Parvoviruses are the smallest of the DNA viruses. They are nonenveloped and icosahedral, with single-stranded, linear DNA. A human parvovirus, B19, has been isolated and identified as the cause of transient aplastic crisis in patients with sickle cell disease and implicated in adult acute polyarthritis. This virus is also the cause of the common childhood disease erythema infectiosum and is associated with fetal death in pregnant women experiencing a primary infection. The parvovirus family is divided into two genera, based on whether their ability to replicate requires coinfection with a helper DNA virus, or if they are capable of independent replication (“autonomous parvoviruses”). Members of the first group are referred to as adenoassociated viruses (AAVs), because they are usually found in infected cells in combination with a helper adenovirus.

A. Epidemiology and pathogenesis

 Transmission of parvoviruses is by the respiratory route. A high titered viremia lasting a few days follows about 1 week after infection, during which time virus is also present in throat secretions. A specific antibody response occurs rapidly, resulting in suppression of the viremia. Replication of parvoviruses requires a host cell in which DNA synthesis is in progress. Therefore, damage is limited primarily to specific tissues that are mitotically active. [Note: In the case of B19 virus, these are primarily tissues of erythroid origin.] Because of the single-stranded nature of the genome, conversion to a double stranded DNA molecule by a cellular DNA polymerase must occur before production of additional single-stranded viral DNA genomes or viral mRNA transcription can begin. Despite the limited amount of genetic material, two or three capsid proteins and two nonstructural regulatory proteins are produced by a combination of alternative RNA splicing patterns and posttranslational processing. The parvovirus life cycle is summarized in Figure 1.

                     Figure 1- Replication of B19 parvovirus. 

B. Clinical significance

The single human pathogen in this family is the autonomous parvovirus, B19. The spectrum of illnesses caused by this virus is related to its unique tropism for cycling erythroid progenitor cells. Although B19 was initially isolated from sickle cell disease patients undergoing a transient aplastic crisis, it has since been recognized that chronic, progressive bone marrow suppression results from B19 infection of immunocompromised patients unable to mount an immune response capable of eliminating the virus.

1. Erythema infectiosum: The observation that 30 to 60 percent of some human populations have antibodies to B19 led eventually to the identification of this virus as the causative agent of the common childhood rash, erythema infectiosum (“fifth disease”) as shown in Figure 2. The characteristic rash (“slapped cheek” appearance) occurs about 2 weeks after initial exposure, when the virus is no longer detectable. The rash is apparently immune-system mediated. Another complication accompanying B19 infection is an acute arthritis that usually involves joints symmetrically. This is consider ably more frequent in adults than in children and usually resolves within several weeks.

Figure 2 : Typical “slapped cheek” appearance of a child infected with parvovirus B19 (“fifth disease”).

2. Birth defects: Spontaneous abortion rate is elevated in women having a primary infection during the first trimester, and primary infection  during the second or third trimester is associated with some instances of hydrops fetalis.

 C. Laboratory identification

Laboratory identification of B19 infection is not routinely done. The large amount of virus present during the viremic (usually asymptomatic) phase permits detection of viral proteins by immunologic methods or of viral DNA by various amplification techniques. Retrospective diagnosis can be made by any of the usual procedures used to demonstrate a specific antibody response.

 D. Treatment and prevention

No antiviral agent or vaccine is available for treating human B19 infections. Isolation of patients with signs of parvovirus disease is not a useful approach to control because subclinical infections occur, and infected individuals shed virus before symptoms appear. Intraveneously administered immunoglobulin G specific for B19 virus may be helpful in immunocompromised patients with chronic infections