Clinical note
Acute parvovirus B19 infection in connection with a flare of systemic lupus erythematodes in a female patient

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Abstract

Background: Since its discovery parvovirus B19-infections could be linked to a growing variety of diseases. Besides the harmless exanthema erythema infectiosum perferentially observed with B19-infections in childhood a panel of rather serious and also chronic courses that may be associated with anemia, thrombocytopenia, arthritis and others have been described. Objective: In a 26-year-old female patient an acute parvovirus B19-infection was followed by a serious episode of systemic lupus erythematosus (SLE). Here we demonstrate the clinical and serological parameters which were observed in the patient during that episode in addition to the nucleotide sequence of the virus isolate. Results and conclusion: In this patient parvovirus B19 was not the initial causative agent for SLE. However the B19 infection was followed by a severe flare of SLE and therefore may be considered as an enhancer of the autoimmune disease. The amount of nucleotide variability observed in the viral genome was in the range known from other B19 isolates. An elevated degree of mutations in antigenic domains was not detectable. Therefore, we would like to emphasize the possible role of parvovirus B19 in the aetiology or the enhancement of autoimmune diseases like SLE and the necessity of an according differential diagnosis.

Introduction

Since its discovery in 1975 parvovirus B19 (Cossart et al., 1975) could be linked to an increasing variety of human diseases. The most common manifestations are erythema infectiosum in children, aplastic anemia in patients with underlying hemolytic anemias, hydrops fetalis in pregnant women, acute or chronic arthritis and also a series of rather rare complications like liver dysfunction, meningitis and others (Anderson and Young, 1997). Neutralizing antibodies against the capsid proteins VP1 and VP2 generally lead to the clearance of the virus. Persistent B-19 infections, however, are known to be established both in immunocompromised (Flunker et al., 1998) and in immunocompetent individuals (Cassinotti et al., 1993). The prolonged presence of the virus is frequently accompanied by the occurrence of IgG-antibodies against the viral nonstructural protein NS1 (von Poblotzki et al., 1995a, von Poblotzki et al., 1995b). Particularly interesting is the fact that B19 infections are frequently accompanied by the development of autoantibodies. Recent reports have shown that the induction of autoimmune reactions may be a common side effect during B19 infections, but generally autoantibody titers are rapidly decreasing after virus elimination from the organism (Kerr and Boyd, 1996). Elevated values of rheuma factors as well as antiphospholipid, antinuclear and antilymphocyte antibodies have been reported to be induced (Sasaki et al., 1989, Soloninka et al., 1989, Vigeant et al., 1994, Kerr and Boyd, 1996). In some cases, however, the autoimmune response may persist and may be associated with the development of rheumatic manifestations (Vigeant et al., 1994). The involvement of parvovirus B19 infections in arthritis, vasculitis, polymyalgia rheumatica and SLE have been described (Nesher et al., 1995, Anderson and Young, 1997, Cimmino, 1997, Nigro et al., 1997). Here we report the case of a 26-year-old, female patient suffering from SLE for a period of 3 years, who presented with a strong onset of a typical SLE flare that was associated with an acute parvovirus B19 infection.

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Materials and methods

IgG and IgM antibodies against the capsid proteins VP1 and VP2 and nonstructural protein NS1 of parvovirus B19 were detected using the RecomBlot Parvovirus B19 IgG/IgM Western Blot system (Mikrogen, Munich, Germany) according to the manufacturer’s protocol.

Nested-PCR for the detection of parvovirus B19 DNA in serum and sequencing of the virus isolate was performed as described previously (Hemauer et al., 1996). The sequence of the parvovirus B19 isolate obtained from the SLE patient was

Results and discussion

A 26-year-old, female patient suffering from SLE for a period of 3 years with antiphospholipid-antibody syndrome and autoimmune hemolytic anemia, presented with a strong onset of a typical SLE flare in May 1997 correlated with fever, muscle and joint pain, nausea and vomiting. These symptoms were similar to previous episodes of SLE, which were characterized by anemia, thrombocytopenia, polyarthralgias and fever. Until may 1997 she did not show any serological parameters indicating the status of

Acknowledgements

This work was supported by the Deutsche Forschungsgemeinschaft DFG (grant Mo620/5-1). Andrea Hemauer has been supported by the Studienstiftung des Deutschen Volkes. The authors thank PD Dr Rainer Straub and PD Dr Thilo Andus for helpful discussion and Dr M. Motz (Mikrogen GmbH, Munich, FRG) for the generous donation of Recomblots.

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    Present address: Rheumaklinik Baden-Baden, Rotenbachtalstr. 5, D-76530 Baden-Baden, Germany.

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