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Overview of hepatitis A virus infection in children

Rubén E Quirós-Tejeira, MD
Section Editors
Morven S Edwards, MD
Elizabeth B Rand, MD
Deputy Editor
Alison G Hoppin, MD


Although the reported cases of hepatitis A virus (HAV) infection have decreased over the past decade, HAV infection is still a frequently reported disease in the United States [1]. HAV is a 27 nm single-stranded, icosahedral, nonenveloped RNA virus that belongs to the Heparnavirus genus of the Picornaviridae. Four well-defined genotypes of HAV have been described in humans, yet they belong to a single serotype [2]. The virus is stable at low pH and moderate temperature, but it is inactivated by high temperature, chlorine, and formalin. These characteristics are relevant for preventive measures.


Hepatitis A virus (HAV) infection occurs worldwide (figure 1). Although it remains one of the most commonly reported vaccine-preventable diseases in the United States and among American travelers [1,3], the incidence in the United States has declined substantially since vaccination was recommended for persons at increased risk (in 1996), for children living in states with the highest incidence of HAV (in 1999), and for all children (in 2006) [4]. The incidence of acute HAV infection in the United States has declined from 12 cases per 100,000 in 1995 to about 0.4 case per 100,000 in 2011 [5,6]. Declines were greatest in states in which routine vaccination of children for HAV was initiated in 1999. In 2013, a total of 1781 cases of hepatitis A were reported in the United States to CDC (0.6 cases per 100,000), a 14 percent increase from 2012, indicating that hepatitis A infection is still an important issue in the United States. This increase is believed to be due to a large hepatitis A outbreak from imported pomegranate arils consumed by people in several southwestern states and Hawaii [1,7]. (See "Hepatitis A virus infection in adults: An overview", section on 'Epidemiology'.)

A similar decline in the incidence of HAV infection was seen in Israel following a universal immunization program for toddlers that was initiated in 1999 [8-10]. The incidence declined from 50.4 cases per 100,000 in 1993 to 1998 to 2.2 to 2.5 cases per 100,000 in 2002 to 2004, and outbreaks in school and day care settings were essentially eliminated.

To what extent the observed reductions in the incidence of HAV infection in these reports can be attributed to improved environmental and hygienic conditions or variation in the epidemic cycle is difficult to evaluate [11]. Nonetheless, the above reports highlight the potential for "herd protection" through the immunization of toddlers or children [4,8,10].

HAV is spread via the fecal-oral route. The majority of patients who acquire the illness have had personal contact with an infected person. In the childcare setting, spread of HAV usually takes place before the index case has been recognized. Outbreaks are usually recognized only after childcare staff members develop symptoms, such as jaundice, since most of the children are asymptomatic or have nonspecific symptoms [3,12]. The potential for broad exposure is compounded in childcare centers that include children who have not yet been toilet-trained [13]. (See 'Clinical manifestations' below.)


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Literature review current through: Sep 2016. | This topic last updated: Mar 31, 2016.
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