SUMMARY Evidence of recent infection with human parvovirus B19 (HPV) was found in two patients with early rheumatoid arthritis (RA) and in four patients with acute inflammatory arthritis (IA). Both of the patients with RA but only one of the four patients with IA carried RA associated haplotypes. No evidence of persistent infection with HPV was found, but evidence of past infection with HPV was significantly more common in patients with RA than in controls. The results confirm the arthritogenic potential of HPV and are consistent with the hypothesis that rheumatoid arthritis may develop in a genetically predisposed patient after an arthritogenic insult such as an HPV infection.

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Associations were sought between major histocompatibility complex (MHC) genes on chromosome 6 and the complement component C3 and immunoglobulin genes located on other chromosomes which might contribute to susceptibility to mild inflammatory arthritis (IA) or definite rheumatoid arthritis (RA). Frequencies of the complement C3F allele were raised in patients with IA but were normal in patients with RA and controls. When associations between C3F and MHC genes were sought frequencies of some MHC genes were greater in patients with C3F than in those without-for example, HLA-B8 and DR3 in patients with RA and DR2 in patients with IA. Conversely, DR4 frequency was lower in patients with IA with C3F than in those without. Thus the C3F allele may act independently or exert an epistatic effect on MHC genes to increase susceptibility or protect against disease.The frequency ofthe immunoglobulin heavy chain aliotype Glm(2) on chromosome 14 was increased in patients with RA but only in those with the phenotype Gml,2,3,17;21,5; no significant associations were found between MHC genes and Gm phenotypes. Further, no associations of MHC, C3F, and immunoglobulin genes were shared by patients with RA and those with UA, indicating a different genetic basis for the two clinical entities.In this paper we have compared the frequencies of C3 and Gm alleles in patients with RA and IA and sought interactions of these alleles with the MHC genes associated with RA. Our aim was to discover if other genes as well as those in the MHC might (a) predispose to RA, (b) predispose to mild inflammatory arthritis, or (c) protect patients with IA from developing definite RA. In patients with RA we found some associations between the C3F allele of the complement component C3 and MHC genes; an association was also found between RA and the Gm allotype Glm(2). The C3F allele may also be relevant in patients with IA, particularly when associated with HLA-B62, DR4, or DR2. Patients and methods PATIENTSThe 61 patients with RA who were typed for MHC antigens, complement component C3, and Gm allotypes are described in the accompanying paper.' Thirty five additional patients with definite or classical RA23 were included in the study on Gm allotype frequencies; no MHC or complement allotypes were determined in these patients.Similarly, 49 patients with IA typed for MHC, C3, and Gm allotypes, are also described in the accompanying paper.' Fifty six additional patients with IA were Gm allotyped; three of these were also typed for MHC and C3 allotypes.

arthritis (RA) were tested for RF specificity towards these IgG monoclonal anti-D antibodies the incidence and titre of reactivity towards an IgG3 monoclonal anti-D antibody was considerably greater than for a polyclonal anti-D antibody of the same Gm allotype, G3m(5). This difference was not explained by the amount of each anti-D antibody which bound to erythrocytes. Furthermore, when patients with RA were divided into groups according to their Gm phenotype, sera from a greater proportion of patients negative for the phenotype G3m(5) reacted to the G3m(5) monoclonal anti-D antibodies than sera from those patients positive for this allotype. Analysis of RF reactivities towards two IgG3 and three IgGl monoclonal anti-D antibodies, each with different Gm allotypic epitopes, indicated, however, that individual serum samples contained RFs with a spectrum of specificities; some sera appeared to react to a single set of Gm alleles, whereas others also reacted to isotypic or iso-allotypic epitopes, or both. Our data suggest that RFs with specificity for Gm allotypes do not arise in patients who carry that particular allotype owing to tolerance induced in fetal-neonatal life. Conversely, RFs with apparent specificity for a Gm allotype formed in patients negative for that allotype may be reacting to a closely related but different epitope. Final proof requires precise specificities for each RF formed, and IgG3 monoclonal anti-D antibodies would be useful reagents for this purpose.

LETTERSshould be limited to those tumors that most frequently occur with DM, and should only be extended in case of abnormal signs and symptoms (1,2,4,5). In our patient, radiographic examination of the knees was performed because of a low-grade arthritis which occurred during Legionella pneumophila pneumonia. Arthritis in the course of DM is rare (3), and the chondrosarcoma of the tibia was an unexpected finding revealed only by accident. In studies of large series of patients with DM and malignancies, sarcoma was described in only a few patients and did not include chondrosarcoma (2,4). To our knowledge, this is the first report of a chondrosarcoma in connection with DM.The relapse of DM after tumor removal, of course, might have been related to incomplete tumor therapy, but this seems unlikely since no signs of tumor metastasis have been found. This might be an example of the unpredictable, rather autonomous course of DM, after successful tumor therapy, which has been observed by others (4).