HSV I and II: (8/17/2007) General Characteristics: Similarities between HSV-I and HSV-II Linear, 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 nonAssociated with transmission by sexual sexual direct contact with infected fluid contact (i.e. STD) with infected fluid Signs and Symptoms: HSV-I Primary infection may be asymptomatic or may be characterized by oral (fever) blisters, ocular lesions, encephalitis Grouped or single vesicular lesions involving the ectoderm (skin, mouth, conjunctiva, nervous system) On dry surfaces, lesions scab before healing. One mucosal surfaces, lesions reepithelialize directly After initial infection, virus becomes latent in sensory nerve root ganglia or trigeminal nerve. Recurrent infection signaled by tingling or buring in the area. Symptoms may last 7 days May also infect fingers or nail area (called herpatic whitlow). HSV-II Primary infections may be asymptomatic and first clinical episode may not be observed for years after primary infection. Lesions begin as small erythematous (red) papules which form vesicles. The vesicles form pustules. Some heal without scarring Genital and anal regions may be affected with lesions. Urethra and cervix may also be infected. Signs and symptoms may also include: bilateral inguinal lymph nodes and systemic symptoms (fever, malaise, myalgia, aseptic meningitis) More likely to recur than HSV-I Recurrences are shorter with no systemic symptoms (though genital lesions do occur) Most recurrences occurs from reactivation of the virus from dorsal root ganglia

May infect the eye which can cause severe corneal damage and may lead to blindness

Can be transmitted from mother to child at birth leading to severe infections with high mortality (~60%). Especially dangerous of birth occurs near time of mothers primary infection

Due to genetic similarity with HSV-II, infection with HSV-I is though to confer some immunity which makes recurrences of HSV-II less severe. Treatment: HSV I and II are inhibited by acyclovir, a nucleoside analog. This drug is converted by the viral enzyme thymidine kinase to a monophosphate which cellular enzymes convert to a triphosphate. This triphosphate inhibits the viral DNA Polymerase ceasing DNA replication. Acyclovir decreases the duration of primary infection. It has a lesser, but marked effect on recurrences and may be taken daily to help suppress future recurrences. Variations of acyclovir such as valacyclovir are also approved for use. The body rapidly converts this drug to acyclovir, but it has better bioavailability. The drug is cleared by glomerular filtration and tubular secretion. The half life of the drug in patients with normal renal function is 3 hours and 20 hours in patients with anuria. Acyclovir shortens the first episode by ~2 days, lesion healing by 4 dyas, and viral shedding by 7 days. Side effects may include nausea, diarrhea, and headache.