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Aciclovir (ACV), also known as acyclovir in the US, is an antiviral medication designed for herpesviruses. It is mostly used to treat herpes simplex virus (cold sores or genital sores) and varicella zoster virus (chickenpox or shingles). It also has weaker activity against cytomegalovirus and Epstein-Barr virus. Aciclovir is a nucleic acid analogue derived from guanosine. It works by blocking the production of the viral DNA. Use of aciclovir has largely been replaced with use of the newer version, valaciclovir.
Mechanism of action[edit | edit source]
Aciclovir inhibits replication of the herpesvirus by targeting the viral DNA polymerase, a viral enzyme which makes copies of the viral genome. The viral DNA polymerase mistakenly incorporates aciclovir into the viral genome instead of guanosine, which effectively terminates the copying of the genome.
Clinical Use[edit | edit source]
Aciclovir is prescribed for active infections of herpes simplex virus (cold sores, genital sores) as well as for active infections of varicella zoster virus (chickenpox, shingles). It is also used to prevent reactivation of these viruses while the viruses are in the latent, inactive state. Even when the virus appears to be in the latent, inactive state, aciclovir can reduce the proinflammatory cytokines produced by infected cells.
Aciclovir as a treatment for ME/CFS[edit | edit source]
In 1988, Straus et al. conducted a double-blind, placebo-controlled study of the efficacy of aciclovir in patients with CFS. One group was given a course of IV aciclovir followed by oral aciclovir. The other group received a placebo. Patients with and without antibodies to Epstein-Barr virus early antigens were included in the study. The researchers concluded that aciclovir, as used in this study, did not ameliorate the symptoms of chronic fatigue syndrome: "Of the 24 patients who completed the trial, similar numbers improved with acyclovir therapy and with placebo (11 and 10, respectively). Neither acyclovir treatment nor clinical improvement correlated with alterations in laboratory findings, including titers of antibody to Epstein-Barr virus."
Learn more[edit | edit source]
References[edit | edit source]
- de Clercq, Erik; Field, Hugh J (Oct 5, 2005), "Antiviral prodrugs – the development of successful prodrug strategies for antiviral chemotherapy", British Journal of Pharmacology, Wiley-Blackwell (published January 2006), 147 (1), pp. 1–11, doi:10.1038/sj.bjp.0706446, PMC , PMID 16284630
- Acyclovir, The American Society of Health-System Pharmacists, retrieved Jan 1, 2015
- Elion, G. B. (Jul 20, 1982). "Mechanism of action and selectivity of acyclovir". The American Journal of Medicine. 73 (1A): 7–13. ISSN 0002-9343. PMID 6285736.
- Halford, W. P.; Gebhardt, B. M.; Carr, D. J. (Nov 10, 1997). "Acyclovir blocks cytokine gene expression in trigeminal ganglia latently infected with herpes simplex virus type 1". Virology. 238 (1): 53–63. doi:10.1006/viro.1997.8806. ISSN 0042-6822. PMID 9375008.
- Straus, Stephen E.; Dale, Janet K.; Tobi, Martin; Lawley, Thomas; Preble, Olivia; Blaese, R. Michael; Hallahan, Claire; Henle, Werner (Dec 29, 1988). "Acyclovir Treatment of the Chronic Fatigue Syndrome". New England Journal of Medicine. 319 (26): 1692–1698. doi:10.1056/NEJM198812293192602. ISSN 0028-4793. PMID 2849717.