LACK OF EVIDENCE FOR HUMAN T-CELL LYMPHOTROPHIC VIRUS TYPE-I OR TYPE-II INFECTION IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS OR RHEUMATOID-ARTHRITIS
Rt. Bailer et al., LACK OF EVIDENCE FOR HUMAN T-CELL LYMPHOTROPHIC VIRUS TYPE-I OR TYPE-II INFECTION IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS OR RHEUMATOID-ARTHRITIS, Journal of rheumatology, 21(12), 1994, pp. 2217-2224
Objective. Human retroviruses including human immunodeficiency virus (
HIV) and human T cell lymphotrophic virus Types I and II (HTLV-I/II) h
ave been associated with forms of connective tissue autoimmune disease
s including systemic lupus erythematosus(SLE) and rheumatoid arthritis
(RA). We looked for evidence of HTLV-I/II infection in a large popula
tion of SLE, RA, and control patients. Methods. One hundred fifteen pa
tients with connective tissue autoimmune disease and other rheumatolog
ical disorders were screened far antibodies to HTLV-I/II by Western im
munoblots (WIB). Due to the transforming characteristic of these retro
viruses, the patients' peripheral blood mononuclear cells (PBMNC) were
cultured in attempts to establish continuous cell lines. Furthermore,
PBMNC culture supernatants were analyzed for reverse transcriptase ac
tivity and/or HTLV-I/II gag antigen production. The presence of HTLV-I
/II proviral sequences in short term culture and fresh PBMNC was deter
mined by Southern blot analysis and polymerase chain reaction (PCR), r
espectively. Results. All 115 patients were HTLV-I/II and HIV seronega
tive. Seventy-four attempts to establish PBMNC cell lines from 65 pati
ents were unsuccessful with a mean culture survival time of 3.6 (+/- 1
.4) months. Reverse transcriptase activity and HTLV-I/II gag antigen p
roduction were not detected in 51 and 16 culture supernatants tested,
respectively. Cells from Il patients tested by Southern blot analysis
and from 57 patients tested by PCR were negative for HTLV-I/II related
sequences. Conclusion. Our results failed to establish an association
between human retroviruses (HTLV-I/II and HIV) and SLE, RA, or other
rheumatological disorders. However, these results do not rule out othe
r exogenous or endogenous retroviruses that may play a role in the ini
tiation and/or promotion of these diseases.