|Other names||Infectious hepatitis|
|A case of jaundice caused by hepatitis A|
|Specialty||Infectious disease, gastroenterology|
|Symptoms||Nausea, vomiting, diarrhea, dark urine, jaundice, fever, abdominal pain|
|Complications||Acute liver failure|
|Usual onset||2–6 weeks after infection|
|Causes||Eating food or drinking water contaminated with Hepatovirus A infected feces|
|Diagnostic method||Blood tests|
|Prevention||Hepatitis A vaccine, hand washing, properly cooking food|
|Treatment||Supportive care, liver transplantation|
|Frequency||114 million symptomatic and nonsymptomatic (2015)|
Hepatitis A is an infectious disease of the liver caused by Hepatovirus A (HAV).Many cases have few or no symptoms, especially in the young. The time between infection and symptoms, in those who develop them, is between two and six weeks. When symptoms occur, they typically last eight weeks and may include nausea, vomiting, diarrhea, jaundice, fever, and abdominal pain. Around 10–15% of people experience a recurrence of symptoms during the six months after the initial infection. Acute liver failure may rarely occur, with this being more common in the elderly.
It is usually spread by eating food or drinking water contaminated with infected feces.Shellfish which have not been sufficiently cooked are a relatively common source. It may also be spread through close contact with an infectious person. While children often do not have symptoms when infected, they are still able to infect others. After a single infection, a person is immune for the rest of his or her life. Diagnosis requires blood testing, as the symptoms are similar to those of a number of other diseases. It is one of five known hepatitis viruses: A, B, C, D, and E.
The hepatitis A vaccine is effective for prevention. [ needs update ] Some countries recommend it routinely for children and those at higher risk who have not previously been vaccinated. It appears to be effective for life. Other preventive measures include hand washing and properly cooking food. No specific treatment is available, with rest and medications for nausea or diarrhea recommended on an as-needed basis. Infections usually resolve completely and without ongoing liver disease. Treatment of acute liver failure, if it occurs, is with liver transplantation.
Globally, around 1.4 million symptomatic cases occur each yearand about 114 million infections (symptomatic and asymptomatic). It is more common in regions of the world with poor sanitation and not enough safe water. In the developing world, about 90% of children have been infected by age 10, thus are immune by adulthood. It often occurs in outbreaks in moderately developed countries where children are not exposed when young and vaccination is not widespread. Acute hepatitis A resulted in 11,200 deaths in 2015. World Hepatitis Day occurs each year on July 28 to bring awareness to viral hepatitis.
Early symptoms of hepatitis A infection can be mistaken for influenza, but some sufferers, especially children, exhibit no symptoms at all. Symptoms typically appear 2 to 6 weeks (the incubation period) after the initial infection.About 90% of children do not have symptoms. The time between infection and symptoms, in those who develop them, is between 2 and 6 weeks with an average of 28 days.
The risk for symptomatic infection is directly related to age, with more than 80% of adults having symptoms compatible with acute viral hepatitis and the majority of children having either asymptomatic or unrecognized infections.
Symptoms usually last less than 2 months, although some people can be ill for as long as 6 months:
Joint pains, red cell aplasia, pancreatitis and generalized lymphadenopathy are the possible extrahepatic manifestations. Kidney failure and pericarditis are very uncommon.If they occur, they show an acute onset and disappear upon resolution of the disease.
|Electron micrograph of Hepatovirus A virions|
Hepatovirus A is a species of virus in the order Picornavirales in the family Picornaviridae and is the type species of the genus Hepatovirus . Humans and vertebrates serve as natural hosts.
A total of nine members of Hepatovirus are recognized.These species infect bats, rodents, hedgehogs, and shrews. Phylogenetic analysis suggests a rodent origin for Hepatitis A.
A member virus of Hepatovirus B (Phopivirus) has been isolated from a seal.This virus shared a common ancestor with Hepatovirus A about 1800 years ago.
Another hepatovirus - Marmota himalayana hepatovirus - has been isolated from the woodchuck Marmota himalayana .This virus appears to have had a common ancestor with the primate-infecting species around 1000 years ago.
One serotype and seven different genetic groups (four human and three simian) have been described.The human genotypes are numbered I–III. Six subtypes have been described (IA, IB, IIA, IIB, IIIA, IIIB). The simian genotypes have been numbered IV–VI. A single isolate of genotype VII isolated from a human has also been described. Genotype III has been isolated from both humans and owl monkeys. Most human isolates are of genotype I. Of the type I isolates subtype IA accounts for the majority.
The mutation rate in the genome has been estimated to be 1.73–9.76 × 10−4 nucleotide substitutions per site per year. The human strains appear to have diverged from the simian about 3600 years ago. The mean age of genotypes III and IIIA strains has been estimated to be 592 and 202 years, respectively.
Hepatovirus A is a picornavirus; it is not enveloped and contains a single-stranded RNA packaged in a protein shell.Only one serotype of the virus has been found, but multiple genotypes exist. Codon use within the genome is biased and unusually distinct from its host. It also has a poor internal ribosome entry site. In the region that codes for the HAV capsid, highly conserved clusters of rare codons restrict antigenic variability.
|Genus||Structure||Symmetry||Capsid||Genomic arrangement||Genomic segmentation|
Humans and vertebrates serve as the natural hosts. Transmission routes are fecal-oral and blood.
Following ingestion, HAV enters the bloodstream through the epithelium of the oropharynx or intestine.The blood carries the virus to its target, the liver, where it multiplies within hepatocytes and Kupffer cells (liver macrophages). Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the virus to host receptors, which mediates endocytosis. Replication follows the positive-stranded RNA virus replication model. Translation takes place by viral initiation. The virus exits the host cell by lysis and viroporins. Virions are secreted into the bile and released in stool. HAV is excreted in large numbers about 11 days prior to the appearance of symptoms or anti-HAV IgM antibodies in the blood. The incubation period is 15–50 days and risk of death in those infected is less than 0.5%.
Within the liver hepatocytes, the RNA genome is released from the protein coat and is translated by the cell's own ribosomes. Unlike other picornaviruses, this virus requires an intact eukaryotic initiation factor 4G (eIF4G) for the initiation of translation.The requirement for this factor results in an inability to shut down host protein synthesis, unlike other picornaviruses. The virus must then inefficiently compete for the cellular translational machinery, which may explain its poor growth in cell culture. Presumably for this reason, the virus has strategically adopted a naturally highly deoptimized codon usage with respect to that of its cellular host. Precisely how this strategy works is not quite clear yet.
No apparent virus-mediated cytotoxicity occurs, presumably because of the virus' own requirement for an intact eIF4G, and liver pathology is likely immune-mediated.
|Genus||Host details||Tissue tropism||Entry details||Release details||Replication site||Assembly site||Transmission|
|Hepatovirus||Humans; vertebrates||Liver||Cell receptor endocytosis||Lysis||Cytoplasm||Cytoplasm||Oral-fecal; blood|
The virus spreads by the fecal–oral route, and infections often occur in conditions of poor sanitation and overcrowding. Hepatitis A can be transmitted by the parenteral route, but very rarely by blood and blood products. Food-borne outbreaks are common, °C. It can survive for months in fresh and salt water. Common-source (e.g., water, restaurant) outbreaks are typical. Infection is common in children in developing countries, reaching 100% incidence, but following infection, lifelong immunity results. HAV can be inactivated by chlorine treatment (drinking water), formalin (0.35%, 37 °C, 72 hours), peracetic acid (2%, 4 hours), beta-propiolactone (0.25%, 1 hour), and UV radiation (2 μW/cm2/min). HAV can also be spread sexual contact specifically oroanal sexual acts.and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection. About 40% of all acute viral hepatitis is caused by HAV. Infected individuals are infectious prior to onset of symptoms, roughly 10 days following infection. The virus is resistant to detergent, acid (pH 1), solvents (e.g., ether, chloroform), drying, and temperatures up to 60
In developing countries, and in regions with poor hygiene standards, the rates of infection with this virus are highand the illness is usually contracted in early childhood. As incomes rise and access to clean water increases, the incidence of HAV decreases. In developed countries, though, the infection is contracted primarily by susceptible young adults, most of whom are infected with the virus during trips to countries with a high incidence of the disease or through contact with infectious persons.
Humans are the only natural reservoir of the virus. No known insect or other animal vectors can transmit the virus. A chronic HAV state has not been reported.
Although HAV is excreted in the feces towards the end of the incubation period, specific diagnosis is made by the detection of HAV-specific IgM antibodies in the blood.IgM antibody is only present in the blood following an acute hepatitis A infection. It is detectable from 1–2 weeks after the initial infection and persists for up to 14 weeks. The presence of IgG antibodies in the blood means the acute stage of the illness has passed and the person is immune to further infection. IgG antibodies to HAV are also found in the blood following vaccination, and tests for immunity to the virus are based on the detection of these antibodies.
During the acute stage of the infection, the liver enzyme alanine transferase (ALT) is present in the blood at levels much higher than is normal. The enzyme comes from the liver cells damaged by the virus.
Hepatovirus A is present in the blood (viremia) and feces of infected people up to 2 weeks before clinical illness develops.
Hepatitis A can be prevented by vaccination, good hygiene, and sanitation.
The two types of vaccines contain either inactivated Hepatovirus A or a live but attenuated virus.Both provide active immunity against a future infection. The vaccine protects against HAV in more than 95% of cases for longer than 25 years. In the US, the vaccine was first used in 1996 for children in high-risk areas, and in 1999 it was spread to areas with elevating levels of infection.
The vaccine is given by injection. An initial dose provides protection lasting one year starting 2–4 weeks after vaccination; the second booster dose, given six to 12 months later, provides protection for over 20 years.
The vaccine was introduced in 1992 and was initially recommended for persons at high risk. Since then, Bahrain and Israel have embarked on elimination programmes.Australia, China, Belarus, Italy, Spain, and the United States have started similar programmes. The incidence of hepatitis A where widespread vaccination has been practised has decreased dramatically. In China and the United States, the incidence of hepatitis A has decreased by 90% since 1990.
In the United States, vaccination of children is recommended at 1 and 2 years of age;hepatitis A vaccination is not recommended in those younger than 12 months of age. It is also recommended in those who have not been previously immunized and who have been exposed or are likely to be exposed due to travel. The CDC recommends vaccination against infection for men who have sex with men.
No specific treatment for hepatitis A is known. Recovery from symptoms following infection may take several weeks or months. Therapy is aimed at maintaining comfort and adequate nutritional balance, including replacement of fluids lost from vomiting and diarrhea.
In the United States in 1991, the mortality rate for hepatitis A was estimated to be 0.015% for the general population, but ranged up to 1.8 -2.1% for those aged 50 and over who were hospitalized with icteric hepatitis.The risk of death from acute liver failure following HAV infection increases with age and when the person has underlying chronic liver disease.
Young children who are infected with hepatitis A typically have a milder form of the disease, usually lasting 1–3 weeks, whereas adults tend to experience a much more severe form of the disease.
Globally, symptomatic HAV infections are believed to occur in around 1.4 million people a year.About 114 million infections (asymptomatic and symptomatic) occurred all together in 2015. Acute hepatitis A resulted in 11,200 deaths in 2015. Developed countries have low circulating levels of hepatovirus A, while developing countries have higher levels of circulation. Most adolescents and adults in developing countries have already had the disease, thus are immune. Adults in midlevel countries may be at risk of disease with the potential of being exposed.
Over 30,000 cases of hepatitis A were reported to the CDC in the US in 1997, but the number has since dropped to less than 2,000 cases reported per year.
The most widespread hepatitis A outbreak in the United States occurred in 2018, in the state of Kentucky. The event was ongoing as of June 30, 2018. As of June 27, 2018, the total number of suspected people affected is 969 people (482 cases in Louisville, Kentucky). In total, six people have died from the virus. A total of 48% of the state's counties have reported of at least one case of hepatitis A. As of June 30, 2018, where the outbreak started is unknown, but it is believed to have started around the fall of 2017 (Another widespread outbreaks in the United States, 2003 United States hepatitis outbreak, affected at least 640 people (killing four) in northeastern Ohio and southwestern Pennsylvania in late 2003. The outbreak was blamed on tainted green onions at a restaurant in Monaca, Pennsylvania. In 1988, more than 300,000 people in Shanghai, China, were infected with HAV after eating clams ( Anadara subcrenata ) from a contaminated river. In June 2013, frozen berries sold by US retailer Costco and purchased by around 240,000 people were the subject of a recall, after at least 158 people were infected with HAV, 69 of whom were hospitalized. In April 2016, frozen berries sold by Costco were once again the subject of a recall, after at least 13 people in Canada were infected with HAV, three of whom were hospitalized. In Australia in February 2015, a recall of frozen berries was issued after at least 19 people contracted the illness following their consumption of the product. In 2017, California (particularly around San Diego), Michigan, and Utah reported outbreaks of hepatitis A that have led to over 800 hospitalizations and 40 deaths.
Yellow fever is a viral disease of typically short duration. In most cases, symptoms include fever, chills, loss of appetite, nausea, muscle pains particularly in the back, and headaches. Symptoms typically improve within five days. In about 15% of people, within a day of improving the fever comes back, abdominal pain occurs, and liver damage begins causing yellow skin. If this occurs, the risk of bleeding and kidney problems is increased.
West Nile fever is an infection by the West Nile virus, which is typically spread by mosquitoes. In about 80% of infections people have few or no symptoms. About 20% of people develop a fever, headache, vomiting, or a rash. In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. Recovery may take weeks to months. The risk of death among those in whom the nervous system is affected is about 10%.
Hepatitis is inflammation of the liver tissue. Some people with hepatitis have no symptoms, whereas others develop yellow discoloration of the skin and whites of the eyes (jaundice), poor appetite, vomiting, tiredness, abdominal pain, and diarrhea. Hepatitis is acute if it resolves within six months, and chronic if it lasts longer than six months. Acute hepatitis can resolve on its own, progress to chronic hepatitis, or (rarely) result in acute liver failure. Chronic hepatitis may progress to scarring of the liver (cirrhosis), liver failure, and liver cancer.
Antiviral drugs are a class of medication used for treating viral infections. Most antivirals target specific viruses, while a broad-spectrum antiviral is effective against a wide range of viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit their development.
Measles is a highly contagious infectious disease caused by measles virus. Symptoms usually develop 10–12 days after exposure to an infected person and last 7–10 days. Initial symptoms typically include fever, often greater than 40 °C (104 °F), cough, runny nose, and inflamed eyes. Small white spots known as Koplik's spots may form inside the mouth two or three days after the start of symptoms. A red, flat rash which usually starts on the face and then spreads to the rest of the body typically begins three to five days after the start of symptoms. Common complications include diarrhea, middle ear infection (7%), and pneumonia (6%). These occur in part due to measles-induced immunosuppression. Less commonly seizures, blindness, or inflammation of the brain may occur. Other names include morbilli, rubeola, red measles, and English measles. Both rubella, also known as German measles, and roseola are different diseases caused by unrelated viruses.
Mumps is a viral disease caused by the mumps virus. Initial signs and symptoms often include fever, muscle pain, headache, poor appetite, and feeling generally unwell. This is then usually followed by painful swelling of one or both parotid salivary glands. Symptoms typically occur 16 to 18 days after exposure and resolve after seven to 10 days. Symptoms are often more severe in adults than in children. About a third of people have mild or no symptoms. Complications may include meningitis (15%), pancreatitis (4%), inflammation of the heart, permanent deafness, and testicular inflammation, which uncommonly results in infertility. Women may develop ovarian swelling, but this does not increase the risk of infertility.
Hepatitis C is an infectious disease caused by the hepatitis C virus (HCV) that primarily affects the liver. During the initial infection people often have mild or no symptoms. Occasionally a fever, dark urine, abdominal pain, and yellow tinged skin occurs. The virus persists in the liver in about 75% to 85% of those initially infected. Early on chronic infection typically has no symptoms. Over many years however, it often leads to liver disease and occasionally cirrhosis. In some cases, those with cirrhosis will develop serious complications such as liver failure, liver cancer, or dilated blood vessels in the esophagus and stomach.
Norovirus, sometimes referred to as the winter vomiting bug, is the most common cause of gastroenteritis. Infection is characterized by non-bloody diarrhea, vomiting, and stomach pain. Fever or headaches may also occur. Symptoms usually develop 12 to 48 hours after being exposed, and recovery typically occurs within 1 to 3 days. Complications are uncommon, but may include dehydration, especially in the young, the old, and those with other health problems.
Hepatitis E is inflammation of the liver caused by infection with the hepatitis E virus (HEV). Hepatitis E has mainly a fecal-oral transmission route that is similar to hepatitis A, but the viruses are unrelated. In retrospect, the earliest known epidemic of hepatitis E occurred in 1955 in New Delhi, but the virus was not isolated until 1983, by Russian scientists investigating an outbreak in Afghanistan. One of five known human hepatitis viruses: hepatitis A, B, C, D, and E, HEV is a positive-sense, single-stranded, nonenveloped, RNA icosahedral virus.
Viral hepatitis is liver inflammation due to a viral infection. It may present in acute form as a recent infection with relatively rapid onset, or in chronic form.
Japanese encephalitis (JE) is an infection of the brain caused by the Japanese encephalitis virus (JEV). While most infections result in little or no symptoms, occasional inflammation of the brain occurs. In these cases, symptoms may include headache, vomiting, fever, confusion and seizures. This occurs about 5 to 15 days after infection.
TT virus (TTV) was the first member of the new family Anelloviridae to be discovered.
Infectious canine hepatitis (ICH) is an acute liver infection in dogs caused by Canine mastadenovirus A, formerly called Canine adenovirus 1 (CAV-1). CAV-1 also causes disease in wolves, coyotes, and bears, and encephalitis in foxes. The virus is spread in the feces, urine, blood, saliva, and nasal discharge of infected dogs. It is contracted through the mouth or nose, where it replicates in the tonsils. The virus then infects the liver and kidneys. The incubation period is 4 to 7 days.
HBsAg is the surface antigen of the hepatitis B virus (HBV). It indicates current hepatitis B infection.
Passive immunity is the transfer of active humoral immunity of ready-made antibodies. Passive immunity can occur naturally, when maternal antibodies are transferred to the fetus through the placenta, and it can also be induced artificially, when high levels of antibodies specific to a pathogen or toxin are transferred to non-immune persons through blood products that contain antibodies, such as in immunoglobulin therapy or antiserum therapy. Passive immunization is used when there is a high risk of infection and insufficient time for the body to develop its own immune response, or to reduce the symptoms of ongoing or immunosuppressive diseases. Passive immunization can be provided when people cannot synthesize antibodies, and when they have been exposed to a disease that they do not have immunity against.
A breakthrough infection is a case of illness in which a vaccinated individual becomes sick from the same illness that the vaccine is meant to prevent. Simply, they occur when vaccines fail to provide immunity against the pathogen they are designed to target. Breakthrough infections have been identified in individuals immunized against a variety of different diseases including Mumps, Varicella, and Influenza. The character of breakthrough infections is dependent on the virus itself. Often, the infection in the vaccinated individual results in milder symptoms and is of a shorter duration than if the infection was contracted naturally.
Human betaherpesvirus 5, sometimes called human cytomegalovirus (HCMV), is the type species of the virus genus Cytomegalovirus, which in turn is a member of the viral family known as Herpesviridae or herpesviruses. It is also commonly called CMV. Within Herpesviridae, HCMV belongs to the Betaherpesvirinae subfamily, which also includes cytomegaloviruses from other mammals.
Hepatitis B vaccine is a vaccine that prevents hepatitis B. The first dose is recommended within 24 hours of birth with either two or three more doses given after that. This includes those with poor immune function such as from HIV/AIDS and those born premature. It is also recommended that health-care workers be vaccinated. In healthy people routine immunization results in more than 95% of people being protected.
Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that affects the liver. It can cause both acute and chronic infection. Many people have no symptoms during the initial infection. In acute infection, some may develop a rapid onset of sickness with vomiting, yellowish skin, tiredness, dark urine and abdominal pain. Often these symptoms last a few weeks and rarely does the initial infection result in death. It may take 30 to 180 days for symptoms to begin. In those who get infected around the time of birth 90% develop chronic hepatitis B while less than 10% of those infected after the age of five do. Most of those with chronic disease have no symptoms; however, cirrhosis and liver cancer may eventually develop. Cirrhosis or liver cancer occur in about 25% of those with chronic disease.
A hepatitis C vaccine, a vaccine capable of protecting against hepatitis C, is not available. Although vaccines exist for hepatitis A and hepatitis B, development of a hepatitis C vaccine has presented challenges. No vaccine is currently available, but several vaccines are currently under development.