Hepatitis A

One of the more common causes of acute hepatitis is hepatitis A virus (HAV), which was isolated by Purcell in 1973. Humans appear to be the only reservoir for this virus. Since the application of accurate serologic investigations in the 1980s, the epidemiology, clinical manifestations, and natural history of hepatitis A have become apparent.

The relative frequency of HAV as a cause of acute hepatitis has declined in Western societies, while in contrast, notification of individual cases has increased, primarily as a result of improved reporting and diagnostic techniques. The nadir of reported cases was in 1987.

Improvements in hygiene, public health policies, and sanitation have had the greatest impact on hepatitis A, and vaccination and passive immunization have successfully led to some reduction in illness in high-risk groups.

Reduced encounters with HAV at a young age have resulted in both a decline in herd immunity and a change to the epidemiology of the illness, with increases in the mean age of occurrence of illness attributed to acute HAV infection in Western societies. Although this phenomenon may lay a framework for potential epidemics in the future, public health policies and newly implemented immunization practices are likely to reduce this potential.

Most patients have no defined risk factors for hepatitis A. Risk factors for the acquisition of hepatitis A include the following:

• Personal contacts
• Institutionalization
• Occupation (eg, daycare)
• Foreign travel
• Male homosexuality
• Illicit parenteral drug use
  
  

  HAV is a single-stranded, positive-sense, linear RNA enterovirus of the Picornaviridae family. In humans, viral replication depends on hepatocyte uptake and synthesis, and assembly occurs exclusively in liver cells. Acquisition results almost exclusively from ingestion (eg, fecal-oral transmission), although isolated cases of parenteral transmission have been reported.

  HAV is an icosahedral nonenveloped virus measuring approximately 28 nm in diameter (see the image below). Its resilience is demonstrated by its resistance to denaturation by ether, acid (pH 3.0), drying, and temperatures as high as 56°C and as low as -20°C. The hepatitis A virus can remain viable for many years. Boiling water is an effective means of destroying it, and chlorine and iodine are similarly effective.