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Invest Ophthalmol Vis Sci. 1999 Feb;40(2):378-84.
Comparative antiviral efficacies of cidofovir, trifluridine, and acyclovir in the HSV-1 rabbit keratitis model.

Romanowski EG, Bartels SP, Gordon YJ.

Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania, USA.

PURPOSE: To determine the relative antiviral inhibitory activity of topical 1% and 0.5% cidofovir, topical trifluridine (Viroptic; Burroughs-Wellcome, Research Triangle Park, NC), and topical acyclovir (Zovirax; The Wellcome Foundation, London, UK) during a 7-day period for the treatment of herpes simplex virus type 1 (HSV-1) keratitis and HSV-1 replication in the New Zealand rabbit ocular model. METHODS: In a series of four experiments using a two-eye design, a total of 80 New Zealand rabbits were inoculated in both eyes with HSV-1 McKrae after epithelial scarification. Forty-eight hours after inoculation, the rabbits were randomly assigned to a treatment group. Five treatment groups (16 rabbits/group) were evaluated: I, 1% cidofovir, twice daily for 7 days; II, 0.5% cidofovir, twice daily for 7 days; III, 3% acyclovir ointment, five times daily for 7 days; IV, 1% trifluridine, nine times daily for 3 days, then 4 times daily for 4 days; and V, control vehicle twice daily for 7 days. HSV-1 dendritic keratitis was graded in a masked fashion by slit-lamp examination on days 2, 3, 5, 7, 9, 11, and 14. Ocular viral cultures were obtained after slit-lamp examination on days 1, 3, 5, 7, 9, 11, and 14. RESULTS: Compared with the control group, all four treatment groups demonstrated significantly lower viral titers, fewer HSV-1-positive eyes/total during the treatment period, lower keratitis scores, fewer eyes with keratitis/total, and a shorter time to resolution of keratitis. Within the treatment groups, the 1% and 0.5% cidofovir treatments were significantly more effective than acyclovir and trifluridine as measured by the previous viral and keratitis parameters. CONCLUSIONS: Topical 1% and 0.5% cidofovir both appeared to be significantly more efficacious than topical trifluridine and acyclovir, during a 7-day course, in the treatment of experimental HSV-1 ocular disease in the New Zealand rabbit keratitis model.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9950596&dopt=Abstract

J Virol. 2001 Apr;75(7):3240-9.
ICP0 is required for efficient reactivation of herpes simplex virus type 1 from neuronal latency.

Halford WP, Schaffer PA.

Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6076, USA.

Relative to wild-type herpes simplex virus type 1 (HSV-1), ICP0-null mutant viruses reactivate inefficiently from explanted, latently infected mouse trigeminal ganglia (TG), indicating that ICP0 is not essential for reactivation but plays a central role in enhancing the efficiency of reactivation. The validity of these findings has been questioned, however, because the replication of ICP0-null mutants is impaired in animal models during the establishment of latency, such that fewer mutant genomes than wild-type genomes are present in latently infected mouse TG. Therefore, the reduced number of mutant viral genomes available to reactivate, rather than mutations in the ICP0 gene per se, may be responsible for the reduced reactivation efficiency of ICP0-null mutants. We have recently demonstrated that optimization of the size of the ICP0 mutant virus inoculum and transient immunosuppression of mutant-infected mice with cyclophosphamide can be used to establish wild-type levels of ICP0-null mutant genomes in latently infected TG (W. P. Halford and P. A. Schaffer, J. Virol. 74:5957-5967, 2000). Using this procedure to equalize mutant and wild-type genome numbers, the goal of the present study was to determine if, relative to wild-type virus, the absence of ICP0 function in two ICP0-null mutants, n212 and 7134, affects reactivation efficiency from (i) explants of latently infected TG and (ii) primary cultures of latently infected TG cells. Although equivalent numbers of viral genomes were present in TG of mice latently infected with either wild-type or mutant viruses, reactivation of n212 and 7134 from heat-stressed TG explants was inefficient (31 and 37% reactivation, respectively) relative to reactivation of wild-type virus (KOS) (95%). Similarly, n212 and 7134 reactivated inefficiently from primary cultures of dissociated TG cells plated directly after removal from the mouse (7 and 4% reactivation, respectively), relative to KOS (60% reactivation). The efficiency and kinetics of reactivation of KOS, n212, and 7134 from cultured TG cells (treated with acyclovir to facilitate the establishment of latency) in response to heat stress or superinfection with a nonreplicating HSV-1 ICP4(-) mutant, n12, were compared. Whereas heat stress induced reactivation of KOS from 69% of latently infected TG cell cultures, reactivation of n212 and 7134 was detected in only 1 and 7% of cultures, respectively. In contrast, superinfection with the ICP4(-) virus, which expresses high levels of ICP0, resulted in the production of infectious virus in nearly 100% of cultures latently infected with KOS, n212, or 7134 within 72 h. Thus, although latent mutant viral genome loads were equivalent to that of wild-type virus, in the absence of ICP0, n212 and 7134 reactivated inefficiently from latently infected TG cells during culture establishment and following heat stress. Collectively, these findings demonstrate that ICP0 is required to induce efficient reactivation of HSV-1 from neuronal latency.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11238850&dopt=Abstract

Int J Dermatol. 1997 Jun;36(6):457-9.
Cost-benefit of oral acyclovir in the treatment of herpes zoster.

Kubeyinje EP.

Skin Clinic, Arar Central Hospital, Saudi Arabia.

BACKGROUND: Oral acyclovir is a costly antiviral agent shown to be effective in the treatment of herpes zoster. Herpes zoster runs a relatively benign course in young, healthy individuals, as compared with elderly and immunologically compromised patients, in whom complications are common. This study attempts to assess the cost-benefit of treatment with oral acyclovir in young healthy adults with herpes zoster. PATIENTS AND METHODS: The records of 42 healthy young adults suffering from herpes zoster and treated with oral acyclovir (800 mg five times daily for 7 days) were compared with those of 40 healthy young adults with herpes zoster seen during the same period but treated without oral acyclovir. The duration of zoster-associated pain and the presence of complications were noted. RESULTS: There was no statistically significant difference in the duration of zoster-associated pain between the two groups of patients (P = 0.11). Other complications of herpes zoster were few and similar in the two groups. CONCLUSIONS: At a cost of $250 to $300 for a 7-day course of oral acyclovir, the use of this antiviral agent in healthy young individuals with herpes zoster is not justified, especially in developing countries with limited resources.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9248895&dopt=Abstract

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