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Introduccion. La infeccion por el virus de Epstein-Barr (VEB) puede dar lugar –tanto como primoinfeccion, reactivacion o infeccion cronica activa– a varias formas clinicas de afectacion del sistema nervioso central. Presentamos un caso de encefalitis por VEB producido por reactivacion virica en un paciente inmunocompetente, que inicialmente simulaba, desde el punto de vista clinico y electroencefalografico, una encefalitis por virus herpes simple tipo 1 (VHS-1). Caso clinico. Varon de 51 años con antecedente de herpes zoster dorsal en los dias previos. Acudio a urgencias por un cuadro de siete dias de duracion de cefalea opresiva holocraneal y febricula; 24 horas antes de su ingreso, padecia somnolencia y alteracion del lenguaje. En la exploracion neurologica presentaba rigidez nucal y disfasia. En el liquido cefalorraquideo se evidencio pleocitosis (422 celulas/mm3) con un 98% de mononucleares, y proteinorraquia y glucorraquia normales. Resonancia magnetica cerebral normal y electroencefalograma con descargas epileptiformes lateralizadas periodicas en la region temporal izquierda. Se trato con aciclovir intravenoso; una insuficiencia renal motivo su cambio a valaciclovir oral con resolucion clinica y mejoria de los parametros licuorales. La reaccion en cadena de la polimerasa en el liquido cefalorraquideo fue positiva para VEB y negativa para el resto de virus neurotropos. En sangre, la serologia para VEB con IgG resulto positiva, y negativa con IgM y anticuerpos heterofilos. Conclusiones. La infeccion por VEB puede dar lugar a una encefalitis aguda diseminada o afectar a varias localizaciones del sistema nervioso central, principalmente el cerebelo. Menos frecuentes son los cuadros imitadores de VHS-1. Cuando la encefalitis se relaciona con reactivacion viral pueden detectarse, como en nuestro caso, factores precipitantes.
The purpose of this study was to complete a systematic review and, if possible, a meta-analysis on the effectiveness of systemic and topical nucleoside antiviral agents in the prevention of recurrent herpes labialis (RHL) in immunocompetent subjects.
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In this prospective single-center study, we evaluated the efficacy and safety of valaciclovir (VACV) in the prevention of cytomegalovirus (CMV) infection after allogeneic bone marrow transplantation (BMT). The study population consisted of 12 patients who underwent allogeneic BMT from an unrelated donor. Patients received acyclovir (ACV) intravenously until they became able to take VACV orally. VACV was administered at a daily dose of 3000 mg and continued until day 100. CMV infection was monitored by CMV antigenemia assay and real-time polymerase chain reaction analysis of plasma. Thirty-five patients who did not receive any form of CMV chemoprophylaxis served as control subjects. CMV infection was detected in 4 (33.3%) of the 12 patients and in 24 (68.6%) of the 35 control subjects (P < .05). The onset of CMV infection was significantly delayed in the VACV group (median, day 43) compared with the control group (median, day 28.5; P < .01). Gastrointestinal symptoms as an adverse event due to VACV administration were observed in 2 patients. The plasma levels of ACV after VACV administration were measured in 8 patients and were similar to those in the healthy subjects. In conclusion, VACV shows normal absorption, even in the early posttransplantation period, and may prevent or delay CMV infection effectively and safely in allogeneic BMT recipients.
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High-dose valaciclovir at up to 8 g/day has been shown to be effective in prophylaxis against cytomegalovirus (CMV) disease in renal transplant recipients. We report our experience with low-dose valaciclovir prophylaxis of up to 3 g/day, adjusted to creatinine clearance. A group of patients at high risk of developing CMV disease who received prophylaxis were selected as the study group. This included all CMV-positive patients who received antilymphocyte therapy (R+, n=20) and all CMV-negative recipients of CMV-positive organs (D+R-, n=15). D+R- patients receiving antilymphocyte therapy were excluded, as most of the patients in the control group had received ganciclovir prophylaxis. A historical control group was used, which consisted of patients who did not receive prophylaxis. Low-dose valaciclovir prophylaxis resulted in a statistically significant decrease (8.5 vs 37%, P=0.004) in CMV disease in the study group at 6 months. On subgroup analysis the decrease was statistically significant only in the R+ group (5 vs 45%, P=0.003), not in the D+R- group (13.3 vs 26.6%, P=0.651). Low-dose valaciclovir prophylaxis seems to be adequate for R+ patients receiving antilymphocyte therapy. The role of low-dose valaciclovir prophylaxis needs to be assessed further in a prospective trial.
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Genital herpes is caused by herpes simplex virus 1 (HSV-1) or 2 (HSV-2). Some infected people experience outbreaks of genital herpes, typically, characterized by vesicular and erosive localized painful genital lesions.
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Three patients were treated with valacyclovir and monitored by clinical examination, Goldmann visual field testing, and electroretinography.
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Genital herpes, a viral infection caused by Herpes simplex virus (HSV), is the most common cause of genital ulceration. Patients with a severe decrease in cellular immunity, such as patients positive for Human immunodeficiency virus (HIV) infection, are more likely to develop atypical, severe, disseminated and/or chronic HSV infections. On the other hand, there is an increase incidence of HIV detection among patients positive for HSV infection, as genital ulcers represent a potential portal of entry of HIV into the host. A case of a 52-year-old homosexual man with a two-month history of multiple erythematous ulcerative lesions on the perianal area, the buttocks, and the third left finger is presented. According to the clinical history, the clinical findings and the laboratory results, a diagnosis of HSV infection was made and treatment with valaciclovir was started, which led to complete regression of lesions 30 days later. The atypical features of the herpetic lesions, along with a past history of atypical pneumonitis one year prior to our observation, prompted to a diagnosis of concurrent HIV infection, later confirmed by laboratory
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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.
To evaluate the treatment effect of prednisolone and/or valaciclovir in Bell's palsy patients with different baseline severity of palsy.
Between 1998 and 2001, 717 men in heterosexual monogamous relationships, without a history of GH, completed a cross-sectional questionnaire on demographic, behavioral, and knowledge factors for GH. Their female partners were symptomatic and HSV-2-seropositive. Risk factors for HSV-2 seropositivity were assessed using logistic regression.
The effect of 1% VVACV on epithelial keratitis induced by inoculation of HSV-1 strain McKrae (25 microL of 10(5) plaque-forming units [PFU]) in the scarified rabbit cornea and stromal keratitis induced by intrastromal injection of HSV-1 strain RE (10 microL of 10(5) PFU) was compared with that of 1% trifluorothymidine (TFT) and balanced salt solution as the vehicle control. Both eyes of 10 rabbits were used in each treatment group. Lesions were evaluated by slit lamp examinations over a 2-week period after infection. Aqueous humor samples and corneas were analyzed for drug concentrations at the end of each experiment. Cytotoxicity of VVACV in comparison with val-acyclovir (VACV), ACV, and TFT was evaluated in cellular proliferation assays.
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The study population comprised patients with localized prostate cancer receiving multiple and/or repeat intraprostatic injections of a replication deficient adenovirus containing the herpes simplex virus thymidine kinase (HSV-tk) gene. Intravenous ganciclovir or oral valaciclovir was given for 14 days after injection. Patients were recruited from 4 different clinical protocols in studies of toxicity and efficacy of suicide gene therapy, and closely monitored for toxicity and side effects during and after treatment. Toxicity was graded according to the Cancer Therapy Evaluation Program common toxicity criteria published by the National Cancer Institute.
MANY SPECIES OF TSETSE FLIES (DIPTERA: Glossinidae) are infected with a virus that causes salivary gland hypertrophy (SGH), and flies with SGH symptoms have a reduced fecundity and fertility. The prevalence of SGH in wild tsetse populations is usually very low (0.2%-5%), but higher prevalence rates (15.2%) have been observed occasionally. The successful eradication of a Glossina austeni population from Unguja Island (Zanzibar) using an area-wide integrated pest management approach with a sterile insect technique (SIT) component (1994-1997) encouraged several African countries, including Ethiopia, to incorporate the SIT in their national tsetse control programs. A large facility to produce tsetse flies for SIT application in Ethiopia was inaugurated in 2007. To support this project, a Glossina pallidipes colony originating from Ethiopia was successfully established in 1996, but later up to 85% of adult flies displayed symptoms of SGH. As a result, the colony declined and became extinct by 2002. The difficulties experienced with the rearing of G. pallidipes, epitomized by the collapse of the G. pallidipes colony originating from Ethiopia, prompted the urgent need to develop management strategies for the salivary gland hypertrophy virus (SGHV) for this species. As a first step to identify suitable management strategies, the virus isolated from G. pallidipes (GpSGHV) was recently sequenced and research was initiated on virus transmission and pathology. Different approaches to prevent virus replication and its horizontal transmission during blood feeding have been proposed. These include the use of antiviral drugs such as acyclovir and valacyclovir added to the blood for feeding or the use of antibodies against SGHV virion proteins. In addition, preliminary attempts to silence the expression of an essential viral protein using RNA interference will be discussed.
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To report the successful long-term treatment of varicella zoster virus-associated progressive outer retinal necrosis (VZV-PORN) with aggressive antiviral combination drugs along with highly active antiretroviral therapy (HAART).
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Among 203 renal transplant recipients, 46 were D+/R- (22.7%) and received prophylaxis. Of the 203 recipients, 21 (10.3%) developed CMV disease over a four-year follow-up period. Within the D+/R- group, CMV disease occurred in 15.2% of patients at 6 months (7/46), and 21.7% at 4 years (10/46). Of the 10 D+/R- patients who developed CMV disease, six were inadvertently on a dose of valaciclovir below that dictated by protocol arising from a failure to increase dosage in parallel with improving recipient renal function. In the D+/R- recipients where the protocol was adhered to, the incidence of CMV disease was 5% (2/40) at 6 months, and 10% (4/40) at 4 years.
Neurological manifestations of mononucleosis are extremely rare, occurring in about 1% of all cases. However, when they occur, appropriate treatment must be undertaken to ensure appropriate symptomatic management and reduce morbidity. We present the case of a 25-year-old graduate student with weeklong complaints of fever, sore throat, fatigue, nausea, and "dizziness." She later developed increased sleep requirements, ataxia, vertigo, and nystagmus with a positive EBV IgM titer confirming acute infectious mononucleosis. The patient was clinically diagnosed with EBV-associated cerebellitis and encephalitis, displaying neurological and psychiatric impairment commonly seen in postconcussion syndrome. MRI showed no acute changes. She was started on valacyclovir and a prednisone taper, recovering by the end of twelve weeks. Though corticosteroids and acyclovir are not recommended therapy in patients presenting with EBV-associated ataxia, clinicians may want to keep a low threshold to start these medications in case more serious neurological sequelae develop.
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Horses hospitalized at a referral veterinary hospital.
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Significant hearing and balance control in patients with MD can be achieved with orally administered antiviral drugs.
Clinical ocular examination, a diagnostic workup including corneal scraping for herpesvirus polymerase chain reaction, in vivo confocal microscopy, and therapeutic outcome.
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We report a patient with history of Hodgkin lymphoma. Six months after treatment, 2-deoxy-2-[18F]fluoro-d-glucose positron emission tomography and/or computed tomography ([18F] FDG PET/CT) scan showed abnormal uptake in right axillary lymph nodes concerning for recurrence. In addition, PET/CT showed a new hypermetabolic skin lesion overlying the right scapula. Clinical evaluation was consistent with shingles, and the patient was treated with valacyclovir. Subsequent PET/CT scan was normal with no evidence of lymphoma. Although there have been reported cases of abnormal FDG in nodes or in skin due to herpes zoster, our case is unique in the literature in that the PET/CT demonstrates abnormalities involving both the skin and associated lymph nodes. The possibility of false positive uptake, not because of recurrent malignancy, must always be considered when abnormal FDG uptake is noted in the follow-up of oncology patients. Careful review of the scan and correlation with clinical findings can avoid false positive interpretation and facilitate patient management.
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To determine whether a single course of valaciclovir, i.e. 500, 1000 or 2000 mg, administered during the prodrome of herpes facialis, could be beneficial.
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Valganciclovir (vGCV) and valacyclovir (vACV) are used in cytomegalovirus (CMV) prophylaxis in renal transplant recipients. The aim of this study was to compare the economic impact of both regimens during 1-year follow-up.