| Literature DB >> 9855214 |
A Mizokami1, K Eguchi, R Moriuchi, Y Futsuki, K Terada, H Nakamura, T Miyamoto, S Katamine.
Abstract
To evaluate the hypothesis, proposed in previous reports from HTLV-I non-endemic areas, that HTLV-I is involved in a significant proportion, about a quarter, of Sjögren's syndrome patients who lack serum antibodies to the virus, we examined for the presence or absence of HTLV-I in DNA samples isolated from salivary gland tissues of 17 seronegative as well as 7 seropositive patients with Sjögren's syndrome in Nagasaki, Japan, where the virus is highly endemic. The nested two-step polymerase chain reaction (PCR), with a sensitivity capable of detecting a single DNA molecule, failed to amplify the HTLV-I tax sequence from DNA of 14 of the 17 seronegative patients. The tax was only amplifiable from the tissue DNA of the remaining three seronegative patients. The detection rate, 3/17 (18%), was, unexpectedly, less than those previously reported from the HTLV-I non-endemic areas. Moreover, in contrast to high viral loads (10(-1) to 10(-3) per cell) in the salivary gland of the seropositive patients, a semiquantitative PCR revealed that the copy number of the HTLV-I tax in the gland tissue of these seronegative patients was very low, 10(-5) per cell. This level is unlikely to be sufficient to promote an inflammatory reaction in the tissue. Our findings might argue against the involvement of "prototype" HTLV-I in the pathogenesis of Sjögren's syndrome in seronegative patients.Entities:
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Year: 1998 PMID: 9855214 DOI: 10.1080/030097498442262
Source DB: PubMed Journal: Scand J Rheumatol ISSN: 0300-9742 Impact factor: 3.641