herpes
Famciclovir as antiviral prophylaxis in laser resurfacing procedures.

Wall SH, Ramey SJ, Wall F.

Plastic Surgery LLP, Shreveport, LA, USA. swallmd aol.com

Latent herpes simplex virus (HSV types I and II) may be reactivated by laser resurfacing procedures, presenting serious postoperative complications in approximately 9 percent of patients. Perioperative prophylactic administration of nucleoside analog antiviral agents has been shown to decrease the duration and severity of postsurgical herpes infection and to prevent recurrence. This study was conducted to assess the efficacy of famciclovir in preventing orofacial herpes virus reactivation and primary infection in patients undergoing laser resurfacing. HSV history was obtained from a total of 121 patients undergoing the procedure. Antiviral prophylaxis with famciclovir was begun 1 to 2 days before surgery and continued for 5 days after surgery. Patients with no history of orofacial herpes (n = 94) received 125 mg of famciclovir twice daily. Those with a history of orofacial herpes (n = 27) received 250 mg of famciclovir twice daily. Postsurgical HSV infection rates in patients receiving famciclovir prophylaxis were compared with those from a similar historical control group of HSV-positive patients (n = 127) who received no prophylaxis. In patients receiving famciclovir prophylaxis, one patient (1.1 percent) in the HSV-negative history group and no patients in the HSV-positive history group had postsurgical herpes infection. Famciclovir significantly reduced postsurgical herpes infection when compared with the 9.4 percent rate of herpes reactivation in patients who received no prophylaxis (p = 0.003). This study suggests that twice-daily famciclovir prophylaxis markedly reduces orofacial herpes virus infection in patients undergoing laser resurfacing.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10654754&dopt=Abstract herpes medicine



herpes
Persistent stress as a predictor of genital herpes recurrence.

Cohen F, Kemeny ME, Kearney KA, Zegans LS, Neuhaus JM, Conant MA.

Department of Psychiatry, University of California, San Francisco, School of Medicine, 94143-0844, USA. fcohen itsa.ucsf.edu

BACKGROUND: Results of several studies suggest that psychological stress and negative mood can trigger genital herpes recurrences, but results are inconsistent. OBJECTIVE: To determine whether short-term or persistent psychological stress or specific negative moods are predictive of genital herpes recurrences in women. METHODS: A prospective cohort study followed up participants for 6 months using weekly assessments of stress and mood, monthly assessments of life change events, and diary reports of genital herpes recurrences confirmed by medical examination when feasible. The community sample consisted of 58 women, aged 20 to 44 years, with a 1- to 10-year history of visible genital herpes recurrence and at least 1 recurrence in the previous 6 months. RESULTS: Persistent stress predicted recurrence in the subsequent week (odds ratio, 1.08 per unit increase in stress; 95% confidence interval, 1.01-1.15; P=.03). After adjusting for recurrence in the previous week, the more weekly persistent stress reported, the greater the likelihood of recurrence the following week. Also, an increased recurrence rate occurred after the month during which participants experienced their highest levels of anxiety (P =.03). There were no significant associations between recurrence and short-term stress, life events, depressive mood, anger, or phase of menstrual cycle. CONCLUSIONS: Persistent stressors and highest level of anxiety predicted genital herpes recurrence, whereas transient mood states, short-term stressors, and life change events did not. Women with herpes can be reassured that short-term stressful life experiences and dysphoric mood states do not put them at risk for increased outbreaks of recurrent genital herpes.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10665891&dopt=Abstract herpes medicine



herpes
Human herpes virus-like particles in pityriasis rosea lesions: an electron microscopy study.

Drago F, Malaguti F, Ranieri E, Losi E, Rebora A.

Section of Dermatology, Department of Health Sciences, DiSEM, University of Genoa, Viale Benedetto XV 7, 16132 Genoa, Italy. rebdermo unige.it

BACKGROUND: In a previous study we detected virions with electron microscopy features of human herpes viruses in the supernatant of cocultured mononuclear cells from patients with acute pityriasis rosea. Because of their morphology and of polymerase chain reaction studies, we ascribed them to human herpes virus 7. OBJECTIVE: To find such virions in the lesional skin of pityriasis rosea patients. METHODS: Skin specimens from lesions of 21 patients with acute pityriasis rosea were examined by elecron microscopy. RESULTS: In 15 (71%) patients, human herpes virus particles in various stages of morphogenesis were detected. Mature enveloped virions appeared as typical human herpes virus virions, measuring about 160-200 nm in diameter and containing an electrodense cylindrical core, a capsid, an envelope with typical spikes and a very distinct tegument layer between the capsid and the envelope. They were very similar to those we reported in the supernatant of co-cultured circulating mononuclear cells from patients with pityriasis rosea. CONCLUSION: Our results confirm our previous findings and provides further evidence of a viral etiology for pityriasis rosea.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12135467&dopt=Abstract herpes medicine



herpes
Examination of the oral mucosa and peripheral blood cells of patients with recurrent aphthous ulceration for human herpes virus DNA.

Brice SL, Cook D, Leahy M, Huff JC, Weston WL.

Department of Dermatology, School of Medicine, University of Colorado, Denver, CO 80262, USA.

OBJECTIVE: The purpose of this study was to exam the oral mucosa and peripheral blood cells of patients with recurrent aph-thous ulceration (RAU) for the presence of the following human herpes viruses: herpes simplex viruses 1 and 2, varicella zoster virus, Epstein-Barr virus, cytomegalovirus, human herpes virus-6, and human herpes virus-7. STUDY DESIGN: Fifty-eight subjects with RAU and 10 control subjects were recruited at an academic referral center and enrolled in this prospective, nonrandomized, case-controlled study. Each of the subjects with RAU was seen during an acute episode, and swab specimens from lesional (RAU-acute/lesion) and clinically normal (RAU-acute/normal) oral mucosa were obtained. Each of 2 subjects with RAU was evaluated during more than one acute episode. Three subjects with RAU were seen between active episodes, and swab specimens were taken from clinically normal (RAU-convalescent) oral mucosa. Swab specimens from clinically normal (control/normal) oral mucosa were obtained from the control subjects. Peripheral blood specimens were obtained from subjects with RAU and control subjects at the time the swab specimens were performed. Through use of polymerase chain reaction, all swab and peripheral blood specimens were examined for the presence of human herpes virus DNA. Statistical significance was determined by means of chi(2) analysis. RESULTS: Herpes simplex virus and human herpes virus-6 were found in a higher percentage of mucosal specimens from the control subjects (herpes simplex virus, 4/10; human herpes virus-6, 5/9) than from the subjects with RAU (RAU-acute/lesion: 3/45 herpes simplex virus, 13/53 human herpes virus-6; RAU-acute/normal: 7/48 herpes simplex virus, 9/53 human herpes virus-6). No difference was demonstrated between RAU-acute/lesion, RAU-acute/normal, and RAU-convalescent mucosal specimens for any of the human herpes viruses. Different human herpes viruses were identified from individual subjects with RAU during subsequent episodes of disease. Epstein-Barr virus (6/35), human herpes virus-6 (3/40), and human herpes virus-7 (7/43) were detected in the peripheral blood mononuclear cells during acute RAU but not in RAU-convalescent or control peripheral blood mononuclear cells. CONCLUSIONS: The detection of human herpes virus DNA from the oral mucosa and peripheral blood mononuclear cells of patients with RAU appears to represent normal viral shedding rather than a direct causal mechanism in this disorder.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10673655&dopt=Abstract herpes medicine



herpes
Viral causes of the acute retinal necrosis syndrome.

Ganatra JB, Chandler D, Santos C, Kuppermann B, Margolis TP.

Francis I. Proctor Foundation, and the Department of Ophthalmology, University of California at San Francisco, 94143-0944, USA.

PURPOSE: The primary goal of this study was to determine the viral cause of the acute retinal necrosis syndrome in 28 patients (30 eyes). A secondary goal was to investigate possible associations between viral cause and patient age, and viral cause and central nervous system disease. METHODS: A retrospective case series in which we reviewed the laboratory results and clinical histories of 28 patients (30 eyes) diagnosed with acute retinal necrosis syndrome, from whom vitreous or aqueous specimens were received, for diagnostic evaluation using previously described polymerase chain reaction-based assays. RESULTS: Varicella-zoster virus, herpes simplex virus, and cytomegalovirus (CMV) DNA were detected in aqueous and/or vitreous specimens from 27 of 28 patients (29 of 30 eyes with a clinical history of acute retinal necrosis syndrome). No sample was positive for DNA from more than one virus. Varicella-zoster virus DNA was detected in 13 patients (15 eyes). Median age was 57 years. Herpes simplex virus type 1 DNA was detected in seven patients (seven eyes). Median age was 47 years. Six of these patients had a history of herpes simplex virus encephalitis. Herpes simplex virus type 2 DNA was detected in six patients (six eyes). Median age was 20 years. Three of these patients had a likely history of meningitis. Cytomegalovirus DNA was detected in one patient who was immunosuppressed iatrogenically. No viral DNA was detected in one patient from whom a sample was taken after 6 weeks of acyclovir therapy. CONCLUSIONS: The data suggest that varicella-zoster virus or herpes simplex virus type 1 cause acute retinal necrosis syndrome in patients older than 25 years, whereas herpes simplex virus type 2 causes acute retinal necrosis in patients younger than 25 years. A history of central nervous system infection in a patient with acute retinal necrosis syndrome suggests that herpes simplex virus is likely to be the viral cause.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10682968&dopt=Abstract herpes medicine



herpes
Genital herpes and public health: addressing a global problem.

Corey L, Handsfield HH.

Fred Hutchinson Cancer Research Center, Department of Laboratory Medicine, University of Washington School of Medicine, Seattle 98109, USA.

Genital herpes can be caused by herpes simplex virus 2 (HSV-2) or, less commonly, by herpes simplex virus 1 (HSV-1). With a seroprevalence of antibodies to HSV-2 of 22% in the general population, genital herpes is 1 of the 3 most prevalent sexually transmitted diseases (STDs) in the United States. A central issue in the public health problem of genital herpes is the high proportion of genital HSV infections that are unrecognized by both patients and clinicians. Persons who are HSV-2 seropositive may be symptomatic but nevertheless fail to recognize genital herpes; they serve as reservoirs for transmission. Physicians and patients must be aware of the subclinical presentation of genital herpes and the potential these patients have for transmitting HSV. Serious consequences of HSV infection include neonatal herpes and increased risk of human immunodeficiency virus transmission. Recommendations to physicians for prevention include using type-specific tests for HSV when screening for other STDs and testing for HSV when evaluating patients with genital ulcers. Researchers must evaluate the performance of type-specific tests and strategies to prevent transmission.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10683059&dopt=Abstract herpes medicine



herpes
Cellular expression of alphaherpes virus gD interferes with entry of homologous and heterologous alphaherpes viruses by blocking access to a shared gD receptor.

Geraghty RJ, Jogger CR, Spear PG.

Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, Illinois, 60611, USA.

Several human and animal alphaherpes viruses can enter cells via human herpes virus entry mediator C (HveC), a receptor for viral glycoprotein D (gD). In previous studies with cells expressing unknown entry mediators, cellular expression of alphaherpes virus gD was shown to inhibit entry of the homologous virus and sometimes also of heterologous alphaherpes viruses. To investigate the mechanism of gD-mediated interference and the basis for cross-interference among alphaherpes viruses, HveC was expressed in cells as the sole entry mediator, in the presence or absence of one of the gDs encoded by herpes simplex virus type 1, pseudorabies virus, or bovine herpes virus type 1. Cells expressing HveC alone were highly susceptible to entry of all three viruses, whereas cells coexpressing HveC and any one of the gDs were at least partially resistant to infection by each virus. Coexpression of gD with HveC did not cause reduced levels of cell-surface HveC but the HveC had reduced ability to bind to exogenous gD. Coimmunoprecipitation experiments revealed that HveC was complexed with gD in lysates of cells expressing both. Thus, cellular expression of gD can interfere with alphaherpes virus entry by blocking ligand-binding sites of the gD receptor(s) used for entry and cross-interference can occur because different forms of alphaherpes virus gD can compete for shared entry receptors. Copyright 2000 Academic Press.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10683337&dopt=Abstract herpes medicine



herpes
[Mechanisms for the therapeutic effect of herpes polyvaccines in chronic ophthalmic herpes and genital herpes]

[Article in Russian]

Barinskii IF, Karpovich LG, Gubanova EI, Belkina IV, Semenova TB, Lazarenko AA, Davydova AA, Samoilenko II, Kasparov AA.

Commercial inactivated culture polyvaccine against herpes simplex viruses (types 1 and 2) developed at D. I. Ivanovsky Institute of Virology promoted cessation of viremia. During the first vaccination viremia coincided with appearance of a focal allergic test on the retina, which is proposed for the diagnosis of herpetic involvement of the posterior compartment of the eye. T-cellular immunity normalized after a course of vaccination. Experimental immunization of rats and vaccination of patients with chronic ophthalmic and genital herpes demonstrated the therapeutic activity of inactivated herpetic polyvaccine in suppositoria.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10695041&dopt=Abstract herpes medicine