Type c viruses and systemic lupus erythematosus

✍ Scribed by Joseph A. Markenson; Paul E. Phillips

• Publisher: John Wiley and Sons
• Year: 1978
• Tongue: English
• Weight: 446 KB
• Volume: 21
• Category: Article
• ISSN: 0004-3591
• DOI: 10.1002/art.1780210217

✦ Synopsis

The hypothesis that microbes might cause the connective tissue diseases arose from a lack of other clearly definable host or environmental causes (1). The complexity of microbial-host relationships now makes it even more difficult to define "prime causes" in these diseases. Nevertheless the general hypothesis is still attractive. Initially, host factors, probably genetic, determine abnormal control of a microbial infection. They allow its persistence at least for a time, its replication with more foreign antigen production, and/or generation of altered self antigens. Then a probably abnormal host immune response to these antigens, circulating and/or in the tissues. results in inflammation in the target organs characteristic for the particular connective tissue disease. Except for vasculitis with hepatitis B virus infection, this hypothesis is based principally on animal models of immunologically mediated chronic disease caused by microbial infection (2). The most applicable model for systemic lupus erythematosus (SLE) is New Zealand (NZ) mouse disease, where an endogenous xe-From the