Shortly after the reeognition of the aequired immunodefieieney syndrome
(AIDS) in 1981 (1-3), it was hypothesized that herpesviruses may play an
important role in the etiology or pathogenesis of this newly identified
syndrome (4,5). This theory was based on the faet that infeetion with
herpesviruses was a prominent elinieal feature in nearly all patients
with AIDS (3-5). Chronie mueocutaneous herpes simplex virus (HSV)
infections were one of the first opportunistie infeetions deseribed in
patients with AIDS (3), and both cytomegalovirus (CMV) and HSV
infections were extremely common in individuals identified to be at
highest risk for aequiring AIDS, such as homosexual men, intravenous
drug users and hemophiliaes (4-8). CMVand Epstein-Barr virus (EBV) were
also prominent infeetions whieh were suspected as possible etiologic
agents of the prolonged fever, wasting, and Iymphadenopathy that often
precedes AIDS, frequently referred to as the chronie Iymphadenopathy
syndrome (9,10). Subsequent elinieal studies have indeed demonstrated
that infeetions with HSV, CMV, EBV, and even varieella- zoster virus
(VZV) are frequent opportunistic infeetions wh ich oeeur among AIDS
patients (11-14). Several of the opportunistie infeetions caused by
herpesviruses include encephalitis, chorioretinitis, hairy leukoplakia,
esophagitis, enteritis, colitis, Burkitt's lymphoma, primary CNS
lymphoma, zoster, and there has even been speculation about the role of
CMV in the pathogenesis of Kaposi's sareoma (15,16). Furthermore, the
herpesviruses, partieularly CMV and EBV have been known to be strongly
associated with immunosuppression, partieularly of cell-mediated immune
functions, which further supported the hypothesis that herpesviruses may
contribute to the immune defects that eharacterize AIDS.
