Failure to demonstrate (cross-reacting) antibodies to human T lymphotropic viruses in patients with rheumatic diseases
✍ Scribed by J. Steven McDougal; M. Susan Kennedy; V. S. Kalyanaraman; Frederic C. McDuffie
- Publisher
- John Wiley and Sons
- Year
- 1985
- Tongue
- English
- Weight
- 485 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0004-3591
No coin nor oath required. For personal study only.
✦ Synopsis
Largely through work published over the past 4 years by Gallo and coworkers, a family of retroviruses, termed human T lymphotropic viruses (HTLV), has been isolated and characterized, and their infectivity and pathogenic potential for humans has been established (1-8). There is now convincing evidence based on isolation and seroepidemiologic studies that HTLV-I causes an adult form of human T cell leukemia (ATL) and that HTLV-111, also known as lymphadenopathy-associated virus (LAV), causes the acquired immunodeficiency syndrome (AIDS) (2-4,6,8). HTLV-I1 was isolated from a patient with hematologic dyscrasia but has not been convincingly linked to any human disease (I).
Although these viruses replicate differently in human cells, and thus, differ in their transforming (HTLV-I and HTLV-11) versus cytopathic (HTLV-IIII LAV) properties, the HTLV family shares many properties, including T cell tropism, similar reverse transcriptases, major structural proteins of similar size, some nucleic acid homologies, and cross-reactive antigens (2-10). Because of the latter feature, one can predict that a person inoculated or infected with one HTLV may mount an antibody response which, in part, reacts with the others.
Branch, 1-1202, Centers for Disease Control,