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HSV I and II:

(8/17/2007)

General Characteristics:

Similarities between HSV-I and HSV-IILinear, double stranded DNA virus

No known animal vector

Humans are the natural reservoir

50% homology of base sequence

Similar glycoprotein surface antigens

Direct contact with infected secretions is primary mode of transmission

Transmission may occur while asymptomatic (i.e. virion have been isolated from saliva

and genital secretions even when clinical symptoms were absent)

Stress activated recurrences (mechanism not understood, but observed factors are light,

fever, and trauma)

Differences between HSV-I and HSV-II

HSV-I HSV-II

Glycoprotein gB1 Glycoprotein gB2

Associated with transmission by non-

sexual direct contact with infected fluid

Associated with transmission by sexual

contact (i.e. STD) with infected fluid

Signs and Symptoms:

HSV-I HSV-II

Primary infection may be asymptomatic ormay be characterized by oral (fever)

blisters, ocular lesions, encephalitis

Primary infections may be asymptomaticand first clinical episode may not be

observed for years after primary infection.

Grouped or single vesicular lesions

involving the ectoderm (skin, mouth,conjunctiva, nervous system)

Lesions begin as small erythematous (red)

papules which form vesicles. The vesiclesform pustules. Some heal without scarring

On dry surfaces, lesions scab beforehealing. One mucosal surfaces, lesions re-

epithelialize directly

Genital and anal regions may be affectedwith lesions. Urethra and cervix may also

be infected.

After initial infection, virus becomes latentin sensory nerve root ganglia or trigeminal

nerve.

Signs and symptoms may also include:bilateral inguinal lymph nodes and

systemic symptoms (fever, malaise,myalgia, aseptic meningitis)

Recurrent infection signaled by tingling or

buring in the area.

More likely to recur than HSV-I

Symptoms may last 7 days Recurrences are shorter with no systemic

symptoms (though genital lesions do occur)

May also infect fingers or nail area (called

herpatic whitlow).

Most recurrences occurs from reactivation

of the virus from dorsal root ganglia

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