Medication Summary

Antiviral agents used to treat herpes simplex virus infections are nucleoside analogs. Acyclovir is the antiviral most commonly used to treat herpes simplex virus (HSV) infections. Other oral medications include famciclovir, which is a prodrug that is converted to penciclovir, and valacyclovir, which is a prodrug that is converted to acyclovir. Oral therapy is effective for non–life-threatening herpes simplex virus infections (eg, primary orolabial, genital), and can be useful in the suppression of recurrent genital herpes simplex virus infections to diminish viral shedding and decrease rates of clinical recurrences. Intravenous (IV) acyclovir is indicated for the treatment of encephalitis, any form of neonatal disease, severe infection in patients who are immunocompromised, and occasionally for cases of severe orolabial or genital disease.^{[11, 12, 13, 14]}

Class Summary

Acyclovir, a synthetic acyclic purine nucleoside analog, is the standard treatment for herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) infections. Activation of the drug requires 3 phosphorylations. Herpes simplex virus thymidine kinase adds the first phosphate. Acyclovir binds 200-300 times more avidly to viral thymidine kinase than to host enzyme. After final cellular phosphorylation, the nucleoside triphosphate effectively inhibits DNA polymerase and acts as a DNA chain terminator. Precursors of acyclovir (ie, valacyclovir, famciclovir) have bioavailability better than that of their active metabolites (acyclovir and penciclovir, respectively). The bioavailability of valacyclovir ranges from approximately 42-64%, while that of acyclovir is between 10-20%.^[75]

The results of a multicenter, retrospective, cohort study suggest that delayed initiation of acyclovir therapy was associated with significantly greater odds of death in neonates with HSV infection.^[76]

Acyclovir (Zovirax)

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Inhibits activity of HSV-1 and HSV-2. Patients experience least pain and fastest resolution of cutaneous lesions with prompt start of therapy, usually within 48 h after rash onset. Selectively incorporated into infected cells. May prevent recurrent outbreaks. Long record of use with excellent safety profile.

Available as PO susp 200 mg/5 mL, tab, cap, injection, and topical formulation. Topical form does not appear to be effective in recurrent mucocutaneous or genital HSV infections and offers no advantage over PO form in treating primary genital HSV infections. For obese patients, calculate IV dose according to ideal body weight.

Valacyclovir (Valtrex)

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Prodrug rapidly converted to active drug acyclovir. More expensive but more convenient dosing regimen and superior bioavailability than that of PO acyclovir. Use in adolescent HSV infection. Available as 500 mg and 1g tablet formulations.

Famciclovir (Famvir)

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Transformed in vivo to active nucleoside analogue penciclovir, which can effectively inhibit HSV DNA synthesis and/or replication. More expensive but more convenient dosing regimen than that of acyclovir. Use in adolescent HSV infection.

Penciclovir (Denavir)

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1% cream approved for treatment of recurrent orolabial HSV infection. Nucleotide derivative active in vitro against HSV-1 and HSV-2. Guanosine analog that inhibits viral DNA synthesis. Negligible systemic absorption after topical use. Repeated application of cream beginning shortly after onset of recurrent HSV symptoms and continued for 4 d shortens healing time to about 1 d. May also shorten duration of viral shedding. Not approved by the FDA for use in children.

Follow-up

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Media Gallery

Primary herpes simplex virus (HSV) gingivostomatitis in an infant is shown. This same patient also had concomitant herpes whitlow as shown in the following image.
Herpes whitlow in an infant.
Cutaneous herpes simplex virus (HSV) lesions in a child in whom sexual abuse is suspected.
Vesicular scalp lesions caused by herpes simplex virus (HSV) in a 7-day-old infant.
Herpes gladiatorum in an adolescent wrestler.
MRI shows abnormal signal intensity in the left temporal lobe of an 18-year-old man with herpes simplex virus (HSV) encephalitis.

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Author

J Michael Klatte, MD Assistant Professor of Pediatrics, University of Massachusetts Medical School; Adjunct Assistant Professor of Pediatrics, Tufts University School of Medicine; Medical Director, Pediatric Antimicrobial Stewardship, Baystate Medical Center

J Michael Klatte, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Mark R Schleiss, MD Minnesota American Legion and Auxiliary Heart Research Foundation Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School

Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Leonard R Krilov, MD Chief of Pediatric Infectious Diseases and International Adoption, Vice Chair, Department of Pediatrics, Winthrop University Hospital; Professor of Pediatrics, Stony Brook University School of Medicine

Leonard R Krilov, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Swetha G Pinninti, MD Assistant Professor of Pediatric Infectious Diseases, Department of Pediatrics, University of Alabama at Birmingham School of Medicine

Swetha G Pinninti, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous author Sherman Alter, MD, to the original writing and development of this article.