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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Absence of human T-lymphotrophic virus type I in patients with systemic lupus erythematosus.

The role of the human T-cell lymphotropic/leukaemia virus type I (HTLV-I) in the pathogenesis of autoimmune diseases of unknown cause, such as systemic lupus erythematosus ( SLE), multiple sclerosis ( MS) or Sjögren's syndrome (SS) has been discussed extensively. We have investigated whether SLE is in any way associated with exogenous HTLV-I. Using enzyme immunoassay (EIA), we found no seroreactivity against HTLV-I antigens in any of 24 SLE patients under investigation. Using a radioimmunoprecipitation assay (RIPA), there was also no expression of retroviral tax-protein demonstrable in 24 individuals with SLE. DNA preparations of peripheral blood cells, as well as isolated CD4- and CD8-positive cells, were examined for HTLV-I sequences ( pol-, env-, gag-, LTR- and tax-region) using polymerase chain reaction (PCR). We were unable to demonstrate any specific HTLV-I PCR products in SLE specimens. Our data suggest that exogenous HTLV-I is not involved in the pathogenesis of SLE. Systemic lupus erythematosus ( SLE) is a multisystem disease of unknown cause characterized by B-cell hyperactivity with hypergammaglobulinaemia and the formation of pathogenic autoantibodies. Patients may also show altered suppressor/helper T-cell ratios. Abnormalities in T-cell function include T-cell lymphopenia, expression of activation antigens and alteration of responses to mitogens and lymphokines. Human retroviruses are known to cause immune aberrations, such as diminished T-cell function and polyclonal B-cell stimulation, which are observed in patients with leukaemias, lymphomas and the acquired immunodeficiency syndrome (AIDS). Human T-cell lymphotropic/leukaemia (HTLV-I) is aetiologically linked with adult virus type I T-cell leukaemia (ATL) and tropical spastic paraparesis. A common feature of the HTLV family is an LTR encoded protein (tax protein, p40tax) which triggers viral protein production in the early stages of a retroviral infection. Detection of p40tax may indicate transcriptional activity of a provirus. Several investigators have examined the possible involvement of HTLV-I in SLE and have produced conflicting results, especially so far as seroreactivity against HTLV-I antigens is concerned. The discovery of HTLV-I like particles in murine lupus might also indicate an important role of exogenous viruses in SLE. Olsen and colleagues describe a high seropositivity to anti-HTLV-I- and anti-HTLV-III antibodies and evidence of viral replication in patients with SLE. Lin et al. also demonstrated anti-HTLV-I antibodies in SLE patients. However, other authors failed to detect anti-HTLV-I antibodies, proviral structures or viral transcripts in SLE. We investigated whether or not there are any indications of the presence of the exogenous retrovirus, HTLV-I, in patients with SLE, at immunological and genetic levels. We found neither immunological nor molecular biological evidence for the existence of HTLV-I in SLE patients. There were some weak suggestions of the presence of possibly endogenous retroviral sequences.[1]


  1. Absence of human T-lymphotrophic virus type I in patients with systemic lupus erythematosus. Lipka, K., Tebbe, B., Finckh, U., Rolfs, A. Clin. Exp. Dermatol. (1996) [Pubmed]
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