Page 104 - AIDSBK23C

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appear and before they ulcerate. Later ulcerative lesions may have no detectable virus.
Serologic testing is mainly of value for detection of past infection, but not acute infection, for
immunocompromised patients are unlikely to mount a significant (fourfold or greater) rise in
anti-HSV titer between acute and convalescent samples.[461]
Microscopically, lesions of HSV and VZV both in tissue biopsies and from cytologic
preparations (Tzanck or Pap smears) demonstrate characteristic acantholytic epithelial or
discohesive parenchymal cells, often multinucleated or in clusters, with mauve to pink to steel-
gray ground glass intranuclear (Cowdry type A) inclusions and nuclear chromatin margination.
The cytoplasm of infected cells is not prominent and, unlike CMV, does not contain inclusion
bodies of any kind. With ulceration, such cells may be infrequent or autolyzed. Epithelial cells
of the skin adnexa (sweat ducts and hair follicles with sebaceous apparatus) may also be
involved.[466]
On average, cells infected with herpes simplex and varicella zoster virus groups do not
reach the size of those with cytomegalovirus, but the larger cells with herpes simplex or varicella
zoster and the smaller cells with cytomegalovirus may be of similar size. The intranuclear
inclusions of cytomegalovirus tend to be darker and larger. Also, in squamous epithelium with
herpetic lesions, ballooning degeneration is common, and CMV is unlikely to be associated with
vesicle formation in mucosal tissues.
For VZV, typical cytologic features most often occur in cells between papillae and
dermal adnexa. Cells infected with HSV or VZV do not often reach the size of cells infected
with CMV, and the intranuclear inclusions of CMV tend to be darker and larger, and
intracytoplasmic inclusions may accompany CMV. Immunoperoxidase staining with primary
antibody against HSV-1, HSV-2, and VZV will help to exclude other viral etiologies such as
CMV, EBV, and HPV.
Acyclovir has been found to be effective therapy for treating most mucocutaneous and
visceral herpetic infections and may be useful prophylactically in persons with frequent
recurrences.[208,461] However, both HSV and VZV infections that are resistant to acyclovir are
found in increasing numbers in immunocompromised patients.[467] The cyclical nature of
herpetic infections means that they may at times regress without therapy, or in spite of it.[457]
Death from either herpes simplex or varicella-zoster viruses is quite rare, and usually results
from central nervous system involvement.[417]
Human herpesvirus 6 (HHV-6) is highly seroprevalent, with a worldwide distribution.
Most persons are infected by the age of two; the probable mode of transmission is through saliva.
In infants, it may cause roseola, and a mononucleosis-like syndrome. This virus is
predominantly tropic to CD4 lymphocytes. HHV-6 infection can coexist with HIV infection,
and may be involved with progression to AIDS, since HHV-6 upregulates CD4 expression and
can, therefore, increase HIV replication to deplete CD4 lymphocytes. Active HHV-6 infection
can be present before the stage of clinical AIDS is reached.[459,468]
Human herpesvirus 7 (HHV-7) is a lymphocytotropic agent for CD4 cells that typically
infects most persons during childhood and may cause skin rashes such as pityriasis rosea. Both
HHV-7 and HIV use CD4 receptors and can interfere with each other. The immunosuppression
accompanying HIV infection may lead to reactivation from latency and increased replication of
HHV-7 in lymph nodes.[469,470]
Human herpesvirus 8 (HHV-8) is also known as Kaposi sarcoma-associated herpes virus
(KSHV) is known to be associated with a variety of neoplastic and proliferative lesions seen with
AIDS. This is a gamma 2 herpesvirus. The gamma herpesviruses establish persistent viral