HIV disease and AIDS, increased in cells transformed by HTLV-I. The subsequent identification of persons in endemic areas, many with AIDS, who were infected with both HIV and HTLV-I (Cortes et al., 1989; Hattori et al., 1989) led to the speculation that interaction of these two viruses may potentiate disease progression. The prevalence of infection with both HIV and HTLV-I or HTLV-II is increasing in populations of intravenous drug abusers in the United States (Lee et al., 1991). This increase offers the possibility of a study group, albeit an unwanted one, in which to assess this additional risk for disease.
HTLV-I has also been implicated as a factor in other disease syndromes, including polymyositis, arthritis, infective dermatitis, mycosis fungoides, and multiple sclerosis (although the latter is controversial). In addition, HTLV-II was recently linked to chronic fatigue syndrome (DeFreitas et al., 1991). It is probable that the full spectrum of diseases and immunological abnormalities associated with the human retroviruses has yet to be delineated. It is also probable that additional human retroviruses exist but have not yet been discovered.
Atherosclerosis, commonly known as hardening of the arteries, is the result of an uncontrolled proliferation of arterial smooth muscle cells, which eventually can block the flow of blood through the vessel. This disease is the underlying cause of strokes and myocardial infarctions and results in more deaths in the United States (and in other industrialized countries) than any other single disease. The burden on the U.S. health care system is estimated to be in excess of $60 billion per year (Levi and Moskovitz, 1982; Kannel et al., 1984).
Although it is well known that smoking, high cholesterol levels, and elevated blood pressure are major risk factors for atherosclerosis, viruses can generate the pathologic events—cell destruction, metabolic changes within cells, and cell transformation—that precede the appearance of atherosclerotic lesions. This observation has led some researchers to conclude that a virus or viruses may play some role in the disease. Supporting this theory are reports that chickens can develop atherosclerotic lesions as a result of infection with an avian herpesvirus (Fabricant et al., 1978, 1980; Minick et al., 1979). In humans, two similar viruses, herpes simplex virus (HSV-1 and HSV-2) and cytomegalovirus (CMV), infect infants and young children worldwide. During infection, the viruses are often found in the blood vessels, potentially exposing the smooth muscle cells to their effects. In one recent study, CMV infection was demonstrated in patients with atherosclerosis; there was no evidence of either HSV-1 or HSV-2 infection in the same individuals (Melnick et al., 1990). Other studies have implicated