Treatment of Acyclovir-Resistant, Foscarnet-Unresponsive HSV Infection With Topical Cidofovir in a Child With AIDS

Lateef, Farooq; Don, Philip C.; Kaufmann, M.; White, Soren M.; Weinberg, Jeffrey M

doi:10.1001/archderm.134.9.1169

Cited by 26 publications

(15 citation statements)

References 5 publications

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“…There have been several reports on the efficacy of CDV in the treatment of ACV r and/or PFA r HSV infections in immunocompromised patients [Lalezari et al, 1994[Lalezari et al, , 1995Snoeck et al, 1994;Lateef et al, 1998;LoPresti et al, 1998;Blot et al, 2000]. CDV thus is an effective antiviral drug for the treatment of ACV r and/or PFA r herpesvirus infections, although it is not yet commercially available.…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

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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“…As described in a recent case report, a severe perianal HSV-2 infection in an AIDS patient that was refractory to both ganciclovir and acyclovir treatment healed virtually completely within 30 days of treatment with intravenous cidofovir at a dose of 5 mg/kg once weekly for a total of 3 weeks (115). In a child with AIDS presenting with a facial HSV ulcer that had developed resistance to acyclovir and did not respond to foscavir either, local application of cidofovir 1% led to a prompt recovery (123).…”

Section: Clinical Usefulness Cidofovirmentioning

confidence: 94%

Clinical Potential of the Acyclic Nucleoside Phosphonates Cidofovir, Adefovir, and Tenofovir in Treatment of DNA Virus and Retrovirus Infections

2003

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The acyclic nucleoside phosphonates HPMPC (cidofovir), PMEA (adefovir), and PMPA (tenofovir) have proved to be effective in vitro (cell culture systems) and in vivo (animal models and clinical studies) against a wide variety of DNA virus and retrovirus infections: cidofovir against herpesvirus (herpes simplex virus types 1 and 2 varicella-zoster virus, cytomegalovirus [CMV], Epstein-Barr virus, and human herpesviruses 6, 7, and 8), polyomavirus, papillomavirus, adenovirus, and poxvirus (variola virus, cowpox virus, vaccinia virus, molluscum contagiosum virus, and orf virus) infections; adefovir against herpesvirus, hepadnavirus (human hepatitis B virus), and retrovirus (human immunodeficiency virus types 1 [HIV-1] and 2 [HIV-2], simian immunodeficiency virus, and feline immunodeficiency virus) infections; and tenofovir against both hepadnavirus and retrovirus infections. Cidofovir (Vistide) has been officially approved for the treatment of CMV retinitis in AIDS patients, tenofovir disoproxil fumarate (Viread) has been approved for the treatment of HIV infections (i.e., AIDS), and adefovir dipivoxil (Hepsera) has been approved for the treatment of chronic hepatitis B. Nephrotoxicity is the dose-limiting side effect for cidofovir (Vistide) when used intravenously (5 mg/kg); no toxic side effects have been described for adefovir dipivoxil and tenofovir disoproxil fumarate, at the approved doses (Hepsera at 10 mg orally daily and Viread at 300 mg orally daily)

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“…HSV infection is not considered to be a useful indicator of HIV‐related immunosuppression or viral burden (102), possibly reflecting the difficulty of being able to delineate infection that would have arisen even in the absence of HIV disease. Resistance by HSV to aciclovir therapy can arise in HIV disease; although cidofovir proved to be clinically effective in a 4‐year‐old boy with HSV‐1 related persistent facial ulceration (103). Alternating aciclovir and cidofovir regimens may be a rational approach for severe HSV infection in immunocompromised hosts, prolonging the effectiveness of both agents by delaying the development of an isolate that is resistant to both therapies (103).…”

Section: Viral Infectionsmentioning

confidence: 99%

“…Resistance by HSV to aciclovir therapy can arise in HIV disease; although cidofovir proved to be clinically effective in a 4‐year‐old boy with HSV‐1 related persistent facial ulceration (103). Alternating aciclovir and cidofovir regimens may be a rational approach for severe HSV infection in immunocompromised hosts, prolonging the effectiveness of both agents by delaying the development of an isolate that is resistant to both therapies (103).…”

Section: Viral Infectionsmentioning

confidence: 99%

Current trends of HIV disease of the mouth

Frezzini

Leão

Porter

2005

J Oral Pathology Medicine

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HIV infection affects residents of all countries of the world, but the greater majority of affected individuals reside in the developing world. In the past decade there have been substantial changes in the management of HIV disease, particularly the introduction of highly active antiretroviral therapy (HAART). Such agents have reduced significantly the morbidity and mortality associated with HIV disease, however, they are not available for most HIV-infected individuals in the developing world. There is now considerable understanding of the molecular epidemiology, transmission and therapy of the common opportunistic oral infections of HIV disease, and as a consequence of improved anti-HIV strategies, the frequency and severity of oral disease associated with HIV infection have reduced considerably, although HAART may predispose to human papilloma virus infection of the mouth and potentially increase the risk of later oral squamous cell carcinoma. Despite advances in clinical care the majority of individuals with HIV disease worldwide will continue to develop oral disease, as they are resident in the developing world and do not have ready access to even simple therapies.

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Treatment of Acyclovir-Resistant, Foscarnet-Unresponsive HSV Infection With Topical Cidofovir in a Child With AIDS

Cited by 26 publications

References 5 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

Clinical Potential of the Acyclic Nucleoside Phosphonates Cidofovir, Adefovir, and Tenofovir in Treatment of DNA Virus and Retrovirus Infections

Current trends of HIV disease of the mouth

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Treatment of Acyclovir-Resistant, Foscarnet-Unresponsive HSV Infection With Topical Cidofovir in a Child With AIDS

Cited by 26 publications

References 5 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

Clinical Potential of the Acyclic Nucleoside Phosphonates Cidofovir, Adefovir, and Tenofovir in Treatment of DNA Virus and Retrovirus Infections

Current trends of HIV disease of the mouth

Contact Info

Product

Resources

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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