Acyclovir for childhood chickenpox. No reason not to treat.
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Acyclovir↗
Biomedical subjects
H H Balfour
Publications and source records attributed to H H Balfour.
Congenital cytomegalovirus infection as a result of nonprimary cytomegalovirus disease in a mother with acquired immunodeficiency syndrome.
A pregnant woman with acquired immunodeficiency syndrome had nonprimary cytomegalovirus (CMV) viremia and died of complications from Pneumocystis carinii pneumonia and CMV sinusitis and pneumonitis. A boy was delivered by cesarean section at 34 weeks of gestation as the mother's health deteriorated and fetal distress developed. The infant died soon after delivery of interstitial pneumonitis and hyaline membrane disease with invasive CMV disease that affected the kidneys, adrenal glands, and placenta; the CMV strains from the mother and neonate were identical.
AIDS-Related Opportunistic Infections↗
Evaluation of CMV-vue antigenemia assay for rapid detection of cytomegalovirus in mixed-leukocyte blood fractions.
The CMV-vue antigenemia assay was evaluated by using mixed-leukocyte (ML) blood fractions. Of 234 ML fractions studied, 32 (14%), 23 (10%), and 20 (8.5%) were positive in the CMV-vue assay and conventional and shell vial cultures, respectively. The CMV-vue assay was more sensitive than shell vial cultures for rapid detection of cytomegalovirus. ML fractions are appropriate specimens for the cytomegalovirus antigenemia assay.
Antigens, Viral↗
Cytomegalovirus retinitis in persons with AIDS. Selecting therapy for a sight-threatening disease.
Almost one third of persons with AIDS acquire retinitis caused by the opportunistic cytomegalovirus (CMV). Both ganciclovir and foscarnet have been approved for treatment of CMV retinitis and are equally effective. However, their side effects are not the same, and each may have a different impact on the overall course of HIV infection and AIDS. The drug chosen should be administered promptly when sight-threatening disease is diagnosed to ensure maximal vision for the longest time.
AIDS-Related Opportunistic Infections↗
The duration of zidovudine benefit in persons with asymptomatic HIV infection. Prolonged evaluation of protocol 019 of the AIDS Clinical Trials Group.
OBJECTIVE: To determine the durability of zidovudine-induced delay in clinical progression of asymptomatic human immunodeficiency virus (HIV) disease and to assess the relationship between this effect and the entry CD4+ cell count. DESIGN AND INTERVENTIONS: Extended follow-up data from subjects participating in protocol 019 of the AIDS [acquired immunodeficiency syndrome] Clinical Trials Group were examined. Subjects were offered a total daily dose of 500 mg of open-label zidovudine after the unblinding of the original randomized trial in 1989. Original treatment groups included placebo, 500 mg of zidovudine, or 1500 mg of zidovudine daily in divided doses. Three distinct analyses were conducted to assess the duration of zidovudine's effect on progression to AIDS or death: (1) analysis of all follow-up information from all subjects, (2) analysis of all subjects but with follow-up of original placebo-assigned subjects censored at the time open-label zidovudine was initiated, and (3) analysis of the effect of initiating zidovudine in subjects initially assigned to receive placebo. SETTING: University-based and university-affiliated AIDS research clinics participating in AIDS Clinical Trials Group protocol 019. PATIENTS: A total of 1565 asymptomatic HIV-infected subjects with entry CD4+ cell counts less than 0.50 x 10(9)/L (500/microL). MAIN OUTCOME MEASURE: Time to progression to AIDS or death. RESULTS: During follow-up of up to 4.5 years (mean, 2.6 years), 232 subjects progressed to AIDS or died. In each of the three analyses described herein, zidovudine was associated with a significant (P = .008, .004, .007) decrease in the risk of such progression. However, each of these analyses also indicated a decreasing placebo:zidovudine relative risk with duration of use (P = .002, .08, .04), suggesting a nonpermanent effect. The duration of benefit appeared to be related to entry CD4+ cell count, with greater benefit in those with higher counts at entry. No significant differences in survival were found between those originally randomized to zidovudine or placebo. CONCLUSIONS: Zidovudine at 500 mg/d caused a significant delay in progression to AIDS or death, but its earlier use in asymptomatic disease was not associated with an additional prolongation of survival compared with delayed initiation. The delay in progression diminished over time especially in subjects with entry CD4+ cell counts less than 0.30 x 10(9)/L (300/microL). Treatment strategies that alter drug regimens before the loss of zidovudine benefit should be explored.
Acquired Immunodeficiency Syndrome↗
A prospective randomized study of acyclovir versus ganciclovir plus human immune globulin prophylaxis of cytomegalovirus infection after solid organ transplantation.
Cytomegalovirus disease occurs frequently after solid organ transplantation and has been associated with decreased patient and allograft survival. We hypothesized that CMV transmission or reactivation begins immediately or soon after transplantation, and that a short-duration ganciclovir (GCV)-based regimen would obviate the need for long-term antiviral agent administration, perhaps serving to interdict CMV infection and disease as well as, or perhaps even more effectively than, a more prolonged, oral acyclovir (ACV)-based form of prophylaxis. A total of 311 patients were stratified according to allograft type, age, and presence or absence or diabetes mellitus, and were then randomized to receive either long-duration ACV prophylaxis (800 mg orally or 400 mg i.v. q.i.d. for 12 weeks after transplantation or 6 weeks after any antirejection therapy) versus short-duration GCV (5 mg/kg/12 hr i.v. for 7 days after transplant or after any antirejection therapy) plus human immune globulin (HIg; Sandoglobulin or Minnesota CMV immune globulin) 100 mg/kg i.v. administered on days 1, 4, and 7 after transplant or after any antirejection therapy. A total of 266 patients (ACV, n = 133; GCV+HIg, n = 133) completed the protocol and were available for follow-up. CMV disease occurred in fewer patients (n = 28, 21.0%) in the ACV group, while significantly more patients (n = 42, 31.6%) in the GCV + HIg group developed group developed CMV disease slightly later (2.83 +/- 0.70 months) than those who received GCV/HIg (2.15 +/- 0.21 months, P > 0.01). Multivariate analysis demonstrated (2.15 +/- 0.21 months, P > 0.1). Multivariate analysis demonstrated that receiving antirejection therapy, a liver transplant, or a donor organ from a CMV-seropositive individual if the recipient was CMV seronegative were major risk factors for the development of CMV disease (P < 0.001), while the difference between ACV versus GCV + HIg prophylaxis was also significant (P = 0.054). No differences in actuarial patient or allograft survival, however, were noted between the 2 prophylaxis groups. Overall, ACV prophylaxis appeared to be more effective in reducing the incidence of posttransplant CMV disease, although this effect was diminished in high-risk groups of patients. Our findings indicate that CMV transmission or reactivation may best be prevented by long-term antiviral agent administration, and that the primary morbidity of CMV disease is the need for rehospitalization when either prolonged ACV or short-duration GCV + HIg prophylaxis is used in this patient population.
Acyclovir↗
Morphine amplifies HIV-1 expression in chronically infected promonocytes cocultured with human brain cells.
Previous studies have shown that morphine promotes the replication of human immunodeficiency virus (HIV)-1 in peripheral blood mononuclear cell cocultures. In the present study, we tested the hypothesis that morphine would amplify HIV-1 expression in the chronically infected promonocytic clone U1 when cocultured with lipopolysaccharide-stimulated human fetal brain cells. Marked upregulation of HIV-1 expression was observed in these cocultures (quantified by measurement of HIV-1 p24 antigen levels in supernatants), and treatment of brain cells with morphine resulted in a bell-shaped dose-dependent enhancement of viral expression. The mechanism of morphine's amplifying effect appears to be opioid receptor-mediated and to involve enhanced production of tumor necrosis factor-alpha by microglial cells.
Acquired Immunodeficiency Syndrome↗
Use of semiquantitative human immunodeficiency virus type 1 culture to guide therapy in a premature infant.
Semiquantitative cultures for human immunodeficiency virus type 1 were used to initiate and guide therapy in an asymptomatic, heavily infected premature infant. The cultures were performed on fivefold serial dilutions of peripheral blood mononuclear cells, and viral growth was detected by the appearance of p24 antigen in the supernatant. While the patient was receiving low-dose zidovudine, her titer diminished from 206 infectious units per 10(6) cells to undetectable levels over 20 weeks, and she remained asymptomatic throughout her 1st year of life. This case suggests that semiquantitative HIV-1 culture should be further evaluated for its ability to guide practical therapeutic decisions in patients who do not fulfill currently established criteria for treatment.
Acquired Immunodeficiency Syndrome↗
Resistance of human immunodeficiency virus type 1 to antiretroviral agents: a review.
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Antiviral Agents↗
Serum p24 antigen level as an intermediate end point in clinical trials of zidovudine in people infected with human immunodeficiency virus type 1. Aids Clinical Trials Group Virology Laboratories.
Serum p24 antigen levels were examined in subjects from three clinical trials of zidovudine to determine whether the pattern of change in serum p24 antigen during the first 8-16 weeks of therapy was associated with human immunodeficiency virus type 1 (HIV-1) disease progression or death. Among 406 patients with AIDS and a first episode of Pneumocystis carinii pneumonia, 65% had measurable pretreatment concentrations of serum p24 antigen (> or = 10 pg/mL). Changes during treatment were not associated with reduced mortality. In 637 mildly symptomatic patients, 24% had measurable concentrations, and changes were marginally associated with increased time until more advanced disease. Among 683 asymptomatic patients, 18% had measurable concentrations, and changes were not associated with increased time until progression. Despite the small number of clinical events and the low rate of serum p24 antigen positivity in the latter two studies, pretreatment serum p24 antigen levels were predictive of clinical outcome; subsequent measurements appear to be of limited use in evaluating zidovudine therapy.
AIDS-Related Complex↗
Phenotypic and genotypic characterization of acyclovir-resistant varicella-zoster viruses isolated from persons with AIDS.
Phenotypic and genotypic analyses were done on 17 varicella-zoster virus (VZV) isolates recovered from 10 persons with AIDS (mean CD4 cell count, 16.4/mm3) who had chronic VZV lesions. Eleven acyclovir-resistant isolates were recovered from 10 patients after a mean of 20.1 weeks of therapy. Six susceptible isolates were recovered before acyclovir treatment (n = 1), early during therapy (n = 4; mean time, 4.2 weeks), or after discontinuation of acyclovir (n = 1). Acyclovir-resistant VZV isolates were deficient in thymidine kinase (TK) or induced a TK with altered substrate specificity; all isolates were susceptible to foscarnet. Ten of 11 acyclovir-resistant mutants contained tk gene mutations, including single nucleotide substitutions in highly conserved binding sites (n = 2) as well as nucleotide deletions (n = 4) and insertions (n = 4). These findings suggest that multiple, nonuniform mutations within the tk gene are associated with acyclovir-resistant VZV phenotypes.
AIDS-Related Opportunistic Infections↗
Foscarnet for suppression of human immunodeficiency virus replication.
The effect of foscarnet against human immunodeficiency virus (HIV) was evaluated in nine HIV-infected individuals; six completed 28 days of induction therapy. The overall mean increase in CD4+ lymphocytes was 64 cells per mm3. The mean decline in the HIV antigen concentration was 108 pg/ml (P = 0.03), and suppression was related to systemic foscarnet exposure by a maximum-effect pharmacodynamic model.
Adult↗
Clinical aspects of chickenpox and herpes zoster.
Chickenpox in immunocompromised individuals is potentially fatal and should be treated with intravenous acyclovir as soon as it is recognized. Data from four double-blind, placebo-controlled trials in the USA provide a sound scientific basis for using acyclovir to treat chickenpox in immunocompetent individuals. Three studies in children and a fourth study in US naval recruits showed statistically significant reductions in the duration of fever, constitutional illness, and time to cutaneous healing, when treatment was initiated within 24 h of rash onset. Although chickenpox is generally mild in children the severity of the disease increases with age and secondary cases in the family tend to be more ill than the primary case. It is recommended that secondary and tertiary cases in a family, and adolescents and adults with chickenpox be treated with acyclovir. In immunocompromised hosts, intravenous acyclovir halts the progression of herpes zoster and is recommended as therapy during new lesion formation. Herpes zoster in otherwise normal hosts is rarely accompanied by visceral dissemination, but carries an increasing risk of post-herpetic neuralgia with increasing age. Published clinical trials have shown a reduction in the duration and severity of acute pain during herpes zoster for patients treated with acyclovir, but results for chronic pain are conflicting with some, but not all, studies showing a beneficial effect.
Acyclovir↗
Management of acyclovir-resistant herpes simplex and varicella-zoster virus infections.
Persons with AIDS who have CD4+ counts < or = 100 and transplant patients, especially bone marrow allograft recipients, may experience clinically significant infections with acyclovir-resistant herpes simplex virus (HSV) or varicella-zoster virus (VZV). Patients who have received prior repeated acyclovir treatment appear to be at the highest risk of harboring acyclovir-resistant strains. Algorithms for the management of these infections were developed at a recent roundtable symposium. The consensus of the panelists was that treatment with foscarnet should be initiated within 7-10 days in patients suspected to have acyclovir-resistant HSV or VZV infections. Foscarnet therapy should be continued for at least 10 days or until lesions are completely healed.
Acquired Immunodeficiency Syndrome↗
Recurrent ocular herpes simplex infection.
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Acyclovir↗
Failure of foscarnet in disseminated herpes zoster.
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Adolescent↗
Current management of varicella zoster virus infections.
A series of randomized, placebo-controlled, double-blind clinical trials conducted from 1980 to the present provide the basis for appropriate management of varicella-zoster virus (VZV) infections. Placebo recipients in these studies have also provided valuable natural history data on the clinical course of VZV infections. The protocols in toto have shown acyclovir (ACV) to be safe and effective for treatment of nearly all forms of acute VZV infection. A number of issues still need to be addressed, including appropriate dosage, importance of early initiation of therapy, cost-benefit ratio, and viral resistance. Considering the data in aggregate, the author recommends ACV treatment for all acute VZV infections in immunocompromised hosts; for acute herpes zoster infections in all adults; and for varicella in otherwise healthy adults and adolescents, and children who contract it from a sibling.
Acyclovir↗
Effect of oral acyclovir on pain resolution in herpes zoster: a reanalysis.
The most frequent complication of herpes zoster is postherpetic neuralgia, usually defined as chronic pain in the area of the exanthem that persists for at least a month after the skin lesions have healed. Several clinical studies of acyclovir showed a reduction in severity and duration of acute pain, but provided no definitive data for chronic pain. In order to determine if acyclovir therapy could reduce chronic pain, we reanalyzed data from the largest U.S. placebo-controlled treatment trial of 187 immunocompetent persons with herpes zoster. By considering pain as a continuum, we found that the median duration of pain in acyclovir recipients was 20 days vs. 62 days for their placebo counterparts (P = 0.02). Thus, acyclovir has been shown to reduce chronic zoster-associated pain. We also noted that the absence of pain at the onset of cutaneous herpes zoster did not preclude its later development.
Acyclovir↗