Valtrex References

31: Herpes. 2004 Aug;11 Suppl 3:170A-174A.

Prevention of herpes simplex virus type 2 transmission with antiviral therapy.

Corey L, Ashley R; Valaciclovir HSV Transmission Study Group.

Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA.

Worldwide, herpes simplex virus type 2 (HSV-2) infection is the biggest cause of genital ulcer disease, and is responsible for the majority of cases of genital herpes. The risk of transmitting genital herpes to a partner is one of the leading causes of psychological distress for those with the disease. Antiviral compounds available for the treatment of genital herpes are known to reduce clinical recurrence rates and HSV shedding. This understanding provided impetus for a randomized, placebo-controlled study to assess the ability to interrupt transmission of HSV using oral valaciclovir therapy (500 mg, once daily). The study enrolled 1484 immunocompetent, heterosexual, monogamous couples in stable relationships where both partners were aware of the source partner's infection and the source partner had symptomatic genital herpes. Valaciclovir reduced the risk of transmitting HSV-2 infection by 48%. Furthermore, valaciclovir reduced the risk of clinical disease in the susceptible partner by 75%. As a result, the International Herpes Management Forum (IHMF) now recommends that physicians offer suppressive valaciclovir therapy to immunocompetent individuals concerned about transmitting genital herpes to a heterosexual partner, and advises safer sex behaviour, including the use of condoms, to prevent genital herpes transmission.

32: J Med Virol. 2004 Aug;73(4):566-73.

Detection of ganciclovir resistance after valacyclovir - Valtrex-prophylaxis in renal transplant recipients with active cytomegalovirus infection.

Alain S, Hantz S, Scieux C, Karras A, Mazeron MC, Szelag JC, Imbert BM, Fillet AM, Gouarin S, Mengelle C, De Wilde A, Cogne N, Champier G, Rogez S, Legendre C, Denis F.

Department of Bacteriology-Virology-Hygien, EA, Teaching Hospital Dupuytren, Limoges, France.

Whether valaciclovir (VCV) prophylaxis could be responsible for ganciclovir (GCV)-resistance of Human cytomegalovirus (HCMV) in transplantation has never been documented. A multicentric retrospective pilot study was undertaken to detect GCV-resistance through mutations within the UL97 gene in renal transplant recipients who experienced active HCMV infection and received valacyclovir - Valtrex prophylaxis. Twenty-three patients who experienced HCMV antigenaemia or DNAemia during or at the end of prophylaxis were included. UL97 genotyping was carried out on peripheral blood samples, using a nested in-house PCR, which amplified the full-length UL97 gene. One patient has a resistance-related mutation (M460I); the major risk factor for emergence of resistance in this patient was the presence of early and persistent antigenaemia. GCV-resistance during VCV-prophylaxis was rare after renal transplantation. However, special attention must be paid to patients developing early active HCMV infection under prophylaxis.

33: Mayo Clin Proc. 2004 Aug;79(8):1055-8.

80-year-old man with fever and ear pain.

Lim LS, Takahashi PY.

Mayo Graduate School of Medicine, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA.

34: Schweiz Rundsch Med Prax. 2004 Jul 28;93(31-32):1253-5.

A 59-year old patient with herpes zoster V1-V2

Hartsleben CH.

Medizinische Universitatspoliklinik, Departement Innere Medizin, Kantonsspital, Basel.

35: N Engl J Med. 2004 Jul 22;351(4):354-61.

Methylprednisolone, valacyclovir - Valtrex, or the combination for vestibular neuritis.

Strupp M, Zingler VC, Arbusow V, Niklas D, Maag KP, Dieterich M, Bense S, Theil D, Jahn K, Brandt T.

Department of Neurology, University of Munich, Munich, Germany.

BACKGROUND: Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. Its assumed cause is a reactivation of herpes simplex virus type 1 infection. Therefore, corticosteroids, antiviral agents, or a combination of the two might improve the outcome in patients with vestibular neuritis. METHODS: We performed a prospective, randomized, double-blind, two-by-two factorial trial in which patients with acute vestibular neuritis were randomly assigned to treatment with placebo, methylprednisolone, valacyclovir - Valtrex, or methylprednisolone plus valacyclovir - Valtrex. Vestibular function was determined by caloric irrigation, with the use of the vestibular paresis formula (to measure the extent of unilateral caloric paresis) within 3 days after the onset of symptoms and 12 months afterward. RESULTS: Of a total of 141 patients who underwent randomization, 38 received placebo, 35 methylprednisolone, 33 valacyclovir - Valtrex, and 35 methylprednisolone plus valacyclovir - Valtrex. At the onset of symptoms there was no difference among the groups in the severity of vestibular paresis. The mean (+/-SD) improvement in peripheral vestibular function at the 12-month follow-up was 39.6+/-28.1 percentage points in the placebo group, 62.4+/-16.9 percentage points in the methylprednisolone group, 36.0+/-26.7 percentage points in the valacyclovir - Valtrex group, and 59.2+/-24.1 percentage points in the methylprednisolone-plus-valacyclovir - Valtrex group. Analysis of variance showed a significant effect of methylprednisolone (P<0.001) but not of valacyclovir - Valtrex (P=0.43). The combination of methylprednisolone and valacyclovir - Valtrex was not superior to corticosteroid monotherapy. CONCLUSIONS: Methylprednisolone significantly improves the recovery of peripheral vestibular function in patients with vestibular neuritis, whereas valacyclovir - Valtrex does not.

36: J Infect Dis. 2004 Jul 15;190(2):396-9. Epub 2004 Jun 11.

Expression of Epstein-Barr virus latent genes in oral epithelium: determinants of the pathogenesis of oral hairy leukoplakia.

Walling DM, Ling PD, Gordadze AV, Montes-Walters M, Flaitz CM, Nichols CM.

Division of Infectious Diseases, Department of Internal Medicine, and Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.

This retrospective study examined expression of Epstein-Barr virus (EBV) latent genes in oral epithelium from human immunodeficiency virus-seropositive subjects, to identify genes associated with the pathogenesis of oral hairy leukoplakia (HLP). Transcription of EBV latent genes was detected in tissues with productive EBV replication and, also, in normal oral epithelial tissues without EBV replication. Expression of the EBV EBNA-2 open-reading frame in oral epithelium was identified as an important cofactor associated with the pathogenesis of HLP. In vitro experiments suggested that a recombinant variant of the EBNA-2 gene may play a role in the pathogenesis of HLP, through modulation of EBNA-2 protein function.

37: J Infect Dis. 2004 Jul 15;190(2):387-95. Epub 2004 Jun 9.

Persistence and transition of Epstein-Barr virus genotypes in the pathogenesis of oral hairy leukoplakia.

Walling DM, Etienne W, Ray AJ, Flaitz CM, Nichols CM.

Division of Infectious Diseases, Department of Internal Medicine, and Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.

This prospective study examined the persistence and transition of Epstein-Barr virus (EBV) in human immunodeficiency virus (HIV)-seropositive subjects with and without oral hairy leukoplakia, a replicative EBV-associated epithelial disease. The intrahost molecular epidemiology of EBV infection was characterized in subjects treated with valacyclovir - Valtrex to suppress EBV replication. Tongue epithelial tissues of HIV-seropositive subjects were found to support not only EBV replication but also persistent, nonproductive EBV infection. EBV appeared to enter the tongue from the blood reservoir of infection and, possibly, from exogenous sources as well. EBV transition from the blood to the tongue appeared to occur even during valacyclovir - Valtrex-mediated suppression of EBV replication, suggesting EBV entry into tongue epithelial tissue as a cell-associated latent infection. In conclusion, these results describe the persistence and transition of EBV as a dynamic interaction between the blood and epithelial reservoirs of EBV infection and suggest a role for entry, persistence, and reactivation of oral epithelial EBV in the pathogenesis of oral hairy leukoplakia.

38: Cutis. 2004 Jul;74(1):31-4.

Therapeutic options for herpes labialis, I: Oral agents.

Elish D, Singh F, Weinberg JM.

Department of Dermatology, St. Luke's-Roosevelt Hospital Center and Beth Israel Medical Center, New York, New York 10025, USA.

Given the prevalence of herpes labialis, effective therapy has the potential to affect the lives of many and presents a challenge for clinicians. Over the last several years, most of the focus of herpes research has been on the treatment of genital herpes. Recently, however, several studies have been published examining the efficacy of therapies specifically for herpes labialis. Several therapeutic agents, both prescription and over-the-counter, are available for controlling and managing the disease. In this series of articles, we review oral and topical therapeutic agents that are available in the treatment of herpes labialis and its associated symptoms. This article will review oral treatment options.

39: Int J STD AIDS. 2004 Jul;15(7):429-33.

Antiviral treatment of genital herpes.

Apoola A, Radcliffe K.

Whittall Street Clinic, Whittall Street, Birmingham B4 6DH, UK.

A review of the randomized, controlled trials in the literature on the treatment of genital herpes infection with aciclovir, famciclovir and valaciclovir. Common clinical questions encountered by physicians, such as the effect of antivirals on symptoms, healing, aborting attacks and subsequent recurrences, are addressed. There is very little comparative data between the three licensed drugs but the little data that there is shows no difference in efficacy, tolerability and toxicity between aciclovir, valaciclovir or famciclovir when taken orally. Choice of therapy would then depend on convenience of dosing and cost.

40: Med Sci Sports Exerc. 2004 Jul;36(7):1104-10.

Valtrex therapy for Epstein-Barr virus reactivation and upper respiratory symptoms in elite runners.

Cox AJ, Gleeson M, Pyne DB, Saunders PU, Clancy RL, Fricker PA.

School of Biomedical Sciences, Faculty of Health, University of Newcastle, Callaghan, NSW, Australia.

PURPOSE: The aim of the study was to examine the effectiveness of prophylactic administration of the antiviral agent Valtrex for control of Epstein-Barr virus (EBV) reactivation and upper respiratory symptoms in elite distance runners. METHODS: Twenty elite male distance runners were randomized into a 4-month double-blind, placebo-controlled cross-over trial. Saliva samples were collected weekly and mucosal immune status assessed by measurement of secretory IgA (SIgA) using an enzyme-linked immunosorbent assay (ELISA). EBV reactivation was monitored at the same time by detection of EBV in saliva using a quantitative real-time polymerase chain reaction. The initial EBV status of the runners was determined by detecting EBV antibodies in serum using an ELISA. Upper respiratory symptoms were recorded using self-reporting illness logs. RESULTS: There was no evidence of any marked change in maximal oxygen uptake (P = 0.86), training volume (P = 0.30), or mucosal immunity (P = 0.21) over the study period. Valtrex treatment resulted in an 82% reduction in the detectable EBV load in saliva for EBV seropositive runners compared with the placebo treatment (P = 0.04). The incidence of upper respiratory symptoms was not reduced by Valtrex treatment. CONCLUSIONS: The prophylactic administration of Valtrex reduced EBV reactivation but was not an effective intervention strategy for limiting upper respiratory symptoms in this cohort of elite distance runners. The upper respiratory symptoms in the distance runners could not be directly attributed to infection and may be of a noninfectious inflammatory nature.