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Declovir (Acyclovir)
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Acyclovir

Declovir is used to decrease pain and speed the healing of sores or blisters in people who have varicella (chickenpox), herpes zoster (shingles; a rash that can occur in people who have had chickenpox in the past), and first-time or repeat outbreaks of genital herpes (a herpes virus infection that causes sores to form around the genitals and rectum from time to time). Declovir is also sometimes used to prevent outbreaks of genital herpes in people who are infected with the virus. Declovir is in a class of antiviral medications called synthetic nucleoside analogues. It works by stopping the spread of the herpes virus in the body. Declovir will not cure genital herpes and may not stop the spread of genital herpes to other people.

Other names for this medication:
Acyclovir, Abduce, Acic, Aciclobeta, Aciclomed, Aciclostad, Aciclovirum, Acifar, Acihexal, Aciklovir, Acitop, Acivir, Acivirex, Acivision, Acix, Actios, Activir, Acycloguanosine, Acyl, Acyrax, Acyvir, Aklovir, Antivir, Asiviral, Avir, Aviral, Avix, Avorax, Blistex, Cicloferon, Cicloviral, Clinovir, Clirbest, Clopes, Clovate, Clovir, Cusiviral, Cyclomed, Cyclovax, Cyclovex, Cyclovir, Danovir, Declovir, Epsin, Eurovir, Hascovir, Hernovir, Herperax, Herpesil, Herpesin, Herpex, Herpin, Herplex, Heviran, Immunovir, Lisovyr, Lovir, Lovire, Lovrak, Medovir, Menova, Ocuvir, Poviral, Ranvir, Remex, Rexan, Scanovir, Sitavig, Sophivir, Soviclor, Supraviran, Telviran, Uniplex, Vilerm, Viraban, Viralex, Viratac, Viratop, Virest, Virestat, Virex, Virless, Virolex, Viromed, Virosil, Virostatic, Virovir, Virucid, Viruderm, Virustat, Virux, Vivorax, Xiclovir, Xorox, Zevin, Ziverone, Zoral, Zorax, Zoraxin, Zovirax,

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Resistance to fluconazole and cross-resistance to amphotericin B in Candida albicans from AIDS patients caused by defective sterol delta5,6-desaturation. Toxicity of busulfan and cyclophosphamide (BU/CY2) in patients with hematologic malignancies.

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Circulating HCV-RNA, HCV genotype, and liver histology in asymptomatic individuals reactive for anti-HCV antibody and their follow-up study. UV-vis spectroscopic analysis shows that the electronic interactions between pendent aryl and heteroaryl groups across the iodonium center can be dictated by substitution. Dysfunctional glucocorticoid receptor with a single point mutation ablates the CCAAT/enhancer binding protein-dependent growth suppression response in a steroid-resistant rat hepatoma cell variant. Twenty-one years later, with another first, the crystal structure of the related Na-galactose transporter has been described and opens new avenues to understand structure-function relationships and intelligent drug design for transporters.

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