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Discusses results of a pilot trial of the combination of topical corticosteroids and a systemic antiviral agent for the treatment of herpes labialis. Study synopsis and medication; Characteristics of the study population; Induction lesions; Initiation of therapy; Lesion maturation and area; Lesion healing time; Lesion pain and virology; Adverse reactions.

Studies the use of the antiviral famciclovir to treat experimental ultraviolet radiation-induced herpes simplex labialis. Dosage and administration; Model of early episodic intervention; Reduction in mean maximal lesion size.

The lips of 196 patients with a historyof sun-induced herpes labialis were exposed to experimental ultraviolet radiation (UVR) and treated with acyclovir (ACV) or placebo at different times and by different routes. Of 98 placebo recipients, 39 (40%) developed 43 lesions inside or within 10 mmof the irradiated zone. The temporal distribution of lesions was bimodal, 11(26%) occurring within 48 h (immediate) and 32(72%)2–7 days after UVR exposure (delayed). Prophylactic peroral ACV begun 7 days before or 5 min after UVR prevented the development of the delayed but not the immediate lesions (P < .001). When peroral ACV was started 48 h after UVR, delayed lesions developed but were less severe (P = .01–.05). Prophylactic topical ACV begun 5 min after UVR did not reduce lesion frequency or severity. ACV therapy can be efficacious, but some rapidly developing lesions are unresponsive to treatment. This suggests that more than one process may contribute to the pathogenesis of herpes labialis. [ABSTRACT FROM PUBLISHER]

Topical antiviral treatments for recurrent infection with herpes simplex virus in immunocompetent patients have been generally ineffective. We investigated whether in vitro drug measures could predict in vivo efficacy. Twelve topical antiviral formulations were evaluated in vitro by measuring inhibition of viral plaque formation in cell culture (ID50) and drug penetration through excised guinea pig skin. In vivo efficacy for each treatment was determined in an experimental cutaneous infection with herpes simplex virus type 1 in guinea pigs and expressed as the percent reduction in lesion number, lesion area, and virus titer in the lesions. The in vitro findings were correlated with the results in the animal model. ID50 was a poor predictor of in vivo efficacy, whereas stronger correlations were found between the degree of skin penetration and in vivo activity. The best correlation was noted by using a summary expression of the in vitro results as follows: the ratio of drug penetration through skin at 37 C to ID50 (r = .95, .94, and .92 for lesion number, area, and virus titer, respectively, P less than .0005). Determination of this in vitro index should be included in the preclinical evaluation of new topical antiviral formulations. [ABSTRACT FROM AUTHOR]

Antiviral activity characterized as human interferon (HuIFN) was demonstrated in vesicle fluid from lesions of recurrent herpes labialis in 18 of 19 otherwise healthy patients. High titers (geometric mean, 20,200 units) were present during the early course of lesion development. Antiviral activity in vesicle fluid was neutralized by antibody to leukocyte (type I) HuIFN (HuIFN-α) in the eight patients in whom it was tested. These results indicate that HuIFN-α is present in the local lesions of recurrent herpes labialis. HuIFN may have a role in the pathogenesis of recurrent herpesvirus infections. [ABSTRACT FROM PUBLISHER]

Primary cultures were established with epidermal cells from the skin of 11 patients with frequent episodes of herpes simplex labialis and 13 control subjects with titers of neutralizing antibody to herpes simplex virus (HSV) type 1 but no history of herpetic disease. Confluent monolayers were exposed to HSV type 1 strain E1l5, and the infection was monitored by assay of the rate of virus appearance in the culture medium. The mean slope of the virus growth curves ([log10 pfu/ml/log10 hr) was 9.0 in cultures from patients vs. 9.5 in cultures from controls, and the respective mean titers of virus 53 hr after infection were 106.8 and 106.5 (differences not statistically significant). Genetically controlled host factors may play some role in the clinical,response to HSV infection, but variation in the susceptibility of epidermal cells, the natural target for HSV, is not one of the critical determinants. [ABSTRACT FROM PUBLISHER]

A meta-analysis of 8 randomized trials (1792 patients, 2947 patient-years of follow-up) showed that acyclovir (⩾3200 mg/day) offered a significant survival benefit (P = .006 by log-rank test) in human immunodeficiency virus (HIV) infection. The treatment effect did not vary significantly in patient subgroups of different CD4 cell counts, hemoglobin levels, age, race, and sex, and with or without AIDS diagnosis. Acyclovir treatment (hazard ratio, 0.78; 95% confidence interval [CI], 0.65–0.93), higher CD4 cell count (P < .001), higher hemoglobin level (P < .001), and younger age (P < .001) reduced the hazard of mortality. Acyclovir decreased herpes simplex virus infections (odds ratio [OR], 0.28; 95% CI, 0.21–0.37) and varicella-zoster virus infections (OR, 0.29; 95% CI, 0.13–0.63) but not cytomegalovirus disease or mortality from lymphoma or Kaposi's sarcoma. A survival advantage was seen specifically in studies with high incidence of clinical herpesvirus infections (⩾25% per year). Given the wide confidence intervals, the small effect in low-risk patients, and recent changes in HIV therapeutics, the results should be interpreted cautiously, but the meta-analysis supports the importance of pathogenetic interactions between herpesviruses and HIV. [ABSTRACT FROM PUBLISHER]

Herpes simplex viruses (HSVs) infect epithelial cells, become localized in neurons, and can reactivate in response to a variety of stimuli, including ultraviolet light and hyperthermia. The sequence of gene activation during viral replication is known, but the molecular linkage between exogenous stimuli and HSV reactivation has not been determined. It was hypothesized that interleukin (IL)- 6 acts as a signal between exogenous stimuli and neurons, stimulating HSV reactivation from latency. Mouse corneas were infected with HSV-1, and ocular reactivation was induced 5–7 weeks later by thermal stress or corneal exposure to ultraviolet light. Anti-IL-6 monoclonal antibodies were administered to the latently infected mice 8–12 h before the reactivation stimulus. Treatment with anti-IL-6 antibodies resulted in significantly lower frequencies of ocular reactivation compared with those in mice treated with a control immunoglobulin. These results support the hypothesis that IL-6 plays a role in HSV reactivation from latency. [ABSTRACT FROM PUBLISHER]