International Journal of Infectious Diseases. Keyserling, S. Dr. This drug is phosphorylated in infected mammalian cells by the viral thymidine kinase to acyclovir monophosphate, which is itself further phosphorylated by host kinases to acyclovir triphosphate, a potent inhibitor of the viral DNA polymerase. Kirk, and Mr. Herpesvirus outbreaks in immunocompromised patients are more frequent and harder to control than those in otherwise healthy individuals and can be life-threatening [8, 13–15]. On physical examination, the patient had an acute ill-looking appearance and presented normal conjunctivae.
The emergence of drug-resistant and multidrug-resistant viruses has been linked to severe complications in immunocompromised individuals (27–30). J Infect Dis 2007; 196:1500–1508. Infants treated with standard, high-dose intravenous acyclovir for active neonatal HSV had normal antibody titers during and after therapy;8 however, the humoral and cellular response to extended antiviral therapy is not known. Inhibition of reactivation in the ganglia was not examined in that study. Participants were randomized to 1000 mg of valacyclovir or 400 mg of acyclovir twice daily for 12 weeks, and after a 2-week washout, the alternative arm for 12 weeks. Adverse reactions to these agents included severe renal insufficiency, hyponatremia, and neutropenia. Resistance may be related to a mutation of either viral TK or viral DNA polymerase.
This may not be the complete list of references from this article. Serial CSF samples were available from 10 of the 22 patients. Get a printable copy (PDF file) of the complete article (793K), or click on a page image below to browse page by page. Get a printable copy (PDF file) of the complete article (839K), or click on a page image below to browse page by page. These references are in PubMed. Because the distribution of ACVr variants in natural populations is relatively high (10(-4), these results suggest that selection of ACVr strains during ACV therapy is possible. Wildy , J.
Full text Full text is available as a scanned copy of the original print version. Even though the latent HSV-1 could not be eliminated completely from the trigeminal ganglia by discontinuous administration of either drug, its titers were markedly reduced. Full text Full text is available as a scanned copy of the original print version. Daily administration of 2 g of oral acyclovir for ten days alleviates some of the clinical signs of herpes simplex virus rectal infection. Virus recovery during latent infection was more frequently obtained from the spinal cord in HSV-1-infected animals and from lumbosacral ganglia in HSV-2-infected animals. However, when a suboptimal therapeutic dose was used and virus was repeatedly inoculated into further mice undergoing therapy, the infection became completely refractory to treatment by passage 4. When treatment was started 24 hours after infection, it had no significant effect under the same circumstances.
HSV-2-seropositive women collected daily samples of genital secretions while receiving acyclovir or placebo, each for 10 weeks. None of the eight rabbits receiving intensive ACV shed virus in their tear film sample during 4 weeks of concurrent epinephrine iontophoresis and antiviral therapy. In the treatment or prophylaxis of chronic herpes infections in immunocompromised patients reductions in sensitivity were observed but these were infrequent. He subsequently developed meningoencephalitis. The duration of virus shedding from lesions present at the time of entry into the study was significantly reduced for men who received acyclovir compared with men who received placebo (P less than 0.05). These results have implications for acyclovir resistance and the development of drugs that potentiate acyclovir action by inhibition of viral ribonucleotide reductase. Seropositive patients were first given intravenous acyclovir until day 30 after transplant.
Forty isolates of herpes simplex virus (HSV) obtained from ocular herpetic infections were assayed for their sensitivity to five antiviral agents. Acyclovir recipients had significantly shorter periods of virus shedding (p less than 0.0002) and lesion pain (p less than 0.01), and more rapid lesion scabbing (p less than 0.004) and lesion healing (p less than 0.04). Herpes simplex virus (HSV) strain 1737, acyclovir-resistant and uniformly thymidine kinase-deficient (tkD) by all conventional assays, clinically reactivated in an AIDS patient in the absence of antiviral drug pressure. Description: Founded in 1904, The Journal of Infectious Diseases is the premier publication in the Western Hemisphere for original research on the pathogenesis, diagnosis, and treatment of infectious diseases, on the microbes that cause them, and on disorders of host immune mechanisms. We report a case of orofacial herpes simplex virus (HSV) infection that was progressive despite multiple courses of acyclovir sodium in a patient with the acquired immunodeficiency syndrome. New Zealand white rabbits less than 30 h old were inoculated subcutaneously with 10(3) 50% tissue culture infectious doses of type 2 herpes simplex virus. Infections caused by herpes simplex virus (HSV) are a significant source of morbidity in immunocompromised patients.
To determine the effectiveness of an antiviral to prevent herpes labialis during a brief, high-risk circumstance, 147 persons with a history of sun-induced recurrences were treated prophylactically with oral acyclovir or matching placebo and were observed during their ski holidays.