[Show abstract][Hide abstract] ABSTRACT:
Since its discovery, human parvovirus B19 has been linked with a broad spectrum of clinical syndromes. An aetiological role for the virus has been confirmed in erythema infectiosum, transient aplastic crisis, persistent infection manifesting as pure red cell aplasia in immunocompromised persons, non-immune hydrops fetalis and arthritis. Less commonly recognised, but receiving increasing attention recently, are the neurological manifestations, a variety of which have been described in patients with either clinically diagnosed or laboratory confirmed B19 infection. The purpose of this review is to summarise present knowledge of B19, its known and potential pathogenic mechanisms and its association with human diseases, particularly those with neurological manifestations. The outcome of the review supports an aetiological role of the virus in neurological disease. However, the pathogenesis remains unknown and elucidating this is a priority. INTRODUCTION Human parvovirus B19 (B19), the first known par-vovirus to infect humans, was discovered during evaluation of serum hepatitis B surface antigen tests using a panel of sera . The first association between B19 infection and a clinical syndrome was with hypoplastic crisis in children with sickle-cell anaemia . Two years later, development of a new serological method for detecting specific anti-B19 IgM antibodies proved the causative role of the virus in erythema infectiosum, a com-mon childhood disease . B19 has also been shown to cause persistent infection manifesting as pure red cell aplasia in immunocompromised persons , non-immune hydrops fetalis [5,6] and arthritis [7,8]. In subsequent years, studies of B19 in humans determined the aetiological rela-tionship of B19 infection with a broad spectrum of diseases. Recent improvements regarding the development of immunological and molecular techniques provided new insight into the virology, pathogenesis and various clinical manifestation of B19 infection.
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