. So it is hygienically controllable. Potential foods should be avoided, proper hygiene should be practiced in day cares, mental faculties, and other care faculties. As well, chlorine treatment of water kill the virus is effective. The use of prophylaxis with the immune serum globulin, if given before or during incubation is 80-90% effective.
Hepatitis B
This is the most damaging of the hepatitis family although it has a very limited tissue tropism and host ranges. As known, HBV attacks the liver, also possibly(???) the kidney and pancreas.
The structure of this virus is a small enveloped DNA virus with several unusual qualities. The genome is small, and circular in shape. Is partly double stranded DNA of only 3200 bases despite the DNA encodes reverse transcriptase and replicates through a RNA intermediate.
Known as the virion or Dane particle, its size amounts to a mere 42 NM in diameter and is unusually unstable for an enveloped virus. Resistance is shown against low pH, freezing, and moderate heat. It assists in transmission to one another and hampers disinfection.
The HBV virion is polymerase with reverse transcriptase activity protein kinase surrounded in a core antigen (HBcA) envelope containing a glycoprotein surface antigen (HBsAg). A HBeAg is a minor component of the virion. The HBcAg and HBeAg components share most of their protein sequences, only HBeAg is processed differently by the cell and is primarily secreted into a serum. The HBsAg containing particles ase then released into the individual and actually outnumber the virions.
HBV replication is unique because it has a very defined tropism for the liver. It replicates through a RNA intermediate and produces releases antigenic decoy particles for immune attacks.
HBV attachment to hepatocytes is mediated by the HBsAg glycoprotiens. The actual receptor and mechanism of entry are not known. On penetration of the cell the partial DNA strand of the genome is completed to form a complete double strand DNA circle devlivered to the nucleus. The DNA is there transcribed into three major classes: 2100, 2400, 3500 nucleotides; and two minor: 900 bases of overlapping mRNAs. The 3500 base mRNA is also larger than the genome. The Hbe and HBc are related rpoteins that are translated from different in-phase start codons of closely related mRNA. This causes difference in the processing, structure and distribution in the cell and virion.
Replication of the genome occurs in the cytoplasm. The 3500 base mRNA is packaged into the cunleo capsid that contains the RNA dependent, DNA polymerase. The DNA is synthesized on a protein primer. While that occurs the RNA is degraded.
The entire genome can be integrated into a host's chromatin. The HBsAg can be detected in the cytoplasm unlike other proteins.
In the US, more than 300 cases per year are reported. The highest rates of seropositivity rate in Italy, Greece, Africa, and southeast Asia. Large number of infectee's are asymtomatic chronic carriers that secrete into their blood stream abd other bodily secretions to spread the virus. The spread is mainly percutaneously or by punctures such as sharing needles, tattooing, acupuncture, ear piercing. Also with close personal contacts like sex or child birth, even mother's milk to their babies. It is basically spread by contaminated blood and blood products.
Presence of HBV in children is less severe than in the cases of adults. Apparent illness shows in 25% of those infected. The infection is characterized by a long incubation period and an insidious onset which includes fever, malaise, and anorexia. This is thereafter followed by nausea, puking, gut rot, more fever and chills. Icteric symptoms of liver damage then set in. eg. Jaundice, dark urine, pale stool. Hepatitis causing death occurs in 1% of infectee's.
No specific treatment for HBV exists but limited studies have shown progress in different types. Transmission can be largely reduced by blood screens of donated blood, avoiding intimate personal contact with a carrier, and " avoid the lifestyles that facilitate the spread of the virus ". Vaccination is recommended for infants, children, and those at high risk. Vaccination for newborns is effective even after exposure. The vaccine is given in a series of three shots and 95% develop a protective antibody.
Hepatitis C
HBC Accounts for 90% of NANBH infection. HCV is a flavivirus with a positive RNA genome that is enveloped.
This virus is spread by needle use, paternally, transfusion recipients, and hemophiliacs on factor VIII or IX are at highest risk. It occurs in 5 to 10% of transfusion recipients (150,000 per year) causing chronic hepatitis to half and to cirrhosis in at least 20% of acute cases.
HCV can cause acute or chronic infections, they can be detected in 1 to 3 weeks after a transfusion. On the other hand it can last longer than ten years for a persistent infection. The chronic infection is worse than HBC, often leading to acute disease and cirrhosis.
Recombinant alpha-interfereon is the only effective treatment. Recreational drug use and transfusions are the most identifiable source of infection. Unfortunately the tests for HCV do not detect current acute cases.
Hepatitis D
Near 15 million people in the world are affected by this virus and is responsible for 40% of the fulmiant hepatitis infection. The genome is a defective satellite virus that can only replicate inside HBV infected cells. It is a viral parasite.
The HDV RNA genome is very small with only 1700 nucleotides. It is single stranded, and circular; which is an unusual shape for a virus. The virion is 35 to 37 NM and consists of the genome and the delta antigen, in a small or large form (22,000 and 24,000). It is surrounded by a HBsAg containing envelope.
The delta agent binds to and is internalized in the same manner as HBV, but, the small delta antigen is an RNA binding protein that is necessary for replication. Production of a large antigen is then started and hence causing the cell's demise. The genome, delta antigen, and HBsAg associate together and are freed from the cell.
From children to adults suffering from HBV these are good candidates for acquiring HDV. The agent has world wide distribution and is endemic in southern Italy, the Amazon basin, Africa and the middle east. Infections in western Europe and North America are usually caused by illicit drug use. It is spread by the same method as HBV and the same groups are at risk.
The delta agent increases the severity of the HBV. Infected individuals are most likely to get fulminant hepatitis.
There is no known treatment for the delta agent, but since HDV depends on the presence of HBV, and the routes of infection are the same. Prevention of HBV will prevent HDV. Immunization for HBV subsequently protects against HDV. If a person already has the HBV then precautions to avoid possible situations must be made.
Hepatitis E
HEV is predominantly spread by the fecal oral route. It resembles a calcivirus or a Norwalk agent in size: 27 to 34 NM. It is found all over the world , but is only problematic in developing countries. Epidemics have been reported in India, Pakistan, Nepal, Burma, N. Africa, and Mexico.
The symptoms and course of the HEV are similar to HAV, causing only acute disease. The mortality rate is 1 to 2 %, which is double that of HAV. HEV infection is especially dangerous for pregnant women.









Mr. Iverson
Biology 30
Marty Kowal