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• W2078412130 abstract "To the Editor: In a recent paper,1 Friedrichs and colleagues published evidence for the role of measles virus (MV) in Paget's disease of bone (PDB). This follows earlier reports2-5 in which the same group showed the presence of measles virus RNA in osteoclast precursors cells in bone marrow aspirates and in the peripheral blood mononuclear cell (PBMC) fraction. Other groups have used similar techniques to show the presence the presence of canine distemper virus (CDV) in osteoclasts and osteoblasts from patients with PDB.6 However, the role of paramyxoviruses in PDB remains controversial because several investigators have been unable to identify MV or CDV transcripts in Pagetic tissue or peripheral blood using a variety of approaches including nested reverse-transcription polymerase chain reaction (RT-PCR)7-10. The story of paramyxovirus involvement in PDB has been rumbling on for almost 30 years now ever since electron microscopy of affected bone showed the presence of tubular structures in osteoclasts that superficially resemble paracrystalline arrays of paramyxovirus nucleocapsids.11 These structures have not been formally identified as viral and their nature has been questioned because of the fact that they also appear in osteoclasts of osteosarcoma patients; in macrophages from patients with oxalosis,12 and in the condition familial expansile osteolysis that resembles Paget's but is caused by an activating mutation in the RANK gene.13 The presence of MV transcripts in osteoclasts has also been reported in the stapes bone of patients with otosclerosis,14 but other groups were not able to confirm this finding.15 In all articles published by the Roodman group1-5 viral sequences were found that clearly belonged to the Edmonston (clade A) genotype of measles virus, only varying by at most two nucleotides in the areas of the N gene of MV that were amplified and sequenced. It is clearly possible that some U.S. patients of the right age group would have been exposed to a virus of clade A, which was first isolated in 1954 from David Edmonston in the United States. However, it is of concern that the sequences so far reported in by this group are all of the same genotype, rather than any of the other 21 known MV genotypes.16 This might be plausible if the patients studied had been from the same locality and were exposed to the same virus at the same time, but this seems highly unlikely considering that tissue samples from many of the patients studied have come from collaborators in New Zealand.1, 5 Five of the reported “mutations” between the patient derived sequences and those of the Edmonston strain are nothing more than corrections of the original MV N gene sequence (Fig. 1). Moreover, in the earlier articles and in this article, the MV sequences reported have mutations in the N gene that would almost certainly affect the functionality of the virus N protein because they involved residues that are strictly conserved. Thus, the G26 and R413 residues reportedly mutated to G26E and R413S are conserved in all morbillivirus and all MV strains, even those isolated from cases of SSPE, the prototypical slow virus infection associated with MV.16 Residues K435 and L473 (reportedly mutated to K435R and L473P) are similarly conserved in all MV strains including those isolated from cases of SSPE.16 Mutations E453G, L467P, and Q486K have been observed in some genotypes of MV but other mutations characteristic of the genotype in question are absent in the Edmonston-like P1-P4 sequences.16 The amino acid sequences of the nucleocapsid proteins of a number of MV strains were aligned. The strains are: Edwt, Edmonston strain (acc. nr: AF266288); Schw, Schwarz vaccine strain (acc. nr: AF266291); X01999, Rozenblatt sequence (17); P1 & P2–4, sequences from Friedrichs paper. Identical residues in the alignment are indicated by a hyphen. Cons: represents a consensus sequence of the morbilliviruses where an asterisk (*) indicates strict conservation; a horizontal line (-) indicates that only conservative changes have been recorded within residue groups: G-P (helix breaking); A-I-L-V-M (small aliphatic); K-R (positive charge); D-E-N-Q (negative charge); H-F-Y (large aliphatic); or T-S (hydroxylated). The most recent article1 shows data on 4 patients, 3 of whom were from the United States and 1 from New Zealand. The RNA was extracted from bone marrow mononuclear cells and RT-PCR was done with primers that would amplify the N gene of the MV. Apart from the fact that no controls were shown in which the reverse-transcriptase step was omitted, to test for contamination with plasmid DNA, the main criticism of the data is that the sequence from patient P1 shows apparent homology with a sequence of MV in the database (accession no. X01999) that is now recognized to be incorrect. This sequence of the Edmonston vaccine strain, which was originally reported by Rozenblatt and colleagues in 1985,17 is now known to contain a sequencing error at position 1598 in the genome, which results in a frame shift causing the protein sequence downstream of this to diverge from the true MV nucleocapsid sequence (Fig. 1). In conclusion, the sequences so far found by the Roodman group are very close to those of the Edmonston strain of virus and the variation that one might expect based on the fact that existence of very specific long-lived genotypes of MV is absent from the study results. Contamination may have given rise to these findings. Second, 1 patient (P1) has been reported to harbor a variety of MVs with homology to a sequence that contains an error and is not thought to exist. We do not consider that the evidence provided here confirms or enhances the validity of the hypothesis that the MV virus is involved in PDB." @default.
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• W2078412130 date "2002-12-01" @default.
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• W2078412130 title "The Pro and Con of Measles Virus in Paget's Disease: Con" @default.
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• W2078412130 doi "https://doi.org/10.1359/jbmr.2002.17.12.2290" @default.
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