Herpesvirus Infections
Clinical Snapshot
Herpes simplex virus (HSV-1 and HSV-2) and varicella-zoster virus (VZV) are related human herpesviruses that share a defining biological feature: after the initial infection, each establishes lifelong latency in sensory nerve ganglia and can reactivate periodically to cause recurrent disease. HSV causes orolabial disease (cold sores, most often HSV-1) and anogenital disease (genital herpes, most often HSV-2, though either type can cause either site through oro-genital contact); VZV causes chickenpox on primary infection and, on reactivation from the dorsal root or cranial nerve ganglia, herpes zoster (shingles) — a painful, dermatomal vesicular rash. Knowledge of HSV type does not change antiviral drug selection, since HSV-1 and HSV-2 are similarly susceptible to all three available agents — drug choice is driven by disease site, severity, and dosing convenience instead.[1] This chapter covers the three antiviral nucleoside analogues (acyclovir, valacyclovir, famciclovir) that treat all of these presentations, the distinct dosing and duration each disease requires, the narrow treatment window that determines how effective zoster therapy will be, and the situations — ophthalmic zoster, disseminated disease in immunocompromised hosts, and pregnancy — that change management. Primary varicella (chickenpox) and routine varicella/zoster immunization schedules are outside this chapter's scope, which focuses on treating established HSV and herpes zoster disease.
Recognize the Condition
Three related presentations covered in this chapter
Orolabial HSV
Primary infection (usually HSV-1, most often acquired in childhood) can be asymptomatic or present as herpetic gingivostomatitis — painful vesicular and ulcerative lesions across the oral mucosa, gums, tongue, and lips, often with fever and cervical lymphadenopathy, most severe in young children. Recurrent disease (herpes labialis, the common "cold sore") is typically far milder and localizes to the vermilion border of the lip. A prodrome of tingling, burning, itching, or pain 2-24 hours before the lesion appears is common and is the ideal moment to start episodic therapy.
Genital HSV
Most anogenital infection is HSV-2, though HSV-1 causes a growing share through oro-genital transmission. Presentation ranges from entirely asymptomatic to painful clustered vesicles or ulcers on the genitals, perianal area, or buttocks, sometimes with fever, myalgia, and tender inguinal lymphadenopathy — most pronounced with a first episode. Recurrent episodes are typically shorter and milder and are often preceded by a localized prodrome (tingling, burning) at the same site.
Herpes zoster (shingles)
Reactivation of latent VZV produces a painful, often burning or stabbing, unilateral rash confined to one or two adjacent dermatomes that does not cross the body's midline. Pain frequently precedes the visible rash by 1-4 days. Lesions progress from erythematous papules to grouped vesicles, then pustules and crusts, typically healing over 2-4 weeks. The most common complication is postherpetic neuralgia — pain persisting after the rash has resolved, which can last weeks to years.[2]
Risk Factors
HSV (orolabial and genital)
- Direct mucocutaneous or secretional contact with an infected partner, including during asymptomatic viral shedding — most transmission occurs when no lesion is visible.
- New or multiple sexual partners, for genital HSV specifically.
- Sun exposure, physical or emotional stress, febrile illness, local trauma, and menstruation are common recurrence triggers for orolabial and, less consistently, genital HSV.
- Immunosuppression (HIV, transplant, chemotherapy, high-dose corticosteroids, biologic therapy) — associated with more frequent, more severe, and longer-lasting recurrences, and a higher risk of antiviral-resistant disease.
- Orogenital contact, which can transmit HSV-1 to the genitals or HSV-2 to the mouth.
Herpes zoster
- Age 50 and older — risk and severity, including postherpetic neuralgia risk, rise steadily with age.
- Any cause of reduced cell-mediated immunity — HIV infection, hematologic or solid organ malignancy, transplant, chemotherapy, high-dose or prolonged corticosteroid use, and other immunosuppressive therapy.
- Physical or emotional stress and other causes of transient immune waning.
- A history of primary varicella (chickenpox) infection at any point in the past — required for zoster to occur at all, since it is caused by reactivation of latent VZV.
Red Flags & Refer
Any of the following changes management beyond outpatient oral antiviral therapy — escalate promptly:
- Herpes zoster involving the ophthalmic (V1) division of the trigeminal nerve, or vesicles on the tip or side of the nose (Hutchinson sign) — same-day ophthalmology referral is required regardless of how long the rash has been present, given the risk of permanent vision loss.[3]
- Disseminated herpes zoster in an immunocompromised patient — a widespread rash (more than 20 lesions) affecting 3 or more dermatomes, or spreading beyond the primary and immediately adjacent dermatome — needs hospitalization for IV acyclovir and specialist input.[2]
- Suspected HSV encephalitis — new headache, fever, altered behaviour or consciousness, seizures, or focal neurologic signs — is a neurologic emergency requiring immediate hospital assessment, CSF PCR, and empiric IV acyclovir while the workup proceeds; do not manage as a routine HSV presentation.
- Neonatal herpes exposure risk at delivery — active genital lesions or a prodrome at the onset of labour — requires immediate obstetric and neonatology involvement, since neonatal HSV carries major morbidity and mortality.[4]
- Eczema herpeticum — widespread HSV superinfection of eczematous skin with fever and malaise — needs urgent dermatology/infectious diseases assessment and usually IV acyclovir.
- Any severely immunocompromised patient (e.g., hematopoietic stem-cell transplant, high-dose immunosuppression, advanced/uncontrolled HIV) with a new HSV or VZV reactivation — involve infectious diseases early given the risk of dissemination and antiviral resistance.
- Signs of aseptic meningitis (severe headache, photophobia, neck stiffness) accompanying a genital HSV episode — HSV-2 is an important cause and needs prompt assessment.
Assessment & Diagnosis
History
- For orolabial disease: ask about prodrome timing, sun/stress/illness triggers, and recurrence frequency over the past year.
- For genital disease: characterize the lesion (single vs. multiple, painful vs. painless, vesicular vs. ulcerative), ask about prodrome and exposure history, and screen for other STIs and HIV risk at the same visit.
- For a dermatomal rash: confirm it is unilateral and does not cross the midline, ask about preceding pain, and assess for herpes zoster risk factors (age, immunosuppression).
- For any of the three presentations, ask specifically about immunosuppression (HIV, transplant, chemotherapy, high-dose corticosteroids, biologic therapy) and pregnancy status, since both change management.
Examination and testing
Viral culture remains an acceptable alternative where NAAT is unavailable, though its sensitivity declines as lesions heal. Type-specific serology (glycoprotein G-based assays distinguishing HSV-1 from HSV-2) has a narrow role — confirming infection in a patient with a compatible history but negative virologic testing, or evaluating a partner in a discordant couple — but should not be used as a general screening test given its low positive predictive value in a low-prevalence population; a positive serology result alone, without a corresponding clinical picture, is not by itself an indication to start treatment.[1]
Herpes zoster is usually diagnosed clinically from the characteristic dermatomal vesicular rash; testing (PCR of vesicular fluid, or a Tzanck smear showing multinucleated giant cells, which does not distinguish HSV from VZV) is reserved for atypical presentations, immunocompromised patients, or disseminated disease. Consider zoster even without a visible rash ("zoster sine herpete") in an older patient with new, severe, unilateral dermatomal pain.
Genital herpes ulcers are typically multiple, small, painful, and vesiculoulcerative, in contrast to the classically single, large, painless chancre of primary syphilis — but there is real overlap in presentation, as the Sexually Transmitted Infections chapter's Syphilis section notes when differentiating the two. Do not rule out syphilis on the basis of an atypical-looking ulcer, and consider concurrent syphilis serology, HIV testing, and screening for other STIs at the same visit as a new genital HSV diagnosis.
Do not delay empiric antiviral treatment while awaiting confirmatory results in a patient with a classic presentation — start therapy based on the clinical picture, since delaying treatment reduces its effectiveness for every condition covered in this chapter.
Treatment Targets
- Shorten the duration and severity of the acute episode for orolabial HSV, genital HSV, and herpes zoster alike, which requires starting antiviral therapy as early as possible in each.
- Reduce the frequency and burden of recurrent orolabial or genital HSV outbreaks with suppressive therapy when the recurrence pattern or patient burden warrants it.
- Reduce — though not eliminate — HSV viral shedding and the risk of transmission to sexual partners.
- Reduce the risk of postherpetic neuralgia by starting herpes zoster antiviral therapy within 72 hours of rash onset, or later if specific extension criteria apply.
- Prevent vision-threatening complications of herpes zoster ophthalmicus through same-day ophthalmology referral, in addition to systemic antiviral therapy.
- Prevent disseminated VZV or HSV disease and its complications (pneumonitis, hepatitis, encephalitis) in immunocompromised patients.
- Prevent neonatal HSV transmission at delivery and limit the impact of maternal VZV exposure or infection in pregnancy.
Choose Initial Treatment
Orolabial HSV
Recurrent cold sore, episodic treatment give the patient an advance prescription and instruct them to self-initiate therapy at the very first sign of prodrome (tingling, burning, itching) — a course started early is far more effective than one started after vesicles have formed.
Frequent recurrences, or a clear trigger such as sun exposure switch from episodic to daily suppressive therapy, or use trigger-specific short-course prophylaxis for sun-triggered disease (see Drug Tables).[5]
Do not rely on topical acyclovir cream alone as adequate therapy — it is meaningfully less effective than an oral agent, needs frequent application, and carries a real risk of self-inoculation; oral therapy is preferred.[5]
Genital HSV
First clinical episode start an oral antiviral immediately based on the clinical diagnosis, without waiting for NAAT/PCR confirmation — treatment is most effective when started early in the episode.[1]
Severe first episode — disseminated infection, aseptic meningitis, hepatitis, or inability to tolerate oral intake — hospitalize for IV acyclovir, then switch to oral once improving to complete the course.[1]
Recurrent episode, infrequent or the patient prefers per-episode control patient-initiated episodic therapy, started within 24 hours of prodrome or lesion onset — provide an advance prescription so the patient does not need to be seen to start it.[1]
Recurrent episode, frequent or a significant burden to the patient daily suppressive therapy — base the decision on a joint discussion of disease burden with the patient rather than a fixed episode-count threshold.[1]
Regardless of regimen, counsel that suppressive therapy reduces but does not eliminate viral shedding and transmission risk — continue barrier protection.[1]
Herpes zoster (shingles)
Within 72 hours of rash onset start an oral antiviral in essentially every patient — acyclovir, valacyclovir, or famciclovir are equally recommended, chosen mainly by dosing frequency and adherence.[2]
Beyond 72 hours still start antiviral therapy if new vesicles are actively forming, the ophthalmic dermatome is involved, the patient is immunocompromised, or the rash/pain is severe — the 72-hour mark is a general target, not an absolute cutoff that closes the treatment window.[2]
Ophthalmic zoster — V1 dermatome involvement, or vesicles on the tip or side of the nose (Hutchinson sign) — same oral antiviral therapy plus same-day ophthalmology referral regardless of how long the rash has been present, given the risk of permanent vision loss.[3]
Disseminated disease or significant immunocompromise hospitalize for IV acyclovir; switch to oral once improving to complete a minimum of 10-14 days total.[2]
Do not rely on topical antiviral therapy for herpes zoster — topical agents are not effective for this indication.[2]
Starting antiviral therapy within the treatment window reduces the duration of viral shedding, acute pain, and new lesion formation; evidence that antivirals reliably prevent postherpetic neuralgia is more limited, so pain control and early recognition of persistent pain remain important regardless of antiviral timing.[6]
A short corticosteroid course may be added in carefully selected, healthy immunocompetent patients with moderate-to-severe acute pain to improve quality of life — it does not reduce postherpetic neuralgia risk and carries meaningful risk (immunosuppression, hyperglycemia, GI bleeding) in older, diabetic, or frail patients, so reserve it for healthy patients rather than adding it routinely.[7]
Non-Pharmacologic Treatment
- Avoid touching, scratching, or picking at active lesions of any of the three conditions to reduce autoinoculation (e.g., spreading HSV to the eye or fingers) and secondary bacterial infection.
- Keep the rash/lesions clean and dry; loose, non-restrictive clothing over a zoster rash reduces discomfort.
- Orolabial HSV: avoid sharing lip balm, razors, cups, or utensils during an active outbreak; for sun-triggered recurrences, use a sunscreen lip balm and consider short-course antiviral prophylaxis before planned sun exposure (see Drug Tables).
- Genital HSV: avoid sexual contact from the first sign of prodrome until lesions have fully healed; barrier protection (condoms) reduces but does not eliminate transmission risk between outbreaks and during suppressive therapy, and should be continued.
- Disclose a genital HSV diagnosis to sexual partners and offer them information/testing — this is a counselling point, not a mandatory-notification requirement the way it is for classic bacterial STIs.
- Cool compresses, loose clothing, and non-adhesive dressings for herpes zoster; avoid topical antibiotics and adhesive dressings, which can irritate the rash and delay healing.
- Vaccine prevention (brief note): the recombinant zoster vaccine (Shingrix) is routinely recommended for immunocompetent adults 50 years of age and older, given as 2 intramuscular doses 2-6 months apart, and can be given starting at least 1 year after an acute zoster episode. NACI now also strongly recommends 2 doses for adults 18 years of age and older who are or will be immunocompromised, using the same interval. The vaccine treats nothing acutely — it is prevention only, for a future episode, and is a distinct topic from the antiviral treatment covered in the rest of this chapter.[8]
Special Populations
Pregnancy — genital and orolabial HSV
Pregnancy — VZV exposure
Pediatrics
Primary HSV gingivostomatitis is more common in children than adults. In a child able to swallow, oral acyclovir suspension 15 mg/kg PO 5 times daily for 7 days accelerates resolution of oral lesions and fever and shortens viral shedding when started early in the illness; supportive care (analgesia, hydration) remains essential regardless.[11] If the child cannot tolerate oral intake, hospitalize for IV acyclovir and IV fluids. Primary varicella (chickenpox) treatment and routine varicella/zoster immunization schedules are outside this chapter's scope.
Immunocompromised patients, including HIV
Recurrent genital HSV episodes in HIV-positive patients are treated with the same three agents at somewhat higher-intensity dosing and longer duration than in HIV-negative patients (see Drug Tables) — involve infectious diseases for guidance and ensure antiretroviral therapy is optimized, since ongoing immune suppression increases the risk of prolonged, refractory disease and antiviral-resistant HSV.[1] Severely immunocompromised patients (hematopoietic stem-cell transplant, high-dose immunosuppression, advanced HIV) are at the highest risk of VZV dissemination and visceral organ involvement, and of acyclovir-resistant HSV/VZV requiring IV foscarnet.[2]
Renal impairment
Acyclovir, valacyclovir, and famciclovir are all renally eliminated and require dose or interval adjustment as renal function declines. With IV acyclovir specifically, ensure adequate hydration and infuse over at least 60 minutes to reduce the risk of crystalline nephropathy from acyclovir precipitation in the renal tubules.
Monitoring & Follow-Up
- Reassess healing and symptom resolution within the expected timeframe for the condition treated — days for a treated HSV outbreak, 2-4 weeks for herpes zoster — and reassess sooner if symptoms are worsening rather than improving.
- For patients on HSV suppressive therapy, periodically reassess adherence, breakthrough recurrences, and whether ongoing suppression is still needed, rather than continuing indefinitely by default — recurrence frequency for many patients decreases over time.[1]
- Reassess renal function periodically in patients on long-term or high-dose antiviral therapy, and adjust doses as needed.
- Track pain trajectory after herpes zoster; screen for postherpetic neuralgia if pain persists beyond acute rash resolution, and manage per the Neuropathic Pain chapter's approach if it does.
- Confirm that a new genital HSV diagnosis included counselling on disclosure, safer sex practices, and the psychosocial impact of the diagnosis — this is a substantial part of management, not an afterthought.
- At a follow-up visit after an acute zoster episode, confirm the patient is aware of their eligibility for the recombinant zoster vaccine (Shingrix) once at least 1 year has passed, if not already vaccinated.[8]
- Confirm ophthalmology follow-through for any patient referred for ocular involvement.
Common Errors to Avoid
- Declining to start herpes zoster antiviral therapy solely because more than 72 hours have passed, without checking for the specific situations (new vesicles still forming, ophthalmic involvement, immunocompromise, severe pain) that still justify starting it.[2]
- Treating herpes zoster ophthalmicus, or any vesicles on the tip or side of the nose, with oral antiviral therapy alone and skipping the same-day ophthalmology referral.[3]
- Relying on topical acyclovir cream as adequate therapy for genital HSV, extensive orolabial disease, or herpes zoster — none of these respond adequately to a topical agent alone.
- Assuming a single "textbook" painless genital ulcer excludes herpes, or a "textbook" cluster of painful vesicles excludes syphilis — real-world presentations overlap significantly.
- Telling a patient on HSV suppressive therapy that barrier protection is no longer needed because transmission risk is eliminated — it is reduced, not eliminated.[1]
- Missing renal dose adjustment for antivirals in older adults or anyone with reduced renal function, especially with IV acyclovir.
- Withholding antiviral therapy for a pregnant patient with genital HSV or a VZV exposure/infection out of unfounded teratogenicity concern, when reassuring safety data exist for every trimester.[9]
- Forgetting to counsel a patient recovering from an acute zoster episode about future recombinant zoster vaccine eligibility.[8]
- Adding a corticosteroid to zoster therapy expecting it to reduce postherpetic neuralgia risk — it does not; use it for quality-of-life reasons only, in carefully selected healthy patients with significant acute pain.[7]
- Missing the opportunity to offer VariZIG, or postexposure oral antiviral prophylaxis if VariZIG is unavailable or out of its window, to a non-immune pregnant patient with a significant VZV exposure.[10]
Clinical Decision Algorithm
Drug Tables
How to use this table: Doses are adult doses unless otherwise labeled, and require patient-specific confirmation, including renal adjustment. Select any drug name to open its complete Pharmasist Drug Database page.
Nucleoside analogues — orolabial HSV
Acyclovir, valacyclovir, and famciclovir are equally acceptable; drug choice is driven by dosing convenience and patient preference rather than a meaningful efficacy difference.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Acyclovir | Primary gingivostomatitis, children: 15 mg/kg PO 5 times daily for 7 days (oral suspension) Recurrent episode, adults: 400 mg PO 5 times daily for 5 days, started at first prodrome Topical cream (adjunct/alternative, less effective than oral): 5% cream applied 5 times daily during waking hours for 4 days, started within 1 hour of prodrome Suppression (frequent recurrences): 400 mg PO twice daily, or 200 mg PO 4 times daily, for up to 4 months, then reassess Sun-exposure prophylaxis: 400 mg PO twice daily starting 12 hours before sun exposure, continued for its duration | Nausea, headache; rare nephrotoxicity if inadequately hydrated | Probenecid can increase acyclovir levels; additive nephrotoxicity with other nephrotoxic drugs | Give an advance prescription for self-initiated episodic use. |
| Valacyclovir | Recurrent episode, adults: 2 g PO twice daily for 1 day Suppression (frequent recurrences): 500 mg PO once daily for up to 4 months, then reassess | Nausea, headache | None clinically significant at these doses | A prodrug of acyclovir with improved oral bioavailability, allowing less frequent dosing. |
| Famciclovir | Recurrent episode, adults: 1500 mg PO as a single dose | Nausea, headache | None clinically significant at these doses | A prodrug of penciclovir; the single-dose regimen aids adherence. |
Nucleoside analogues — genital HSV
Start therapy on clinical suspicion; do not delay for NAAT/PCR confirmation. Extend the first-episode course if healing is incomplete at 10 days.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Acyclovir | First clinical episode: 400 mg PO 3 times daily for 7-10 days Recurrent episode (episodic): 800 mg PO twice daily for 5 days, or 800 mg PO 3 times daily for 2 days Suppression: 400 mg PO twice daily, reassessed periodically Severe/disseminated disease, adults: 5-10 mg/kg IV every 8 hours until clinical improvement, then switch to oral to complete a total course of at least 10 days HIV-positive, recurrent episode: 400 mg PO 3 times daily, or 200 mg PO 5 times daily, for 5-10 days | Nausea, headache; rare nephrotoxicity | Probenecid can increase levels; additive nephrotoxicity with other nephrotoxic drugs | IV route reserved for severe/disseminated disease or inability to tolerate oral intake. |
| Valacyclovir | First clinical episode: 1 g PO twice daily for 7-10 days Recurrent episode (episodic): 500 mg PO twice daily for 3 days, or 1 g PO once daily for 5 days Suppression, under 10 recurrences/year: 500 mg PO once daily, reassessed periodically Suppression, 10 or more recurrences/year: 1 g PO once daily, reassessed periodically HIV-positive, recurrent episode: 1 g PO twice daily for 5-10 days | Nausea, headache | None clinically significant at these doses | The only agent with a true once-daily suppressive dose; also reduces transmission risk to a discordant partner. |
| Famciclovir | First clinical episode: 250 mg PO 3 times daily for 7-10 days Recurrent episode (episodic), option 1: 1 g PO twice daily for 1 day Recurrent episode (episodic), option 2: 500 mg PO once, then 250 mg PO twice daily for 2 days Recurrent episode (episodic), option 3: 125 mg PO twice daily for 5 days Suppression: 250 mg PO twice daily, reassessed periodically HIV-positive, recurrent episode: 500 mg PO twice daily for 5-7 days | Nausea, headache | None clinically significant at these doses | Comparable efficacy to acyclovir/valacyclovir; several equally valid episodic regimens exist. |
Nucleoside analogues — herpes zoster (shingles)
Most effective within 72 hours of rash onset; still reasonable beyond 72 hours if new vesicles are still forming, the ophthalmic dermatome is involved, or the patient is immunocompromised.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Acyclovir | Standard course, adults: 800 mg PO 5 times daily for 7 days Disseminated disease or significant immunocompromise: 10-15 mg/kg IV every 8 hours; switch to oral once improving, to complete a minimum of 10-14 days total | Nausea, headache; rare nephrotoxicity if inadequately hydrated | Additive nephrotoxicity with other nephrotoxic drugs | Requires the most frequent dosing of the three agents. |
| Valacyclovir | Standard course, adults: 1000 mg PO 3 times daily for 7 days | Nausea, headache | None clinically significant at these doses | Simpler 3-times-daily dosing than acyclovir, at comparable efficacy. |
| Famciclovir | Standard course, adults: 500 mg PO 3 times daily for 7 days | Nausea, headache | None clinically significant at these doses | Comparable efficacy to valacyclovir. |
Combination topical product
A topical option for patients who prefer it; oral therapy remains preferred given the modest effect size of topical agents overall.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Acyclovir / hydrocortisone cream | Recurrent orolabial HSV: Apply 5 times daily during waking hours for 5 days, starting immediately at the first sign of prodrome | Cheilitis, application-site skin reaction, lip swelling | None clinically significant | For recurrent orolabial HSV only. |
Antiviral resistance — alternative agent
Reserve for confirmed or strongly suspected acyclovir-resistant HSV/VZV in an immunocompromised patient.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Foscarnet | Adults: 40 mg/kg IV every 8-12 hours until lesions have healed | Nephrotoxicity; electrolyte disturbances (hypocalcemia, hypomagnesemia, hypokalemia); genital/perineal ulceration; seizure risk with electrolyte derangement | Additive nephrotoxicity with other nephrotoxic drugs; QT-prolonging drugs may compound electrolyte-related arrhythmia risk | Requires IV hydration and close renal/electrolyte monitoring; use under infectious diseases direction. |
Passive immunoprophylaxis — VZV post-exposure
For a significant VZV exposure in a non-immune high-risk patient; does not treat established disease. See Special Populations for the full pregnancy exposure pathway.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Varicella-Zoster Immune Globulin | Adults and pregnant patients: 125 IU/10 kg IM as a single dose (minimum 125 IU, maximum 625 IU), ideally within 96 hours and up to 10 days after exposure Neonates/infants up to 10 kg: 125 IU IM as a single dose (62.5 IU if 2 kg or under) | Injection-site discomfort; rare hypersensitivity | None clinically significant | Give as soon as possible after a significant exposure. |
Prevention — vaccine (not a treatment for active disease)
Brief cross-reference only — see Non-Pharmacologic Treatment for the full eligibility discussion.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Recombinant zoster vaccine (glycoprotein E antigen) | Adults 50 years and older: 2 doses IM, 2-6 months apart Immunocompromised adults 18 years and older: 2 doses IM, 2-6 months apart | Injection-site pain, redness, and swelling; myalgia, fatigue, headache, shivering, fever, GI symptoms | None clinically significant | Preferred over the older live-attenuated zoster vaccine; can be started at least 1 year after an acute zoster episode. |
Evidence note: drug inventory, dosing, adverse effects, and comments reflect standard Canadian practice, cross-checked against current CDC STI treatment guidance[1], IDSA herpes zoster management guidance[2], and Cochrane systematic review evidence on orolabial HSV prevention and postherpetic neuralgia[5][6].
References
- Sexually Transmitted Infections Treatment Guidelines, 2021 — MMWR Recommendations and Reports, Centers for Disease Control and Prevention (Workowski KA, Bachmann LH, Chan PA, et al.). MMWR Recomm Rep 2021;70(4):1-187
- Recommendations for the Management of Herpes Zoster — Clinical Infectious Diseases, Infectious Diseases Society of America (Dworkin RH, Johnson RW, Breuer J, et al.). Clin Infect Dis 2007;44(Suppl 1):S1-S26
- Herpes Zoster Ophthalmicus: A Review for the Internist — American Journal of Medicine (Vrcek I, Choudhury E, Durairaj V). Am J Med 2017;130(1):21-26
- Management of Genital Herpes in Pregnancy: ACOG Practice Bulletin, Number 220 — Obstetrics & Gynecology, American College of Obstetricians and Gynecologists. Obstet Gynecol 2020;135(5):e193-e202
- Interventions for prevention of herpes simplex labialis (cold sores on the lips) — Cochrane Database of Systematic Reviews (Chi CC, Wang SH, Delamere FM, et al.). Cochrane Database Syst Rev 2015;(8):CD010095
- Antiviral treatment for preventing postherpetic neuralgia — Cochrane Database of Systematic Reviews (Chen N, Li Q, Yang J, et al.). Cochrane Database Syst Rev 2014;(2):CD006866
- Herpes Zoster and Postherpetic Neuralgia: Prevention and Management — American Family Physician, American Academy of Family Physicians (Saguil A, Kane S, Mercado M, Lauters R). Am Fam Physician 2017;96(10):656-663
- Summary of the National Advisory Committee on Immunization (NACI) Statement: Updated Recommendations on Herpes Zoster Vaccination for Adults Who Are Immunocompromised — Canada Communicable Disease Report, Public Health Agency of Canada (Krishnan R, Baclic O, Howarth A, Tuite A, Andrew M). Can Commun Dis Rep 2026;52(1/2):1-7
- Use of Acyclovir, Valacyclovir, and Famciclovir in the First Trimester of Pregnancy and the Risk of Birth Defects — JAMA (Pasternak B, Hviid A). JAMA 2010;304(8):859-866
- Management of Varicella Infection (Chickenpox) in Pregnancy — SOGC Clinical Practice Guideline No. 274 — Journal of Obstetrics and Gynaecology Canada, Society of Obstetricians and Gynaecologists of Canada (Shrim A, Koren G, Yudin MH, Farine D). J Obstet Gynaecol Can 2012;34(3):287-292
- Treatment of herpes simplex gingivostomatitis with aciclovir in children: a randomised double blind placebo controlled study — BMJ (Amir J, Harel L, Smetana Z, Varsano I). BMJ 1997;314(7097):1800-1803
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.