Successful treatment of progressive acyclovir-resistant herpes simplex virus using intravenous foscarnet in a patient with the acquired immunodeficiency syndrome

Sall, R. K.

doi:10.1001/archderm.125.11.1548

Cited by 10 publications

(8 citation statements)

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“…The efficacy of PFA in the treatment of ACV r herpes virus infections was first demonstrated by Vinckier et al [1987] and confirmed by many investigators [Youle et al, 1988;Chatis et al, 1989;Sall et al, 1989;Safrin et al, 1990;Safrin et al, 1991a,b;Hardy, 1992;Verdonck et al, 1993;Safrin et al, 1994;Jones and Paul, 1995;Naik et al, 1995;Breton et al, 1998;Alvarez-McLeod et al, 1999]. As shown in Figure 1, PFA was definitely effective in the treatment of ACV r HSV-1 infection in our patient.…”

Section: Discussionsupporting

confidence: 83%

Bone marrow transplantation in a child with Wiskott‐Aldrich syndrome latently infected with acyclovir‐resistant (ACV^r) herpes simplex virus type 1: Emergence of foscarnet‐resistant virus originating from the ACV^r virus

Saijo

Yasuda

Yabe

et al. 2002

Journal of Medical Virology

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A human leukocyte antigen (HLA)-matched unrelated bone marrow transplantation (BMT) was performed in a 13-year-old patient with the congenital immunodeficiency syndrome, Wiskott-Aldrich syndrome. The patient had a history of acyclovir (ACV)-resistant (ACV(r)) herpes simplex virus type 1 (HSV-1) infections prior to BMT. After BMT, the skin lesions caused by HSV-1 relapsed on the face and genito-anal areas. Ganciclovir (GCV) therapy was initiated, but the mucocutaneous lesions worsened. An HSV-1 isolate recovered from the lesions during this episode was resistant to both ACV and GCV. The ACV(r) isolate was confirmed to have the same mutation in the viral thymidine kinase (TK) gene as that of the previously isolated ACV(r) isolates from the patient. After treatment switch to foscarnet (PFA), there was a satisfactory remission but not a complete recovery. Although the mucocutaneous lesions improved, a PFA-resistant (PFA(r)) HSV-1 was isolated 1 month after the start of PFA therapy. The PFA(r) HSV-1 isolate coded for the same mutation in the viral TK gene as the ACV(r) HSV-1 isolates. Furthermore, the PFA(r) isolate also expressed a mutated viral DNA polymerase (DNA pol) with an amino acid (Gly) substitution for Val at position 715. This is the first report on the clinical course of a BMT-associated ACV(r) HSV-1 infection that subsequently developed resistance to foscarnet as well.

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Section: Discussionsupporting

confidence: 83%

Bone marrow transplantation in a child with Wiskott‐Aldrich syndrome latently infected with acyclovir‐resistant (ACV^r) herpes simplex virus type 1: Emergence of foscarnet‐resistant virus originating from the ACV^r virus

Saijo

Yasuda

Yabe

et al. 2002

Journal of Medical Virology

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“…30 As for TK-dependent drugs, crossresistance between DNA polymerase inhibitors is not always found: this is illustrated by successful intravenous PFA treatment (40 mg/kg per 8 h for 7 days) in progressive vidarabine-resistant (10 mg/kg per day), ACV-resistant HSV infection in a patient with AIDS. 70 However, clinical resistance to PFA (6-to 15 g per day, i.v.) associated with in vitro PFA resistance has also been described in a HIV-infected woman with recurrent and chronic multidermatomal shingles.…”

Section: Mechanisms Of Drug Resistancementioning

confidence: 99%

Chronic verrucous varicella zoster virus skin lesions: clinical, histological, molecular and therapeutic aspects

Nikkels

Snoeck

Rentier

et al. 1999

Clinical and Experimental Dermatology

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SummaryThe outbreak of HIV infection introduced a new phenomenon in varicella zoster virus (VZV) pathology, namely the long-standing wart-like skin lesions that are frequently associated with resistance to thymidine kinase (TK)-dependent antiviral agents. This paper reviews the clinical, histological, and molecular aspects and the therapeutic management of these verrucous lesions. The majority of lesions are characterized by chronically evolving, unique or multiple wart-like cutaneous lesions. The main histo-pathological features include hyperkeratosis, verruciform acanthosis and VZVinduced cytopathic changes with scant or absent cytolysis of infected keratinocytes. The mechanism that establishes the chronic nature of the lesions appears to be associated with a particular pattern of VZV gene expression exhibiting reduced or nondetectable gE and gB synthesis. Drug resistance to TKdependent antiviral agents is a result of nonfunctional or deficient viral TK. This necessitates alternative therapeutic management using antiviral agents that target the viral DNA polymerase.

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“…To decrease recurrences, or to prevent dissemination, almost all patients received chronic suppressive treatment with acyclovir. Prolonged therapeutic regimens at inadequate doses could enhance the emergence of resistances to this agent [9,15,[17][18][19][20]25,[28][29][30]. In these strains, deficient or altered viral thymidine kinase function has been reported [9,10,15,19,20,[28][29].…”

Section: Discussionmentioning

confidence: 99%

“…In these strains, deficient or altered viral thymidine kinase function has been reported [9,10,15,19,20,[28][29]. Foscarnet has been found to be effective in acyclovir-resistant herpetic infections [21,23,25,27,[29][30], as this viral DNApolymerase inhibitor does not require phosphorylation by viral thymidine kinase for antiviral activity.…”

Section: Discussionmentioning

confidence: 99%

Atypical herpes zoster in a patient with AIDS

Fernández-Díaz

Herranz

Lucas

et al. 1995

Acad Dermatol Venereol

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Objective To report a case of persistent infection by varicella-zoster virus (VZV) in an HIV-infected patient who presented with atypical, hyperkeratotic viral lesions and a partial response to acyclovir.Methods Viral changes found on histopathological examination; definitive diagnosis of VZV infection was established by viral culture.Results Lesions of chronic hyperkeratotic herpes zoster responded partially to acyclovir therapy, and complete resolution was achieved with intravenous foscamet. Absence of visceral involvement.Conclusion Prolonged acyclovir therapy for herpes virus infections in HIV-seropositive patients may represent an important pathogenic factor for the appearance of atypical clinical forms associated with drug-resistant viral strains.

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Successful treatment of progressive acyclovir-resistant herpes simplex virus using intravenous foscarnet in a patient with the acquired immunodeficiency syndrome

Cited by 10 publications

References 0 publications

Bone marrow transplantation in a child with Wiskott‐Aldrich syndrome latently infected with acyclovir‐resistant (ACV^r) herpes simplex virus type 1: Emergence of foscarnet‐resistant virus originating from the ACV^r virus

Bone marrow transplantation in a child with Wiskott‐Aldrich syndrome latently infected with acyclovir‐resistant (ACV^r) herpes simplex virus type 1: Emergence of foscarnet‐resistant virus originating from the ACV^r virus

Chronic verrucous varicella zoster virus skin lesions: clinical, histological, molecular and therapeutic aspects

Atypical herpes zoster in a patient with AIDS

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Successful treatment of progressive acyclovir-resistant herpes simplex virus using intravenous foscarnet in a patient with the acquired immunodeficiency syndrome

Cited by 10 publications

References 0 publications

Bone marrow transplantation in a child with Wiskott‐Aldrich syndrome latently infected with acyclovir‐resistant (ACVr) herpes simplex virus type 1: Emergence of foscarnet‐resistant virus originating from the ACVr virus

Bone marrow transplantation in a child with Wiskott‐Aldrich syndrome latently infected with acyclovir‐resistant (ACVr) herpes simplex virus type 1: Emergence of foscarnet‐resistant virus originating from the ACVr virus

Chronic verrucous varicella zoster virus skin lesions: clinical, histological, molecular and therapeutic aspects

Atypical herpes zoster in a patient with AIDS

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Bone marrow transplantation in a child with Wiskott‐Aldrich syndrome latently infected with acyclovir‐resistant (ACV^r) herpes simplex virus type 1: Emergence of foscarnet‐resistant virus originating from the ACV^r virus

Bone marrow transplantation in a child with Wiskott‐Aldrich syndrome latently infected with acyclovir‐resistant (ACV^r) herpes simplex virus type 1: Emergence of foscarnet‐resistant virus originating from the ACV^r virus