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Infectious Disease Online

Pathology of Herpes Simplex Virus Infection

Dr Sampurna Roy MD


Dermatopathology Quiz Case 182

Diagnosis: Herpes Infection showing intraepidermal blister. There is balloon degeneration of the keratinocytes with 'ground glass' nuclei. Some multinucleated giant cells are present. The dermis is showing edema, inflammatory cellular infiltrate and fibrinoid necrosis of the blood vessels.

Dermatopathology Quiz Case 169

Diagnosis: Herpes Labialis (Cold Sore) Herpes Simplex Infection





Herpes simplex virus can be divided into two types on the basis of antigenicity, pathogenicity and genetic properties. 

Herpes simplex type II is the major cause of urogenital infections, whereas Herpes simplex type I is more often isolated from nongenital infections.

Herpes simplex viruses have a worldwide distribution, and direct contact with infected secretions is the principal mode of spread.

Visit: Herpes Virus (Herpesviridae); Herpes Zoster (Shingles) ; Chickenpox ; Herpes Simplex Pancreatitis

Clinical presentation:

Herpes simplex causes disease of the skin and mucosa such as acute gingivostomatitis, recurrent stomatitis, oral ulcers (cold sores), herpetic keratoconjunctivitis, herpetic esophagitis, and genital herpes.

It also causes systemic disease as in disseminated herpetic infection of infants, acute necrotizing encephalitis of the adult, and infections in the immunodeficient host.

Cytopathologic changes in Herpes Infection:

Two types of cytopathology seen in herpes simplex infections are rounding and degeneration of the cells with inclusion body formation and cell fusion with formation of syncytia.


The intranuclear inclusion is the characteristic cellular lesion, and it consists of a single, eosinophilic, well-demarcated inclusion body surrounded by a halo and marginated chromatin.

By electron microscopy the inclusion body consists of paracrystalline arrays of viral capsids and electron-dense glycoprotein.

Herpetic infection of skin and mucosa:


Herpetic infection of skin and mucosa is manifested by the appearance of red papules that quickly become vesiculated.

Histologically there is degeneration of the cells in the stratum malpighii and the stratified squamous epithelium.

In early stages one observes ballooning of the epidermal cells and clearing of the nuclear chromatin.

There is acantholysis and formation of a unilocular vesicle.

The typical inclusion bodies (Cowdry type A) can be seen in the epidermal cells.

The upper dermis or submucosal portions of the affected regions show an inflammatory infiltrate around capillaries.

The histologic lesion of herpes simplex in skin and mucosa is practically indistinguishable from that caused by herpes zoster.

Immunohistochemistry using fluorescent antibodies or immuno-peroxidase can, however, make the distinction between these viruses and even allows typing of the herpesvirus.

Disseminated Herpetic Disease:

Disseminated herpetic infection of the newborn affects neonates in the first 4 weeks of life as well as an older group of infants in whom it causes hepatoadrenal necrosis.

Autopsies of infants dying from disseminated herpetic disease show multiple military foci of necrosis surrounded by hemorrhagic borders in the liver, adrenal gland, and brain.

Microscopically these foci consist of a zone of central coagulative necrosis surrounded by an area of hyperemia with a sparse mononuclear inflammatory inflammatory reaction.

Inclusion bodies characteristic of the herpetic infection are found in nuclei of the parenchymal cells surrounding the necrotic zone.

Pathologic combination may be complicated by the presence of gram-negative septicemia.

Morphologic manifestations of disseminated intravascular coagulation (DIC) may be also prominent.

The virus can be easily easily demonstrated in the lesions by electron microscopic examination.

Acute necrotizing encephalitis:    

Herpes simplex virus has been shown to be a cause of acute necrotizing encephalitis of the adult.

Patients with this syndrome may display a picture of encephalitis or a clinical picture of an expanding lesion, often of the temporal lobe.

In fatal cases the brain shows asymptomatic necrosis particularly prominent in the temporal lobes but also involving the hippocampus and the posterior occipital cortex.

Hemorrhage may be prominent. In the early stages of the disease the histopathologic picture is that of acute necrosis associated with a diffuse meningoencephalitis.

Inclusion bodies within the nuclei of neurons and glial cells can be seen but on occasion are difficult to find.

Reactivation and dissemination of herpetic lesions are not uncommon in immuno-compromised hosts.

Esophageal and upper respiratory tract lesions are commonly found at autopsy in patients who have undergone intense chemotherapy.

Dissemination occasionally occurs, and a picture similar to the disseminated disease in newborns can be seen.

Dissemination with fatal outcome also occurs in some severely burned patients.

Evidence is accumulating that herpes simplex virus (HSV) infection is implicated in oncogenesis. HSV antigens have been observed in some oral cancers.   

Further reading:

Herpes simplex keratitis.

Trends in Herpes Simplex Virus Type 1 and Type 2 Seroprevalence in the United States. 

Isolation of herpes simplex virus from the genital tract during symptomatic recurrence on the buttocks.

Clinical assessment of assays for diagnosis of herpes simplex infection.

Herpes simplex virus infection presenting as a piriform sinus mass.

Chlamydia trachomatis and herpes simplex virus 2 infection in vulvar intraepithelial neoplasia associated with human papillomavirus.

Reactivation of genital herpes simplex virus type 2 infection in asymptomatic seropositive persons.

Fulminant herpes colitis in a patient with Crohn's disease.




Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)

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