Aciclovir

What it is

Acyclovir is a laboratory-made copy of a building block of DNA, a purine nucleoside analogue, used against herpes-family viruses. The herpes virus's own enzyme, thymidine kinase, switches it on inside infected cells, and the activated form then blocks the virus's DNA-copying enzyme. Because the activation step depends on a viral enzyme, the drug concentrates its action in cells the virus has already entered. It is taken by mouth, applied to the skin or eye, or given into a vein, and most of it leaves the body unchanged in the urine.

What the research says

The evidence is strongest for severe herpes infections and weakest for preventing the long-term pain that can follow shingles. In biopsy-proved herpes simplex encephalitis a randomised trial found lower mortality with acyclovir than with vidarabine. Taken continuously, it reduces the number of people with recurrent genital herpes who have at least one further outbreak, though Cochrane rates that evidence low quality. For chickenpox in otherwise healthy children it shortens fever by about a day, and Cochrane calls the clinical importance uncertain. A Cochrane review rated as high quality found that oral aciclovir started within 72 hours of the shingles rash does not significantly reduce postherpetic neuralgia, and a large randomised trial found daily acyclovir did not reduce HIV-1 transmission even though it cut genital ulcers by 73%.

Evidence grade: Well established.

How it works

Drug class: Synthetic purine (guanosine) nucleoside analogue antiviral; herpesvirus DNA polymerase inhibitor

Acyclovir is a man-made look-alike of a DNA building block. Herpes simplex and varicella-zoster viruses carry their own enzyme, thymidine kinase, which converts acyclovir into a form the cell's own enzymes then finish activating. The finished molecule jams the virus's DNA-copying machinery in three ways: it competes with the real building block, it gets built into the growing viral DNA chain and stops it, and it disables the viral copying enzyme. Because the first activation step needs a viral enzyme, uninfected cells are largely spared. (Source 1)

What it is used for

• A randomised trial in people with biopsy-proved disease found mortality of 28% with acyclovir versus 54% with vidarabine, and more survivors functioning normally. This is the use with the clearest survival benefit. Evidence: established. (Source 2)
• Pooled placebo-controlled trials show fewer people have at least one recurrence on continuous acyclovir (risk ratio 0.48), but Cochrane rates the evidence low quality because of risk of bias and inconsistency, and found a small-study effect that shrinks the estimate. Evidence: limited. (Source 3)
• The label records placebo-controlled trials showing shorter acute infection and faster lesion healing. The label also states plainly that acyclovir is not a cure and that there are no data on whether it prevents passing the infection to others. Evidence: limited. (Source 1)
• Three randomised trials pooled by Cochrane found about one day less fever and fewer lesions, with no difference in complications or side effects versus placebo. Cochrane says the clinical importance remains uncertain. Evidence: limited. (Source 4)
• Cochrane found high quality evidence that oral aciclovir does not significantly reduce the incidence of postherpetic neuralgia at four or six months, although there was some evidence of less pain at four weeks. Evidence: not-supported. (Source 5)
• In 3408 serodiscordant African couples, daily acyclovir 400 mg twice daily did not reduce HIV-1 transmission (hazard ratio 0.92) despite lowering plasma HIV-1 RNA and cutting HSV-2 genital ulcers by 73%. Evidence: not-supported. (Source 6)

Interactions

• Probenecid (pharmacokinetic study): Probenecid blocks the kidney's handling of acyclovir, so blood levels stay higher for longer. This has been measured for intravenous acyclovir. (Source 1)
• Other medicines that can damage the kidneys (label): Combining acyclovir with other drugs that stress the kidneys raises the chance of kidney injury and of reversible brain and nerve effects. In one hospital cohort the rate of acute kidney injury rose with the number of such drugs given alongside intravenous acyclovir. (Source 1)
• Food and meals generally (pharmacokinetic study): Food does not meaningfully change how much acyclovir is absorbed, so tablets can be taken with or without a meal. Keeping fluid intake up matters more than meal timing, because the drug can crystallise in the kidney when urine is concentrated. (Source 1)
• Alcohol (theoretical): No specific alcohol interaction is documented for acyclovir on the US label or in the reviews read here. Alcohol and aldehyde dehydrogenase are the enzymes that make acyclovir's main metabolite, CMMG, which has been linked to neurotoxicity, so a pharmacological interaction is biologically plausible but has not been tested in people. This is theory, not a measured interaction. (Source 7)

Stopping it

• There is no withdrawal syndrome described for acyclovir, and no tapering schedule. For long-term suppression of genital herpes the US label sets a one-year review point rather than indefinite use, because the natural pattern of recurrences changes over time. (Source 8)
• Suppression does not change the underlying infection, so stopping returns a person to their own recurrence rate. Cochrane's suppression trials only ran two to 12 months, so there is no long-term randomised evidence on what happens after stopping. (Source 3)
• When acyclovir is stopped because of neurotoxicity in someone with poor kidney function, the neurological symptoms described in a dialysis case series resolved gradually after the drug was withdrawn. (Source 9)

What goes wrong

About a third of patients given intravenous acyclovir in one hospital cohort developed acute kidney injury. (Source 10)

• Cohort study, Low certainty.
• Size: 99 patients.
• Who: Patients aged 12 to 80 receiving IV acyclovir, 2019 to 2023, with pre-existing renal disease or raised baseline creatinine excluded.
• How long: Retrospective over the treatment admissions.
• Result: AKI incidence 34.3% (95% CI 24.9 to 43.7); dose reduction needed in 29.3% of AKI cases; AKI rose with the number of concomitant nephrotoxic drugs (P = 0.004)
• Funding: not stated.

The incidence of AKI was 34.3% (n = 34, 95% confidence interval [CI]: 24.9-43.7).

Acyclovir was an independent risk factor for a first episode of acute kidney injury in a national cohort of children treated for cancer. (Source 11)

• Cohort study, Low certainty.
• Size: 1,525 children.
• Who: Paediatric cancer patients treated at one national centre, 2015 to 2021.
• How long: During cancer treatment, with kidney follow-up at one year (n = 1,159)
• Result: 37% experienced AKI; acyclovir identified alongside ifosfamide, amphotericin B and busulfan as a strong independent risk factor; a single AKI episode raised later CKD risk 2.6-fold.
• Funding: not stated.

A competing risk model identified treatment with ifosfamide, amphotericin B, acyclovir, and busulfan as strong, independent risk factors for a first episode of AKI.

Acyclovir and valacyclovir can cause neuropsychiatric toxicity in people with severe kidney impairment, including those on dialysis. (Source 9)

• Case series, Very low certainty.
• Size: Three patients.
• Who: Adults on automated peritoneal dialysis treated for herpes zoster.
• How long: Symptoms appeared 2 to 4 days after starting treatment.
• Result: Confusion, psychomotor agitation, hallucinations, dysarthria, ataxia, involuntary leg movements; all resolved after the drug was stopped.
• Funding: not stated.

Here, we report three cases of automated peritoneal dialysis patients treated for herpes zoster who developed neurotoxicity following acyclovir or valacyclovir administration.

Acyclovir kidney injury is attributed largely to the drug crystallising inside the kidney tubules, while the neurotoxicity mechanism is still unknown. (Source 7)

• Expert review, not systematic, Very low certainty.
• Size: Narrative review, no pooled sample.
• Who: People receiving acyclovir, mainly intravenously.
• How long: Not applicable.
• Result: 15 to 20% of acyclovir is converted to the metabolite CMMG; serum CMMG above 10 micromol/mL and CSF above 1 micromol/mL have been linked to neurotoxicity.
• Funding: not stated.

Acyclovir nephrotoxicity is primarily attributed to the crystallization of acyclovir within the renal tubules

Reports to the FDA adverse event system for neonates given acyclovir show disproportionate signals for skin, general, liver and kidney events. (Source 12)

• Survey study, Very low certainty.
• Size: 130 reports comprising 409 adverse events.
• Who: Neonates 28 days old or younger with acyclovir as primary suspect drug, 2004 to Q3 2024.
• How long: Spontaneous reports, no fixed follow-up.
• Result: Skin and subcutaneous tissue disorders ROR 6.22; general disorders ROR 4.27; hepatobiliary ROR 3.85; renal and urinary ROR 3.84; strongest preferred term infusion site necrosis/edema ROR 939.92 (95% CI 97.56 to 9055.25)
• Funding: not stated.

Four system organ classes showed positive risk signals: skin and subcutaneous tissue disorders (ROR = 6.22, PRR = 5.88, lower limit of 95% confidence interval [CI] of the information component [IC025] = 1.98, lower limit of 95% CI of EBGM [EBGM05] = 4.16)

The label records nausea and vomiting about four times as often as placebo in genital herpes treatment trials, and malaise at placebo-level rates in shingles trials. (Source 13)

• Official position, Moderate certainty.
• Size: 298 acyclovir and 287 placebo patient-treatments (genital herpes); 323 and 323 (zoster)
• Who: Adults in the registration trials summarised on the US label.
• How long: 10 days (genital herpes); 7 to 10 days (zoster); one year (suppression)
• Result: Nausea and/or vomiting 2.7% vs 0.7% placebo; malaise in zoster trials 11.5% vs 11.1% placebo; one-year suppression nausea 4.8% and diarrhoea 2.4%, against diarrhoea 2.7%, nausea 2.4% and headache 2.2% in 589 controls treated only intermittently.
• Funding: industry data submitted for registration.

nausea and/or vomiting in 8 of 298 patient treatments (2.7%). Nausea and/or vomiting occurred in 2 of 287 (0.7%) patients who received placebo.

Rare but serious harms recorded in post-marketing use include renal failure and thrombotic thrombocytopenic purpura or haemolytic uraemic syndrome, which has caused deaths in immunocompromised patients. (Source 14)

• Official position, Low certainty.
• Size: Not quantified; spontaneous post-marketing reports.
• Who: People taking acyclovir, including immunocompromised patients.
• How long: Not applicable.
• Result: Reported events include renal failure, renal pain, raised urea and creatinine, haematuria, Stevens-Johnson syndrome, toxic epidermal necrolysis, hepatitis and TTP/HUS with fatalities.
• Funding: regulatory position.

Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS), which has resulted in death, has occurred in immunocompromised patients receiving acyclovir therapy.

What the evidence supports

In biopsy-proved herpes simplex encephalitis, acyclovir halved mortality compared with vidarabine in a randomised trial. (Source 2)

• Randomized trial, Moderate certainty.
• Size: 208 randomised; 69 with biopsy-proved disease (37 vidarabine, 32 acyclovir)
• Who: Patients who underwent brain biopsy for presumptive herpes simplex encephalitis.
• How long: 10 days of treatment; outcomes at 6 months.
• Result: Mortality 28% with acyclovir vs 54% with vidarabine (P = 0.008); functioning normally at 6 months 12/32 (38%) vs 5/37 (14%), P = 0.021.
• Funding: not stated.

The mortality in the vidarabine recipients was 54 percent, as compared with 28 percent in the acyclovir recipients (P = 0.008).

Continuous suppressive acyclovir reduced the proportion of people with at least one genital herpes recurrence, on low quality evidence. (Source 3)

• Systematic review, Low certainty.
• Size: 2,049 participants across nine parallel-group acyclovir-versus-placebo trials (26 trials, 6,950 participants in the whole review)
• Who: Non-pregnant, HIV-negative adults with at least four genital herpes recurrences a year; mean 11 recurrences a year.
• How long: Two to 12 months of treatment.
• Result: Pooled RR of at least one clinical recurrence 0.48 (95% CI 0.39 to 0.58); adjusted for small-study effects 0.61 (95% CI 0.49 to 0.75)
• Funding: not stated.

there was a low quality evidence that the risk of having at least one clinical recurrence was reduced with acyclovir (nine parallel-group trials, n = 2049; pooled RR 0.48, 95% confidence interval (CI) 0.39 to 0.58)

In otherwise healthy children with chickenpox, acyclovir shortened fever by about one day and reduced the maximum number of lesions. (Source 4)

• Systematic review, Low certainty.
• Size: Three randomised trials (Jadad quality 3 to 4)
• Who: Otherwise healthy children and adolescents aged 0 to 18 with chickenpox.
• How long: Treatment courses of about 5 to 7 days.
• Result: Days with fever -1.1 days (95% CI -1.3 to -0.9); maximum lesions -76 (95% CI -145 to -8)
• Funding: not stated.

Acyclovir was associated with a reduction in the number of days with fever (-1.1 days, 95% CI -1.3 to -0.9) and in reducing the maximum number of lesions (-76 lesions, -145 to -8).

What the evidence does not support

Cochrane concluded the clinical importance of treating chickenpox in otherwise healthy children with acyclovir remains uncertain. (Source 4)

• Systematic review, Low certainty.
• Size: Three randomised trials.
• Who: Otherwise healthy children and adolescents with chickenpox.
• How long: Short courses within the trials.
• Result: Results 'less supportive' for days to no new lesions and days to relief of itching; no clinically important difference in complications or adverse effects versus placebo.
• Funding: not stated.

The clinical importance of acyclovir treatment in otherwise healthy children remains uncertain.

Oral aciclovir started within 72 hours of the shingles rash did not significantly reduce postherpetic neuralgia, on high quality evidence. (Source 5)

• Systematic review, High certainty.
• Size: 609 participants across three trials for the four-month outcome (six RCTs, 1,211 participants in the review)
• Who: Mostly immunocompetent adults with herpes zoster treated within 72 hours of rash onset.
• How long: Outcomes at four weeks, four months and six months.
• Result: PHN at four months RR 0.75 (95% CI 0.51 to 1.11); at six months RR 1.05 (95% CI 0.87 to 1.27); some evidence of less pain at four weeks.
• Funding: not stated.

There is high quality evidence that oral aciclovir does not reduce the incidence of PHN significantly.

Daily acyclovir did not reduce HIV-1 transmission between serodiscordant partners, despite cutting HSV-2 genital ulcers by 73%. (Source 6)

• Randomized trial, High certainty.
• Size: 3,408 couples at 14 African sites; 84 genetically linked seroconversions.
• Who: Couples where one partner had HIV-1 (CD4 at least 250) plus HSV-2 and was not on antiretroviral therapy.
• How long: Up to 24 months; 92% and 84% retention.
• Result: Hazard ratio 0.92 (95% CI 0.60 to 1.41; P = 0.69); plasma HIV-1 RNA fell 0.25 log10 copies/mL; HSV-2-positive genital ulcers fell 73% (RR 0.27, 95% CI 0.20 to 0.36)
• Funding: not stated in the abstract (Partners in Prevention HSV/HIV Transmission Study Team)

Daily acyclovir therapy did not reduce the risk of transmission of HIV-1, despite a reduction in plasma HIV-1 RNA of 0.25 log10 copies per milliliter

Where the evidence is mixed

The apparent size of acyclovir's suppressive benefit shrinks once small-study bias is accounted for, and no dose-response relationship was found. (Source 3)

• Systematic review, Low certainty.
• Size: 16 parallel-arm trials in the network meta-analysis; 22 trials analysed for recurrence.
• Who: Adults with recurrent genital herpes.
• How long: Two to 12 months.
• Result: Adjusted pooled RR 0.61 (95% CI 0.49 to 0.75) after correcting for the small-study effect; no clear dose-response by daily dose.
• Funding: not stated.

We found evidence of a small-study effect for acyclovir placebo-controlled trials (adjusted pooled RR 0.61, 95% CI 0.49 to 0.75).

Where the research disagrees

Whether starting aciclovir early in shingles prevents the long-term nerve pain that can follow

• Cochrane review authors (Chen and colleagues, 2014), Systematic review and meta-analysis of six RCTs, 1,211 participants: "There is high quality evidence that oral aciclovir does not reduce the incidence of PHN significantly." (Source 5)
• US prescribing information for acyclovir tablets (DailyMed, 2026), Regulatory position based on the registration trials: "There are no data on treatment initiated more than 72 hours after onset of the zoster rash. Patients should be advised to initiate treatment as soon as possible after a diagnosis of herpes zoster." (Source 1)

How confident we can be that suppressive acyclovir prevents genital herpes recurrences

• Cochrane review authors (Le Cleach and colleagues, 2014), Systematic review and network meta-analysis, 26 trials: "Owing to risk of bias and inconsistency, there is low quality evidence that suppressive antiviral therapy with acyclovir, valacyclovir or famciclovir in pacients experiencing at least four recurrences of genital herpes per year decreases the number of pacients with at least one recurrence as compared with placebo." (Source 3)
• US prescribing information for acyclovir tablets (DailyMed, 2026), Regulatory position; the label approves the regimen but requires yearly re-evaluation: "Chronic Suppressive Therapy for Recurrent Disease: 400 mg 2 times daily for up to 12 months, followed by re-evaluation." (Source 8)

How much

• Reference intake: There is no reference intake for a prescription antiviral. Dosing is set by the prescriber and differs by indication: the US label (DailyMed, acyclovir tablet, 2026) gives 800 mg every 4 hours five times daily for 7 to 10 days for acute herpes zoster, and 200 mg five times daily for 10 days for an initial genital herpes episode. (Source 8)
• Upper limit: There is no dietary upper limit. The highest oral regimen on the US label (2026) is 800 mg five times daily for herpes zoster, and the label's dosage section requires the dose to be modified in renal impairment. (Source 8)
• Studied: Celum and colleagues (2010) gave acyclovir 400 mg orally twice daily for up to 24 months to HSV-2-positive partners in 3,408 serodiscordant couples. (Source 6)
• Studied: The label's one-year suppression trial used 400 mg (two 200 mg capsules) twice daily in 586 patients. (Source 13)
• Studied: Whitley and colleagues (1986) gave intravenous acyclovir 30 mg per kilogram per day for 10 days in herpes simplex encephalitis. (Source 2)
• Studied: Cochrane's suppression review pooled trials lasting two to 12 months in people with at least four recurrences a year. (Source 3)

A common belief, and what the research shows

The belief: Acyclovir clears herpes from the body and stops you passing it on.

What the research shows: The US label states plainly: "Patients should be informed that acyclovir is not a cure for genital herpes. There are no data evaluating whether acyclovir will prevent transmission of infection to others." The largest randomised test of that idea went the other way for a related question: in 3,408 couples, daily acyclovir cut HSV-2 genital ulcers by 73% yet "Daily acyclovir therapy did not reduce the risk of transmission of HIV-1, despite a reduction in plasma HIV-1 RNA of 0.25 log10 copies per milliliter".

Questions and answers

What is it?

Acyclovir is a prescription antiviral medicine, not a nutrient. It is a synthetic copy of a DNA building block that works against herpes simplex viruses 1 and 2 and varicella-zoster virus, the virus behind chickenpox and shingles. It comes as tablets, capsules, liquid, creams and ointments, and as an infusion into a vein for severe infection. (Source 1)

What does it do in the body?

Inside a cell the virus has infected, a viral enzyme called thymidine kinase switches acyclovir on. The activated drug then jams the virus's DNA-copying enzyme, so the virus cannot make new copies of itself. Because that first switch depends on a viral enzyme, the drug acts mostly where the virus already is. It suppresses the virus while you take it; it does not remove the virus from the body. (Source 1)

Is it good or bad for you?

It depends entirely on the situation. In herpes simplex encephalitis, a life-threatening brain infection, a randomised trial found mortality of 28% with acyclovir versus 54% with the older drug, so the benefit is large. For shingles, a Cochrane review rated high quality found it does not reduce the long-term nerve pain that can follow. In people with poor kidney function or on high intravenous doses it can injure the kidneys or cause confusion and hallucinations. The same drug is clearly worth it in one setting and of uncertain value in another. (Source 2)

How do you get more of it?

Acyclovir is only available on prescription in the oral and intravenous forms; some topical creams for cold sores are sold over the counter in various countries. Trials have used widely different amounts for different conditions: 200 mg five times a day for ten days for a first genital herpes episode, 400 mg twice a day for suppression, and 800 mg five times a day for shingles. There is no food or supplement that supplies it, and nothing here is advice about what anyone should take. (Source 8)

If it is harmful, what reduces it?

Acyclovir leaves the body mainly through the kidneys, unchanged, with a plasma half-life of about 2.5 to 3.3 hours in people with normal kidney function, so it clears within a day or so of the last dose. When it has built up and caused confusion or kidney injury, the reported management is stopping the drug, adjusting the dose to kidney function, keeping fluid intake up, and in severe cases dialysis; a case series in peritoneal dialysis patients described symptoms resolving after the drug was withdrawn. (Source 7)

Why might someone be low in it or missing it?

Nobody is naturally low in acyclovir, because the body does not make it. People who might not be getting enough of it when they need it include those who cannot swallow or absorb tablets, those prescribed a reduced dose because of kidney impairment, and those whose virus has become resistant. Resistance arises when the virus loses or alters the thymidine kinase enzyme that activates the drug, which is mainly a problem in immunocompromised people. (Source 1)

Which whole foods contain it or feed it?

No whole food contains acyclovir; it is a laboratory-made molecule. Food is relevant only in that it does not interfere with absorption, so tablets work equally well with or without a meal. The fluid you drink matters more than what you eat, because the drug can crystallise inside the kidney tubules when urine is concentrated. (Source 1)

What happens if you do not have it?

What happens without acyclovir depends on the infection. Untreated herpes simplex encephalitis is often fatal: in the randomised trial the comparison arm had 54% mortality. For frequently recurring genital herpes, people off suppressive treatment have more outbreaks, since the drug reduces the proportion with at least one recurrence from the placebo rate. For shingles pain lasting months, the Cochrane evidence suggests taking aciclovir makes no significant difference either way. (Source 2)

How can you test for it?

Routine blood level testing of acyclovir is not standard. What is monitored is kidney function, because the dose has to be adjusted to it and because kidney injury is the main dose-related harm; in one hospital cohort 34.3% of patients given it intravenously developed acute kidney injury. Research has linked levels of the metabolite CMMG above 10 micromol/mL in serum and 1 micromol/mL in cerebrospinal fluid to neurotoxicity, but this is a research measure rather than a validated routine test. The infection itself is tested for separately, by PCR or serology, not by measuring the drug. (Source 7)

References

1. DailyMed, U.S. National Library of Medicine (American Health Packaging). ACYCLOVIR- acyclovir tablet (prescribing information). 2026. Read the source
2. The New England Journal of Medicine (abstract read via Europe PMC REST). Vidarabine versus acyclovir therapy in herpes simplex encephalitis. 1986. PMID 3001520, DOI 10.1056/NEJM198601163140303. Read the source
3. Cochrane Database of Systematic Reviews (abstract read via Europe PMC REST). Oral antiviral therapy for prevention of genital herpes outbreaks in immunocompetent and nonpregnant patients. 2014. PMID 25086573, DOI 10.1002/14651858.CD009036.pub2. Read the source
4. Cochrane Database of Systematic Reviews (abstract read via Europe PMC REST). Acyclovir for treating varicella in otherwise healthy children and adolescents. 2005. PMID 16235308, DOI 10.1002/14651858.CD002980.pub3. Read the source
5. Cochrane Database of Systematic Reviews (abstract read via Europe PMC REST). Antiviral treatment for preventing postherpetic neuralgia. 2014. PMID 24500927, DOI 10.1002/14651858.CD006866.pub3. Read the source
6. The New England Journal of Medicine (author/institutional PDF copy, University of Washington CFAR). Acyclovir and Transmission of HIV-1 from Persons Infected with HIV-1 and HSV-2. 2010. PMID 20089951, DOI 10.1056/NEJMoa0904849. Read the source
7. Medicines (Basel) (abstract read via Europe PMC REST). The Role of Metabolites in Acyclovir-Induced Neurotoxicity and Nephrotoxicity. 2026. PMID 41718166, DOI 10.3390/medicines13010006. Read the source
8. DailyMed, U.S. National Library of Medicine (American Health Packaging). ACYCLOVIR- acyclovir tablet (prescribing information): DOSAGE AND ADMINISTRATION. 2026. Read the source
9. Peritoneal Dialysis International (abstract read via Europe PMC REST). Neurotoxicity from acyclovir and valacyclovir in patients undergoing peritoneal dialysis: Still rare, but still present. 2026. PMID 41610264, DOI 10.1177/08968608261415988. Read the source
10. Sultan Qaboos University Medical Journal (abstract read via Europe PMC REST). Assessing Renal Dysfunction Incidence Related to Intravenous Acyclovir Usage. 2026. PMID 42549298, DOI 10.18295/2075-0528.2996. Read the source
11. Nephrology Dialysis Transplantation (abstract read via Europe PMC REST). Nephrotoxicity and kidney outcomes in pediatric oncology patients. 2026. PMID 40844823, DOI 10.1093/ndt/gfaf169. Read the source
12. Medicine (Baltimore) (abstract read via Europe PMC REST). Safety analysis of acyclovir use in neonates based on the FDA Adverse Event Reporting System: A retrospective observational pharmacovigilance study. 2026. PMID 42675701, DOI 10.1097/MD.0000000000050426. Read the source
13. DailyMed, U.S. National Library of Medicine (American Health Packaging). ACYCLOVIR- acyclovir tablet (prescribing information): ADVERSE REACTIONS. 2026. Read the source
14. DailyMed, U.S. National Library of Medicine (American Health Packaging). ACYCLOVIR- acyclovir tablet (prescribing information): WARNINGS and PRECAUTIONS. 2026. Read the source