Mucocutaneous herpes simplex virus infections in immunocompromised patients

Whitley, Richard J.; Barton, N.; Collins, Eric B.; Whelchel, John D.; Diethelm, Arnold G.

doi:10.1016/0002-9343(82)90098-5

Cited by 48 publications

(8 citation statements)

References 12 publications

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“…The results also indicated that lesion areas decreased at a significantly greater rate among ACV-treated subjects in Utah. Measurement of the rate of change of lesion severity may be the most sensitive means of identifying statistically significant differences between treatment and placebo groups in trials of topical therapy, as we noted in our prior study (8) and as was found as well by Whitley et al (10) in their trial of topical ACV-PEG in immunocompromised subjects.…”

Section: Discussionsupporting

confidence: 70%

“…Topical ACV-PEG has effected a 32% reduction in the time to complete crusting and a 41% reduction in the duration of virus shedding as compared with placebo treatment among primary first-episode cases of herpes genitalis (2). In nonprimary first-episode genital disease, recurrent herpes labialis and genitalis, and recurrent herpes infections in immunocompromised patients, topical ACV-PEG has mainly influenced the duration of virus excretion (2,4,8,10).…”

mentioning

confidence: 99%

“…The modest response of HSV infections to topical ACV-PEG may be related to delayed initiation of treatment, inadequate penetration of ACV into lesions from the PEG vehicle, or both (2,4,8,10). In our previous study of topical 5% ACV-PEG in recurrent herpes labialis, treatment was given four times per day for 5 days after an initial clinic visit; 98% of patients had lesions in the papule, vesicle, or ulcer stage when treatment was begun (8).…”

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confidence: 99%

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Early, patient-initiated treatment of herpes labialis with topical 10% acyclovir

Spruance¹,

Crumpacker²,

Schnipper³

et al. 1984

Antimicrob Agents Chemother

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To determine whether topical acyclovir in polyethylene glycol could reduce the severity of herpes simplex labialis if applied immediately after onset of a recurrence, 10% acyclovir in polyethylene glycol ointment or polyethylene glycol alone was prospectively dispensed to 352 patients in a double-blind, randomized trial. Sixty-nine subjects initiated treatment in the prodrome (57%) or erythema (43%) stage and were followed by clinical and virological criteria, The healing time (6.0 days), maximum lesion area (42 mm2), vesicle or ulcer formation (91%), and maximum lesion virus titer (4.8 logl0 PFU) in the drug recipients were not reduced in comparison with those who received the vehicle (5.2 days, 30 mm2, 75%, and 4.5 log10 PFU, respectively). Topical acyclovir in polyethylene glycol was ineffective for the treatment of herpes labialis despite an optimum therapeutic opportunity.

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Section: Discussionsupporting

confidence: 70%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Early, patient-initiated treatment of herpes labialis with topical 10% acyclovir

Spruance¹,

Crumpacker²,

Schnipper³

et al. 1984

Antimicrob Agents Chemother

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“…Herpes simplex viruses constitute a serious problem in the immunocompromised host, leading to more severe complications [Whitley et al, 1982;Herget et al, 2005;Fatahzadeh and Schwartz, 2007] and a higher probability of developing antiviral resistance (between 5% and 10% of isolates can become resistant to acyclovir) [Englund et al, 1990;Levin et al, 2004]. Furthermore, sequential resistance to acyclovir and foscarnet has been described in HIV-infected patients with low CD4 T-cell counts [Safrin et al, 1994;Schmit and Boivin, 1999].…”

Section: Discussionmentioning

confidence: 99%

Neurovirulence and latency of drug‐resistant clinical herpes simplex viruses in animal models

Dambrosi

Martin

Yim³

et al. 2010

Journal of Medical Virology

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Herpes simplex virus (HSV) resistance to acyclovir or foscarnet results from mutations in viral thymidine kinase (TK) and/or DNA polymerase (pol) genes. Replication kinetics and virulence of TK and/or DNA pol clinical mutants were assessed using models of mouse encephalitis and cotton rat genital infection. Replication capacities in Vero cells of a DNA pol altered strain (L850I) and a TK/DNA pol mutant (C467deletion/A912V) were significantly lower than those of unrelated wild-type (WT) strains, while a double DNA pol mutant (S724N/P920S) demonstrated replication kinetics similar to the WT. The replication of a TK-deficient mutant (G439.5addition) was impaired (low m.o.i.) or unaltered (high m.o.i.) compared to that of a WT virus depending on the viral inoculum. Compared to a survival rate of 6% for mice infected intranasally with WT HSV-1 or -2 viruses, G439.5add, C467deletion/A912V and L850I strains were associated with survival rates of 100% (P < 0.05) whereas mice infected with the S724N/P920S mutant had a survival rate of 33% (P = 0.08). Brain viral titers were higher in mice infected with WT HSV-1 or -2 strains and the double DNA pol mutant. All strains except the DNA pol mutant L850I were able to establish latency in the dorsal root ganglia of cotton rats. A good correlation was generally found between replication kinetics of DNA pol mutants and their neurovirulence potential in mice whereas such correlation was not straightforward for TK mutants.

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“…In the United States, acyclovir ointment (Zovirax Ointment) is approved for use in immunocompromised patients and penciclovir cream (Denavir) for use in otherwise healthy adults. 3,4 In other countries, 1 or more ethical drug treatments, including penciclovir cream, acyclovir cream, 5 and idoxuridine in dimethyl sulfoxide, 6 are generally available. There is experimental evidence that high-dose peroral nucleoside analogue therapy may be highly effective, possibly because of delivery of high concentrations of drug to the site of the infection.…”

Section: Discussionmentioning

confidence: 99%