Acute viral Hepatitis: Types, Symptoms, Treatment

Acute viral hepatitis (AVH) is a systemic infection that mainly affects liver caused by hepatotropic viruses (hepatitis A to E). The condition can be self-limiting or can progress to fibrosis (scarring), cirrhosis or liver cancer.

Other viruses like cytomegalovirus (CMV), herpes simplex, Coxsackie and adenovirus can also cause hepatitis in certain situations.

Most cases of acute viral hepatitis are caused by one of five viral agents:

Hepatitis A virus (HAV),
Hepatitis B virus (HBV),
Hepatitis C virus (HCV),
The HBV-associated delta agent or hepatitis D virus (HDV), and
Hepatitis E virus (HEV).

All these human hepatitis viruses are RNA viruses, except for hepatitis B, which is a DNA virus but replicates like a retrovirus.

In particular, types B and C lead to chronic disease in hundreds of millions of people and, together, are the most common cause of liver cirrhosis and cancer.

Acute viral hepatitis caused by hepatitis A to E is the most common cause of liver disease worldwide.

Hepatitis A and E are typically caused by the ingestion of contaminated food or water. Hepatitis B, C, and D usually occur as a result of parenteral contact with infected body fluids. Common modes of transmission for these viruses include receipt of contaminated blood or blood products, invasive medical procedures using contaminated equipment and for hepatitis B transmission from mother to baby at birth, from family member to child, and also by sexual contact.

Hepatitis A virus

HAV is an RNA virus belonging to the Picornavirus family which is non enveloped, 27 nano micron size, has a 7.5 kb genome. HAV is transmitted fecal orally.

Hepatitis A has an incubation period of ~4 weeks. Its replication is limited to the liver, but the virus is present in the liver, bile, stools, and blood during the late incubation period and acute preicteric/ presymptomatic phase of the illness.

Despite slightly longer persistence of the virus in the liver, fecal shedding, viremia, and infectivity diminish rapidly once jaundice becomes apparent.

Antibodies to HAV (anti-HAV) can be detected during acute illness when serum aminotransferase activity is elevated and fecal HAV shedding is still occurring. This early antibody response is predominantly of the IgM class and persists for several (~3) months, rarely for 6–12 months.

During convalescence, however, anti-HAV of the IgG class becomes the predominant antibody. Therefore, the diagnosis of hepatitis A is made during acute illness by demonstrating anti-HAV of the IgM class.

After acute illness, anti-HAV of the IgG class remains detectable indefinitely, and patients with serum anti-HAV are immune to reinfection.

Risk factors of Hepatitis A virus

Risk factors for hepatitis A virus are:

Unhygienic condition,
Poor sanitation,
Consumers of high-risk food, e.g. raw shellfish,
People traveling to endemic areas and
Gay and intravenous drug abuses

Hepatitis B virus

Hepatitis B virus is a DNA virus that causes both acute and chronic diseases. HBV is now recognized as one of a family of animal viruses, hepadnaviruses (hepatotropic DNA viruses), and is classified as hepadnavirus type 1

The pathological consequences of persistent Chronic Hepatitis B include the development of chronic hepatic insufficiency, cirrhosis and hepatocellular carcinoma (HCC) .

Hepatitis B virus can be classified into seven genotypes A to G based on nucleotide divergence.

Hepatitis B virus (HBV) is transmitted through exposure to infective blood, semen, and other body fluids. HBV can be transmitted from infected mothers to infants at the time of birth or from family members to infants in early childhood.

Transmission may also occur through transfusions of HBV-contaminated blood and blood products, contaminated injections during medical procedures, and through injection drug use. HBV also poses a risk to healthcare workers who sustain accidental needle stick injuries while caring for infected-HBV patients. Safe and effective vaccines are available to prevent HBV.

The antigen expressed on the surface of the nucleocapsid core is the hepatitis B core antigen (HBcAg), and its corresponding antibody is anti-HBc.

Early during the course of acute hepatitis B, HBeAg appears transiently; its disappearance may be a harbinger of clinical improvement and resolution of infection. Persistence of HBeAg in serum beyond the
first 3 months of acute infection may be predictive of the development of chronic infection, and the presence of HBeAg during chronic hepatitis B tends to be associated with ongoing viral replication, infectivity, and inflammatory liver injury

The first virologic marker detectable in serum within 1–12 weeks, usually between 8 and 12 weeks, is HBsAg. Circulating HBsAg precedes elevations of serum aminotransferase activity and clinical symptoms by 2–6 weeks and remains detectable during the entire icteric or symptomatic phase of acute hepatitis B and beyond.

In typical cases, HBsAg becomes undetectable 1–2 months after the onset of jaundice and rarely persists beyond 6 months. After HBsAg disappears, antibody to HBsAg (anti-HBs) becomes detectable in serum and remains detectable indefinitely thereafter.

The other readily detectable serologic marker of HBV infection, HBeAg, appears concurrently with or shortly after HBsAg.

Hepatitis D The delta hepatitis agent, or HDV, the only member of the genus Deltavirus, is a defective RNA virus that co-infects with and requires the helper function of HBV (or other hepadnaviruses) for its replication and expression.

Hepatitis C virus

Hepatitis C virus (HCV) is mostly transmitted through exposure to infective blood. This may happen through transfusions of HCV-contaminated blood and blood products, contaminated injections during medical procedures, and through injection drug use. Sexual transmission is also possible but is much less common.

There is no vaccine for HCV.

Hepatitis C virus is a linear, single-strand, positive-sense, 9600-nucleotide RNA virus.

Hepatitis E virus

Hepatitis E virus (HEV) is mostly transmitted through the consumption of contaminated water or food. Hepatitis E virus (HEV) is an enterically transmitted virus that causes clinically apparent hepatitis. Safe and effective vaccines to prevent HEV infection have been developed but are not widely available.

The clinical manifestations after acute liver injury associated with viral hepatitis are determined by the immunologic responses of the host. This is because none of these viruses have shown to be directly cytopathic to hepatocytes.

Signs and symptoms of Acute Viral Hepatitis

The prodromal or initial symptoms of acute viral hepatitis are systemic and quite variable. This initial phase is known as the acute phase.

Constitutional symptoms of viral hepatitis can mimic flu symptoms and they include:

Anorexia,
nausea and vomiting,
fatigue, malaise,
arthralgias,
myalgias,
headache,
photophobia,
pharyngitis,
cough, and coryza
may precede the onset of jaundice by 1–2 weeks.

A low-grade fever between 38° and 39°C is often present in hepatitis A and E than in hepatitis B or C.

The acute phase is not usually dangerous, but in certain people, it can result in acute liver failure and death. It may also progress to a chronic infection. This is most likely with HBV or HCV.

Dark urine and clay-colored stools may be noticed before the onset of clinical jaundice.
With the onset of clinical jaundice, the constitutional prodromal symptoms usually diminish, but in some patients, mild weight loss is common and may continue during the entire icteric phase.

The liver becomes enlarged and tender and may be associated with right upper quadrant pain and discomfort. Infrequently, patients present with a cholestatic picture, suggesting extrahepatic biliary obstruction.

Splenomegaly and cervical adenopathy are present. A few spider angiomas appear during the icteric phase and disappear during convalescence.

During the recovery phase, constitutional symptoms disappear, but usually, some liver enlargement and abnormalities in liver biochemical tests are still evident.

A substantial proportion of patients with viral hepatitis never become icteric.

Infection with HDV can occur in the presence of acute or chronic HBV infection; the duration of HBV infection determines the duration of HDV infection. When acute HDV and HBV infections occur simultaneously, clinical and biochemical features may be indistinguishable from those of HBV infection alone, although occasionally they are more severe.

HDV superinfection appears as a clinical exacerbation or an episode resembling acute viral hepatitis in someone already chronically infected with HBV. Superinfection with HDV in a patient with chronic hepatitis B often leads to clinical deterioration.