Herpes Simplex Virus

Infection with HSV1 is almost universal. This is known because, although many infections are sub-clinical, virtually 100% of adults have antibodies in their serum. Most individuals become infected in the first few years of life.
Virus is shed from the infected area and spread occurs as a result of direct contact with lesions. For example, through kissing (HSV1) or sexual intercourse (HSV2).
Virus may also, however, be shed in saliva and genital secretions and can thus be transmitted in the absence of clinical lesions.

There are 2 clinical patterns of disease:

a) Primary Infection , and

b) Recurrent disease

Most primary infections are silent.
In clinically apparent cases, vesicles usually develop at between 1-3 days post exposure and remain localized to the site of inoculation. However, in immunocompromised individuals the virus may disseminate.

The primary eruption is often associated with fever and cervical lymphadenopathy. The illness is self limiting and lesions usually heal within 14 days.

Herpetic Whitlow
Inoculation of virus into the fingers - an occupational hazard of doctors, nurses and dentists.
May be mistaken for a paronychia and incised .

Conjunctivitis, Keratitis

Herpetic lesion on the cornea - is called a dendritic ulcer because of its branching appearance. Pain and photophobia are prominant features. Conjunctivitis and oedema of the lids commonly accompany primary infection. Lesions usually heal within 3 weeks.

Exposure may occur:
1) at birth, if the mother has genital herpes at the time of delivery. (This is only a significant risk if the mother is experiencing a primary infection).

2) In the post natal period, if the infant is handled by people with herpetic lesions.

The disease may take one of three forms:-

Cutaneous lesions:-
These are confined to the skin, and the prognosis is good.
Generalized infection:-
This is a serious condition, with a high fatality rate. Virus disseminates throughout the organs. Cinical features include jaundice, hepatosplenomegaly, thrombocytopenia, pneumonia and encephalitis. Lesions on the skin may be trivial.
Encephalitis:-
Direct infection of brain tissue.

Following primary oro-facial infection, the virus enters sensory nerve endings and travels up the axon and establishes a latent infection in the trigeminal ganglion.

The viral genome persists in an episomal form (plasmid) in the nucleus of the neurone. No viral genes are expressed. This state of latency may persist for many years.

In a percentage of people,
the virus will reactivate: - A cycle of viral replication occurs in the neurone and virus particles travel down the axon to reinfect the skin or mucous membrane in the area supplied by the nerve.

1. Cold sores (follows gingivo-stomatitis):
Following one of a variety of stimuli, vesicles erupt on the muco-cutaneous junctions of the nose or mouth. These are more localized than the primary infection and heal more rapidly (7-10 days). The eruption is often preceeded by paraesthesia of the involved area.

2. Recurrent genital herpes:
Recurrence with HSV 2 infections is more common than with HSV 1. Lesions are less extensive and heal more rapidly than the primary infection.

3. Keratitis:
The virus reaches the cornea via the ophthalmic branch of the trigeminal nerve; the clinical lesion is termed a dendritic ulcer. It heals more rapidly than the primary infection.

LABORATORY DIAGNOSIS

Direct detection by electron microscopy of herpesvirus particles in vesicle fluid

Culture: Isolation from clinical material from skin lesions may be inoculated onto cell monolayers which are monitored for the development of characteristic cytopathic effect. This is usually detected within three days

Serology is not very useful because there is a high prevalence of antibody in the normal population.

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