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The human herpesviruses, including Herpes simplex virus (HSV), Varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesvirus 6 (HHV-6), human herpesvirus 7 (HHV-7), and human herpesvirus 8 (HHV-8) may produce a variety of clinically significant manifestations either as self-limited infections or non-resolving opportunistic infections.
Both HSV types 1 (HSV-1) and 2 (HSV-2) primarily infect skin and mucus membranes (mucocutaneous infections) to produce inflammation, often vesicular, progressing to sharply demarcated ulcerations.
Thus, vesicular HSV or VZV lesions may later appear or recur away from the initial site of involvement.
After an initial host response in which both cell-mediated and humoral mechanisms take part, the infection usually becomes latent, with HSV or VZV present but not actively replicating within ganglia. Diagnosis of HSV or HZV infections is suggested by the appearance of crops of clear vesicles in groups on mucocutaneous surfaces.
Ulceration may obscure the features and make diagnosis difficult unless a Tzanck preparation, biopsy, or viral culture is done to establish the diagnosis.
Chronic HZV infections may be characterized by pseudocarcinomatous hyperplasia, verrucous epidermal hyperplasia, and massive hyperkeratosis.
Reactivation of VSV as HZV with shingles may often occur as an early manifestation of immune compromise.
Internal organ involvement with HSV and HZV is infrequent, and disseminated infections are uncommon, but the clinical course can be one of recurrences.
Herpetic mucocutaneous lesions of immunocompromised patients, including those with AIDS, have been reported to be more extensive, more severe, and longer-lasting, with more ulceration, necrosis, and pain than in immunocompetent patients. Viral culture remains the most sensitive clinical method for HSV or HZV diagnosis; methods for antigen detection are less sensitive. Microscopically, lesions of HSV and HZV both in tissue biopsies or 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.
For HZV, typical cytologic features most often occur in cells between papillae and dermal adnexae. Grossly, HSV produces areas of necrosis most commonly in temporal lobe, inferior frontal lobe, insula, or cingulate gyrus. Additional visceral organ involvement with HSV or HZV is quite uncommon, even in immunocompromised hosts.
Acyclovir has been found to be effective therapy for treating most mucocutaneous herpetic infections and may be useful prophylactically in persons with frequent recurrences. Microscopic diagnosis of CMV is based upon finding the characteristic intranuclear inclusions within enlarged cells, in most cases presents no problems.
Treatment for CMV infection has received increasing attention since the observation that the drug 9-(1,3-dihydroxy-2-propoxymethyl) guanine, commonly known as ganciclovir, inhibited in vitro replication of human herpesviruses, including CMV.


There are no specific clinical features of acute EBV infection, aside from infectious mononucleosis. HHV-6 demonstrates T-lymphocyte tropism, and it has been found to replicate in a variety of cell types, including CD4+ lymphocytes.
HHV-7 is quite common, with serologic evidence for previous infection in about 85% of adults in the U.S.
A human herpesvirus-like agent (HHV-8) has been identified in skin lesions of Kaposi's sarcoma (KS) in both classical and AIDS-associated forms as well as in the KS of HIV negative homosexual males. All forms of KS have a male predominance, but this is even more pronounced with AIDS where it is seen most frequently in homosexual and bisexual males who have a 10-fold risk compared with intravenous drug users, though the incidence of KS with AIDS appears to be decreasing slightly over time. 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. From these initial sites, HSV or VZV spreads to nerve endings and is transported intra-axonally to neurons in ganglia, from which spread is then via peripheral sensory nerves back to other, usually adjacent, skin and mucosal sites.
It is unclear just how reactivation of HSV, or VZV as HZV, occurs but lack of cell-mediated immunity in immunocompromised patients may be implicated.
Multiple herpetic lesions tend to ulcerate due to persistence for prolonged periods (with or without therapy), excoriation, or secondary infection. Culture sensitivity is higher when the herpetic vesicular lesions first appear and before they ulcerate. The cytoplasm of infected cells is not prominent and, unlike CMV, does not contain inclusion bodies of any kind.
On average, cells infected with HSV or HZV do not reach the size of those with CMV, and the intranuclear inclusions of CMV tend to be darker and larger, and intracytoplasmic inclusions may accompany CMV. The clinical course and radiologic findings of HSV encephalitis may closely mimic those of progressive multifocal leukoencephalopathy (PML), though computed tomograpahic or magnetic resonance imaging scans showing evidence of hemorrhage, a mass effect, or gray matter involvement more strongly suggest herpes. Microscopically, herpetic lesions can have petechiae with fibrinoid necrosis, perivascular mononuclear inflammatory cell infiltrates, and Cowdry type A inclusions in either neurons or glial cells. However, with AIDS deeper infection is more frequent, with the complication of chorioretinitis reported. Reported involvement includes findings of hepatitis, glomerulonephritis, adrenalitis, and arthritis. Anorectal herpetic lesions often respond to acyclovir therapy and may disappear following treatment. The clear halo that often surrounds intranuclear inclusions also helps in distinguishing CMV.


Several reports have detailed the clinical use and response of AIDS patients treated with ganciclovir Previous attempts to treat CMV with adenine arabinoside, alpha-interferon, and acyclovir met with poor results. This agent appears to be sexually transmissible independently of HIV and accounts for the increased incidence of KS in certain risk groups. Kaposi's sarcoma occurs in the following clinical patterns: classic (sporadic), endemic African (benign nodular, aggressive, florid, and lymphadenopathic), iatrogenic (seen in immunocompromised patients such as recipients of organ transplants, those patients on immunosuppressive drug therapy, or patients with connective tissue diseases), and epidemic (AIDS-associated). Excretion of HSV-1 can be detected in 2 to 9% of asymptomatic adults, while HSV-2 can be isolated from the genital tract in up to 5% of males and up to 8% of females in sexually transmitted disease clinics. Immunoperoxidase staining with primary antibody against HSV-1, HSV-2, and HZV will help to exclude other viral etiologies such as CMV, EBV, and human papillomavirus (HPV).
Herpes simplex virus and adenovirus may produce intranuclear inclusions, but the cells are never as large as CMV, and do not have the cytoplasmic basophilic inclusions of CMV.
Kaposi's sarcoma is infrequently seen in persons whose risk for AIDS is parenteral exposure to HIV, blacks, and children.
However, either body region may be infected by either subtype to produce clinically and histologically indistinguishable disease, which is not surprising, given the 50% homology between the genomes of HSV-1 and -2. The typical patient with HSV or HZV has a grouped vesicular skin eruption that ruptures, crusts, and heals in seven to ten days. 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. However, both HSV and HZV infections have been reported that are resistant to acyclovir. In some cases the plane of sectioning may miss the intranuclear inclusion body of the CMV cell, and the cytoplasmic basophilic granular bodies may resemble bradyzoites of Toxoplasma gondii pseudocysts. Infection may be associated with a history of severe pain, often persisting for months after the skin lesions resolve.
However, bradyzoites are more uniform in size, and the pseudocyst usually has a more prominent border. In questionable cases, immunohistochemical staining or electron microscopy can provide adequate differentiation.



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