Page 102 - AIDSBK23C

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HERPESVIRUS INFECTIONS

The human herpesviruses, including herpes simplex virus (HSV), varicella zoster virus
(VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpes virus 6 (HHV-6)
may appear in the course of HIV infection and produce a variety of clinically significant
manifestations either as self-limited or non-resolving opportunistic infections.[457]
Cytomegalovirus produces the greatest morbidity as well as resultant mortality and has been
discussed separately above. Epstein-Barr virus plays a role in development of both oral hairy
leukoplakia and malignant lymphomas in AIDS.[458] HHV-6 has been found to replicate in a
variety of cell types, including CD4+ lymphocytes, and has been implicated as a cause for
roseola, HHV-6 may act as a cofactor in the acceleration of HIV infection to AIDS in patients
who are infected with both viruses. However, evidence of any pathogenic role of HHV-6 in
enhancing the progression to AIDS has been indefinite. The association of HHV-7 with human
disease has not been recognized.[459]
Herpes simplex types 1 and 2 are sexually transmissible agents of importance in patients
both with and without HIV infection. Recurrent mucocutaneous herpes simplex virus infections
of more than one month’s duration satisfy definitional criteria for diagnosis of AIDS in patients
proven to have HIV infection.[392] Clinically, the recurrent herpetic lesions of AIDS patients
are more of a chronic nuisance than a life-threatening condition. Ulcerated or excoriated lesions
may subsequently become secondarily infected. However, coinfection with HSV-2 has been
associated with an increased HIV viral load and more rapid disease progression.[460]
Both HSV types 1 (HSV-1) and 2 (HSV-2) primarily infect skin and mucus membranes
to produce inflammation, often vesicular, progressing to sharply demarcated ulcerations. Herpes
simplex type 1 involves predominantly the oral cavity while HSV-2 more often involves the
genital region. However, either body region may be infected by either subtype to produce
clinically and histologically indistinguishable disease.[461]
Varicella zoster virus (VZV) infections typically begin as childhood chickenpox, and the
virus becomes latent in dorsal root ganglia. VZV may reactivate years later in adults who are
immunocompromised, including those with AIDS. However, children with HIV infection are
also at risk for VZV infection. The classic presentation in reactivation is “shingles” with painful
skin vesicles appearing in a dermatomal distribution, most commonly thoracic, lumbar, or
cervical. The vesicles may develop into blisters within 2 weeks to a month. VZV is not a
disseminated disease involving multiple organ systems and does not cause death, but is a
debilitating nuisance for persons who have it. Skin dissemination can occur in the form of
multiple dermatomal distributions. Persons who have VZV involvement of the ophthalmic
division of the trigeminal nerve may also have ocular involvement in the form of acute retinal
necrosis, progressive outer retinal necrosis, or progressive herpetic retinal necrosis. About 8 to
15% of patients, particularly elderly persons, may develop post-herpetic neuralgia. Central
nervous system involvement by VZV can lead to encephalitis, ventriculitis, periventriculitis,
vasculopathy, and myelitis.[462]
All herpesviruses exhibit latency following initial infection. Either HSV or VZV
infection initially occurs through mucosal surfaces or through abraded skin via contact with a
person who is excreting virus through active, usually ulcerative, lesions. Viral replication begins
within epithelium and underlying dermis or within submucosa. From these initial sites, HSV or
VZV spreads to nerve endings and is transported intra-axonally to neurons in ganglia, from