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PubMed1999

Determination of acyclovir in plasma by solid-phase extraction and column liquid chromatography.

After oral administration, valacyclovir, the L-valyl ester of acyclovir, converts to the antiherpes virus drug, acyclovir. The bioavailability of acyclovir after valacyclovir administration is between 3- to 4.5-fold higher than that achieved after oral acyclovir administration. Therefore, despite the drug's short terminal half-life (3 hours), acyclovir plasma concentrations obtained after oral administration of the prodrug offer a more convenient dosage regimen in patients with herpes zoster than that required after acyclovir administration. Acyclovir is also used for viral infection prophylaxis in patients with hematologic disorders and in those who have undergone solid organ transplantation. We have described a simple and selective liquid chromatographic method for the determination of acyclovir in plasma using a new polymeric reversed-phase sorbent for solid-phase extraction. A mean acyclovir absolute recovery of 90% was found after elution of the drug from the cartridge with the mobile phase. This procedure allowed us to measure 62.5 ng/mL of acyclovir with an acceptable precision using a plasma volume of 250 microL, and no drug was found to interfere with the assay. This method is suitable for the therapeutic monitoring of acyclovir in patients who have been given a wide variety of coadministered drugs.

Acyclovir↗
PubMed1999

Advances in antiviral therapy.

Multiple agents for the treatment and prevention of viral illnesses have been developed during the past few years. While in many cases this has been in direct response to the human immunodeficiency virus type 1 epidemic, a number of new antiviral agents are relevant to the practice of general pediatrics. This article reviews recent advances in the therapy of some common and a few unusual viral illnesses of children. The indication and efficacy of the newly developed agents valacyclovir, famciclovir, cidofovir, oral and intraocular ganciclovir, adefovir, respiratory syncytial virus immune globulin, palivizumab, and imiquimod are discussed, as well new uses of acyclovir, lamivudine, and ribavirin. Many of the antivirals discussed, including valacyclovir and cidofovir, have not yet been studied in children, but they hold promise for improving the treatment of pediatric viral infections.

Antiviral Agents↗
PubMed2003

Systemic acyclovir reaction subsequent to acyclovir contact allergy: which systemic antiviral drug should then be used?

Allergic contact dermatitis caused by acyclovir is rare. We report the 5th case of systemic acyclovir reaction subsequent to acyclovir contact dermatitis, with investigations made to determine an alternative antiviral treatment. A 23-year-old woman, after dermatitis while using Zovirax cream, went on to develop urticaria after oral acyclovir. Patch tests were performed with the components of Zovirax cream (acyclovir, propylene glycol and sodium lauryl sulfate) and with other antiviral drugs. Patch tests were positive to Zovirax cream, acyclovir, valacyclovir and propylene glycol. Patch and prick tests with famciclovir were negative, but its oral administration caused an itchy erythematous dermatitis on the trunk and extremities. Our patient developed a systemic acyclovir reaction subsequent to acyclovir allergic contact dermatitis, with cross-reactions to valacyclovir and famciclovir. Their common chemical structure is the 2-aminopurine nucleus. It is probably this part of the molecule that provokes both contact allergy and systemic reactions. The only antiviral drugs not having this core are foscarnet and cidofovir, and these could therefore be alternatives.

Acyclovir↗
PubMedDate not supplied

Penciclovir cream--improved topical treatment for herpes simplex infections.

Human herpesviruses can be found worldwide and cause many viral infections in immunocompetent as well as in immunocompromised patients. Herpes simplex virus (HSV) diseases can be the cause of life-threatening disease, especially in neonates. After initial infection, HSV persists latently in host neurons with the risk of periodical reactivation over a lifetime. The development of acyclovir, a potent and specific nucleoside inhibitor of the herpes DNA polymerase, was a milestone in the history of antiviral drugs in the late 1970s. During the last decades a better understanding of the replication and disease-causing state of HSV types 1 and 2 has been achieved enabling the development of new and potent antiviral compounds. In the mid-1990s, for example, valacyclovir and famciclovir were launched as prodrugs of acyclovir with improved bioavailability. Despite the numerous drugs available for the systemic treatment of HSV infections, the topical application of a cream containing an antiviral agent is still the most convenient method of treating herpes simplex labialis/facialis in the general population. For some time, the topical standard treatment for recurrent HSV infections has been acyclovir cream, despite the fact that the evidence for efficacy in recurrent episodes has been equivocal. Penciclovir, a novel acyclic nucleoside analogue, has demonstrated efficacy against HSV types 1 and 2 and seems to have a pharmacological advantage due to a prolonged half-life of its active form in HSV-infected cells. This review discusses and compares the topical treatment modalities available for HSV infections. As a conclusion, different studies are available that have shown that it is possible to reduce viral replication and hasten lesion resolution with 1% penciclovir treatment beyond the prodromal phase of the HSV infection. Comparing data of topical treatment with acyclovir and penciclovir revealed a superiority for penciclovir cream showing a significant decrease in time to lesion healing, lesion area and pain. While systemic acyclovir or valacyclovir may be valid drugs especially for HSV prophylaxis, 1% penciclovir cream should be preferred as topical treatment since there are good therapeutic results independent of the phase of development of herpetic eruptions.

Acyclovir↗
PubMed2003

Short-course oral antiviral treatment for recurrent genital herpes.

OBJECTIVE: To evaluate the literature regarding short-course oral therapy for recurrent genital herpes. DATA SOURCES: Literature was accessed through MEDLINE (1966-March 2003), IOWA Drug Information Service (1966-March 2003), and International Pharmaceutical Abstracts (1966-March 2003). DATA SYNTHESIS: Data are available describing short-course (2 or 3 d) therapy with acyclovir and valacyclovir. Short-course acyclovir therapy was superior to placebo. Three- and 5-day regimens of valacyclovir were equivalent. Early initiation of therapy may be more important than duration of therapy. CONCLUSIONS: More head-to-head studies are needed to determine the most efficacious and cost-effective short-course regimens for recurrent genital herpes.

Administration, Oral↗
PubMed2003

Novel agents and strategies to treat herpes simplex virus infections.

The quiet pandemic of herpes simplex virus (HSV) infection has plagued humanity since ancient times, causing mucocutaneous infection, such as herpes labialis and herpes genitalis. Disease symptoms often interfere with everyday activities and occasionally HSV infections are the cause of life-threatening or sight-impairing disease, especially in neonates and the immunocompromised patient population. After primary or initial infection the virus persists for life in a latent form in neurons of the host, periodically reactivating and often resulting in significant psychosocial distress for the patient. Currently, no cure is available. In the mid-1950s the first antiviral, idoxuridine, was developed for topical treatment of herpes disease and, in 1978, vidarabine was licensed for systemic use to treat HSV encephalitis. Acyclovir (Zovirax), a potent, specific and tolerable nucleosidic inhibitor of the herpes DNA polymerase, was a milestone in the development of antiviral drugs in the late 1970s. In the mid-1990s, when acyclovir became a generic drug, valacyclovir (Valtrex) and famciclovir (Famvir), prodrugs of the gold standard and penciclovir (Denavir), Vectavir), a close analogue, were launched. Though numerous approaches and strategies were tested and considerable effort was expended in the search of the next generation of an antiherpetic therapy, it proved difficult to outperform acyclovir. Notable in this regard was the award of a Nobel Prize in 1988 for the elucidation of mechanistic principles which resulted in the development of new drugs such as acyclovir. Vaccines, interleukins, interferons, therapeutic proteins, antibodies, immunomodulators and small-molecule drugs with specific or nonspecific modes of action lacked either efficacy or the required safety profile to replace the nucleosidic drugs acyclovir, valacyclovir, penciclovir and famciclovir as the first choice of treatment. Recently though, new inhibitors of the HSV helicase-primase with potent in vitro antiherpes activity, novel mechanisms of action, low resistance rates and superior efficacy against HSV in animal models have been discovered. This review summarises the current therapeutic options, discusses the potential of preclinical or investigational drugs and provides an up-to-date interpretation of the challenge to establish novel treatments for herpes simplex disease.

Animals↗
PubMed2005

Splenectomy for severe autoimmune cytopenias after allogenic stem cell transplantation: case report.

Autoimmune cytopenias are rare but serious complications after hematopoietic stem cell transplantation (HSCT). We per-formed splenectomy in 2 patients who had severe autoimmune cytopenias after allogeneic HSCT (allo-HSCT) that were resist-ant to immunosuppressive treatment. The first patient underwent unrelated allo-HSCT for chronic granulocytic leukemia(CGL) in July 2000. Seven months later, red blood cell and platelet counts went down. The results of a direct Coombs test were intermittently positive. The patient was resistant to therapy with steroids and high-dose immunoglobulin. After a splenectomy was performed in February 2001, the hemoglobin concentration and platelet count improved. Her blood counts remained stable, with a hemoglobin level of approximately 110 g/L and a platelet count >100 x 109/L. She continued therapy with itraconazole, valacyclovir, and penicillin. Some months later, the patient was readmitted for fulminant septic infection, which had a fatal outcome. The second patient underwent related allo-SCT for CGL in January 2003. Seven months later, he was readmitted for intraocular bleeding accompanied by severe thrombocytopenia with antiplatelet antibodies. The patient was resistant to steroid and high-dose immunoglobulin therapy. A splenectomy was performed in September 2003. His platelet count normalized and remains stable. The patient continues therapy with itraconazole, valacyclovir, and penicillin and has not experienced any serious infection. We assume that splenectomy is an effective treatment for resistant immune cytopenias after allo-HSCT. However, severe late infections can compromise the outcome.

Adult↗
PubMed2002

Oral antivirals revisited in the treatment of herpes zoster: what do they accomplish?

Oral antiviral agents currently represent the most important therapeutic keystone in the treatment of herpes zoster. Three oral antiviral agents are available for the treatment of herpes zoster: acyclovir, its derivative valacyclovir, and famciclovir. Meta-analysis of published data has shown that oral acyclovir significantly reduces various herpes zoster-related symptoms as well as the duration, intensity and prevalence of zoster-associated pain (ZAP). However, this drug does not influence postherpetic neuralgia. The newer agents famciclovir and valacyclovir exhibit a better oral bioavailability than acyclovir. These agents have demonstrated similar efficacy to acyclovir with ZAP and they require less frequent administration. When initiated within 72 hours, oral antiviral therapy of herpes zoster is beneficial in selected, elderly immunocompetent patients, reducing the duration and intensity of ZAP and providing more rapid skin lesion healing. Oral antivirals are also of benefit in immunocompromised patients with uncomplicated herpes zoster. However, signs of cutaneous and visceral dissemination should be monitored; if signs occur, intravenous antiviral therapy is indicated.

Administration, Oral↗
PubMed1999

Drug treatment of common STDs: part I. Herpes, syphilis, urethritis, chlamydia and gonorrhea.

In 1998, the Centers for Disease Control and Prevention released guidelines for the treatment of sexually transmitted diseases. Several treatment advances have been made since the previous guidelines were published. Part I of this two-part article describes current recommendations for the treatment of genital ulcer diseases, urethritis and cervicitis. Treatment advances include effective single-dose regimens for many sexually transmitted diseases and improved therapies for herpes infections. Two single-dose regimens, 1 g of oral azithromycin and 250 mg of intramuscular ceftriaxone, are effective for the treatment of chancroid. A three-day course of 500 mg of oral ciprofloxacin twice daily may be used to treat chancroid in patients who are not pregnant. Parenteral penicillin continues to be the drug of choice for treatment of all stages of syphilis. Three antiviral medications have been shown to provide clinical benefit in the treatment of genital herpes: acyclovir, valacyclovir and famciclovir. Valacyclovir and famciclovir are not yet recommended for use during pregnancy. Azithromycin in a single oral 1-g dose is now a recommended regimen for the treatment of nongonococcal urethritis.

Anti-Infective Agents↗
PubMed2000

Does treatment of acute herpes zoster prevent or shorten postherpetic neuralgia?

OBJECTIVE: Our goal was to determine if any treatment of acute herpes zoster alters the incidence or duration of postherpetic neuralgia (PHN), a common sequela in elderly patients. SEARCH STRATEGY: We systematically searched MEDLINE and The Cochrane Library. We also examined the reference lists of identified trials and reviews. SELECTION CRITERIA: We included all randomized controlled trials of treatments of zoster published in English that included assessment of pain at any time after rash healing. DATA COLLECTION/ANALYSIS: Forty-two trials met inclusion criteria, and 2 reviewers independently evaluated them for methodologic quality and the statistical and clinical significance of results. MAIN RESULTS: Four placebo-controlled trials of oral acyclovir with 692 patients provided marginal evidence for reduction in pain incidence at 1 to 3 months following zoster onset. Famciclovir significantly reduced duration but not incidence of PHN in one placebo-controlled trial of 419 patients. Valacyclovir significantly reduced duration but not incidence of PHN in one acyclovir-controlled trial of 1141 patients. Steroids had no effect on PHN. Amitriptyline for 90 days reduced pain incidence at 6 months in one placebo-controlled trial of 80 patients. A single trial of percutaneous electrical nerve stimulation (PENS) in 50 patients suggested a decrease in pain incidence at 3 and 6 months compared with famciclovir. CONCLUSIONS: There is limited evidence that current interventions prevent or shorten PHN. Famciclovir and valacyclovir have been shown to reduce the duration of PHN in single published trials. Well-designed and larger trials of amitriptyline and PENS should be conducted.

Acute Disease↗
PubMedDate not supplied

[Efficacy of cidofovir in an HIV infected patient with an acyclovir and foscarnet resistant herpes simplex virus infection].

BACKGROUND: We report the case of an AIDS patient, whose persistant HSV2 ulceration was clinically and phenotypically resistant to acyclovir and foscarnet. Only five clinical isolates of simultaneous acyclovir and foscarnet resistance have been previously described. CASE REPORT: This patient, without history of opportunistic infection, was hospitalized for a recurrent scrotal ulceration resistant to several antiviral treatment such as acyclovir, valacyclovir or foscarnet. The CD4 count was stable at 150/mm(3) and the HIV viral load was below detection level. The last recurrence appeared rapidly under valacyclovir therapy which had been introduced after 65 days of foscarnet therapy. Thus, the patient received a new dose of foscarnet. After initial efficacy, the ulceration increased once again. HSV2 phenotypic determination was done and detected, at that time, a double resistance to acyclovir and foscarnet. Healing was obtained with intravenous cidofovir. DISCUSSION: Foscarnet and acyclovir resistance in an HSV2 isolate is rare. This report presents several particularities. First, whereas the earlier published patients with an acyclovir and foscarnet resistant strain were widely immunocompromised, this was not the case for our patient. Secondly, in contrast with most precedent observations in which acyclovir-resistant strain disappeared after foscarnet therapy, in our case the acyclovir resistant strain remained after foscarnet therapy. Finally, few reports concerned the clinical efficacy of cidofovir in HSV infection. In this case, we proved that intravenously cidofovir was highly and rapidly effective on acyclovir and foscarnet resistant strains.

AIDS-Related Opportunistic Infections↗
PubMed2005

Observations on recovery from and recurrence of HSV-2 infections in adult mice that were rescued from lethal vaginal infection by antiviral therapy.

An adult mouse model for studies of latency and recurrence after vaginal HSV-2 infection is not available at present, largely because the infection kills most mice within 14 days. We describe here an antiviral therapy that rescues most vaginally infected mice from death. Vaginally infected mice were nearly all rescued by combined treatment with one dose of monoclonal anti-HSV glycoprotein D 3 days after infection plus valacyclovir in the drinking water on days 3, 4, 5, 7, 9, 11, 13, and 15 after infection. At 60 days after infection, PCR measurements revealed that most rescued mice had viral DNA in their lumbosacral dorsal root ganglia, lumbosacral spinal cords, and paracervical autonomic ganglia, consistent with the possibility that latent infections were established. At this time, immunolabeling revealed CD45+ lymphoid cells in these neural tissues in rescued mice but not in normal control mice. In vivo depletion of T lymphocytes with monoclonal antibodies caused a recurrence of herpes illness symptoms earlier and in a larger proportion of rescued mice than was observed in non-depleted rescued mice. Interestingly, many rescued mice (46/114) spontaneously developed a syndrome of typical herpes illness symptoms that began with ruffled fur on a mouse that previously had sleek fur and progressed to arched backs, feeble gait, hindlimb paralysis, and death or euthanasia, or in some cases to recovery to health. This high incidence of apparent spontaneous recurrence of HSV-2 infection in rescued mice suggests that it may be possible, with some refinement of the procedure, to obtain an effective adult mouse model for studies of therapeutic vaccination to inhibit or prevent HSV-2 recurrence after genital tract infection.

Acyclovir↗
PubMed2005

The functional evaluation of human peptide/histidine transporter 1 (hPHT1) in transiently transfected COS-7 cells.

Recently, the expression of the human peptide/histidine transporter (hPHT1, SLC15A4) mRNA was observed in the GI tract and in Caco-2 cells, suggesting that it may participate in the intestinal absorption of peptide-based agents. This study aims to elucidate the: (i) protein expression pattern of hPHT1 (SLC15A4) in human small intestine; (ii) cloning of the hPHT1 full-length sequence; (iii) functional characterization of hPHT1 in transiently transfected COS-7 cells. The expression of hPHT1 was measured using Western blot and immunohistochemical analysis. The hPHT1 full-sequence was amplified from BeWo cells, inserted into the pcDNA3.1-V5/His TOPO plasmid and transiently transfected into COS-7 cells to investigate the uptake kinetics of [3H]histidine and [3H]carnosine. Time, pH and sodium-dependent uptake studies were performed in mock (empty vector) and hPHT1-COS-7 cells. Results demonstrated hPHT1 protein expression in different intestinal regions. Histidine and carnosine uptake was linear in hPHT1-COS-7 cells over 15 min and was found to be pH-dependent. These substrates and valacyclovir showed significantly higher uptake at pH 5.0 in the hPHT1 transients when contrasted to the mock COS-7 cells, whereas glycylsarcosine uptake was significantly lower and unaffected by pH. Other di- and tripeptides also showed affinity for hPHT1. This study presents the initial functional characterization, the protein expression of the hPHT1 transporter and provides insight into a potentially different route for increasing peptide and peptide-based drug transport.

Acyclovir↗
PubMed2005

Lymphocytic myocarditis after lung transplantation.

This study reports the development of lymphocytic myocarditis in a bilateral lung allograft recipient. A 23-year-old woman developed congestive heart failure and severe left ventricular dysfunction 32 months after a bilateral lung allograft for cystic fibrosis. She had taken oral acyclovir for infectious mononucleosis that was diagnosed 11 months previously. Her viral load for Epstein-Barr virus (EBV) increased, and an echocardiogram revealed a left ventricular ejection fraction of 25% and endomyocardial biopsy revealed lymphocytic myocarditis. She received valacyclovir (1 g x 3 times daily) and made a full recovery 6 months later.

Acyclovir↗
PubMed2006

Simultaneous modulation of transport and metabolism of acyclovir prodrugs across rabbit cornea: An approach involving enzyme inhibitors.

The aim of this study is to identify the class of enzymes responsible for the hydrolysis of amino acid and dipeptide prodrugs of acyclovir (ACV) and to modulate transport and metabolism of amino acid and dipeptide prodrugs of acyclovir by enzyme inhibitors across rabbit cornea. l-Valine ester of acyclovir, valacyclovir (VACV) and l-glycine-valine ester of acyclovir, gly-val-acyclovir (GVACV) were used as model compounds. Hydrolysis studies of VACV and GVACV in corneal homogenate were conducted in presence of various enzyme inhibitors. IC(50) values were determined for the enzyme inhibitors. Transport studies were conducted with isolated rabbit corneas at 34 degrees C. Complete inhibition of VACV hydrolysis was observed in the presence of Pefabloc SC (4-(2-aminoethyl)-benzenesulfonyl-fluoride) and PCMB (p-chloromercuribenzoic acid). Similar trend was also observed with GVACV in the presence of bestatin. IC(50) values of PCMB and bestatin for VACV and GVACV were found to be 3.81+/-0.94 and 0.34+/-0.08muM respectively. Eserine, tetraethyl pyrophosphate (TEPP) and diisopropyl fluorophosphate (DFP) also produced significant inhibition of VACV hydrolysis. Transport of VACV and GVACV across cornea showed decreased metabolic rate and modulation of transport in presence of PCMB and bestain respectively. The principle enzyme classes responsible for the hydrolysis of VACV and GVACV were carboxylesterases and aminopeptidases respectively. Enzyme inhibitors modulated the transport and metabolism of prodrugs simultaneously even though their affinity towards prodrugs was distinct. In conclusion, utility of enzyme inhibitors to modulate transport and metabolism of prodrugs appears to be promising strategy for enhancing drug transport across cornea.

Acyclovir↗
PubMed2004

Enhanced systemic T-cell activation after in situ gene therapy with radiotherapy in prostate cancer patients.

PURPOSE: In situ cytotoxic gene therapy can potentially trigger a systemic immune response, which could impact occult metastatic disease. We are currently conducting three clinical trials using in situ adenoviral vector mediated herpes simplex virus-thymidine kinase (HSV-tk) gene delivery followed by the HSV-tk prodrug ganciclovir (GCV) or valacyclovir (VCV). This study evaluates the systemic T-cell response after gene therapy in each trial. METHODS AND MATERIALS: The study protocol included three separate clinical trials in the Baylor Prostate Cancer SPORE Program: Trial A gene therapy in prostate cancer patients failing radiotherapy (36 patients), Trial B neoadjuvant gene therapy in pre-radical prostatectomy patients (22 patients), and Trial C gene therapy in combination with radiotherapy for prostate cancer (27 patients). Heparinized blood was collected at the time of vector injection and at selected intervals afterward. A complete blood count was performed, and peripheral blood lymphocytes were analyzed by fluorescent antibody cell sorting after labeling with dual color-labeled antibody pairs. RESULTS: The pretreatment mean percentage of activated CD8+ T cells (DR+CD8+ T cells) was 12.23%, 16.72%, and 14.09% (Trials A, B, and C, respectively). Two weeks posttreatment, this increased to 22.87%, 26.15%, and 39.04% (Trials A, B, and C, respectively), and these increases were statistically significant (p = 0.0188, p = 0.0010, p < 0.0001, respectively). The increase of DR+CD8+ T cells was significantly larger in Trial C than in Trial A (p = 0.0044) or Trial B (p = 0.0288). Total CD8+ T cells significantly increased at 2 weeks posttreatment in Trial B and C (p = 0.0013, p = 0.0004, respectively). Interestingly, only in Trial C were significant increases in activated CD4+ T cells seen at 2 weeks (p = 0.0035). CONCLUSIONS: This is the first report of systemic T-cell responses after HSV-tk+GCV/VCV gene therapy under three clinical trial conditions. There was an increase in activated CD8+ T cells in the peripheral blood after vector injection, suggesting the potential for activation of components of cell-mediated immune response in all trial conditions. The addition of radiotherapy to in situ gene therapy seems to further increase the total CD8+ T cells and activated CD4+ T cells.

Acyclovir↗
PubMed2006

Sustained long-term immune responses after in situ gene therapy combined with radiotherapy and hormonal therapy in prostate cancer patients.

PURPOSE: To explore long-term immune responses after combined radio-gene-hormonal therapy. METHODS AND MATERIALS: Thirty-three patients with prostate specific antigen 10 or higher or Gleason score of 7 or higher or clinical stage T2b to T3 were treated with gene therapy that consisted of 3 separate intraprostatic injections of AdHSV-tk on Days 0, 56, and 70. Each injection was followed by 2 weeks of valacyclovir. Intensity-modulated radiation therapy was delivered 2 days after the second AdHSV-tk injection for 7 weeks. Hormonal therapy was initiated on Day 0 and continued for 4 months or 2.3 years. Blood samples were taken before, during, and after treatment. Lymphocytes were analyzed by fluorescent antibody cell sorting (FACS). RESULTS: Median follow-up was 26 months (range, 4-48 months). The mean percentages of DR+CD8+ T cells were increased at all timepoints up to 8 months. The mean percentages of DR+CD4+ T cells were increased later and sustained longer until 12 months. Long-term (2.3 years) use of hormonal therapy did not affect the percentage of any lymphocyte population. CONCLUSIONS: Sustained long-term (up to 8 to 12 months) systemic T-cell responses were noted after combined radio-gene-hormonal therapy for prostate cancer. Prolonged use of hormonal therapy does not suppress this response. These results suggest the potential for sustained activation of cell-mediated immune responses against cancer.

Acyclovir↗
PubMed2001

Longitudinal analysis of varicella-zoster virus DNA on the ocular surface associated with herpes zoster ophthalmicus.

PURPOSE: Longitudinal analysis of varicella-zoster virus DNA on the ocular surface of patients with herpes zoster ophthalmicus. METHODS: Clinical specimens were obtained from the bulbar conjunctival surface with a cotton-tipped swab at weekly intervals for 6 consecutive weeks from 21 patients with acute ophthalmic zoster with a skin rash duration of less than 7 days. All patients received oral valacyclovir 1000 mg three times daily for 10 days without additional corticosteroids. The swabs were analyzed by means of polymerase chain reaction for the presence of varicella-zoster virus and herpes simplex virus type 1 DNA. Conjunctival swabs were also obtained from a control group of 20 patients with cataract. RESULTS: On inclusion, varicella-zoster virus DNA was present on the ocular surface of 19 of the 21 patients. Six varicella-zoster virus DNA-positive patients had no signs of ocular inflammation. All control swabs were negative for both varicella-zoster virus and herpes simplex virus DNA. The duration of varicella-zoster virus DNA detection from rash onset varied from 2 to 34 days. The number of days between the onset of herpes zoster skin rash and the latest positive varicella-zoster virus DNA test was significantly longer in patients whose age was equal to or above the median age of 66 years than in the younger patients (Mann-Whitney test: P =.0004). At 6-week follow-up, all conjunctival swabs were negative for varicella-zoster virus DNA. However, at that time, the eyes of seven patients were still inflamed. CONCLUSION: The duration of varicella-zoster virus DNA shedding in herpes zoster ophthalmicus is highly variable and age dependent, and is probably related to the host immune response.

Acyclovir↗