scholarly journals Efficacy of Brincidofovir (BCV) Prophylaxis Against Herpes Simplex Virus (HSV) and Varicella Zoster Virus (VZV) in Hematopoietic Cell Transplantation (HCT) Recipients

2016 ◽  
Vol 22 (3) ◽  
pp. S172-S173
Author(s):  
Yeon Joo Lee ◽  
Seong Jin Kim ◽  
Yao-Ting Huang ◽  
Daniel Burack ◽  
Esperanza B. Papadopoulos ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Varicella Zoster Virus ◽  
Cell Transplantation ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Varicella Zoster ◽  
Simplex Virus

Treatment of Severe Acyclovir-Resistant Herpes Simplex Virus Infection with Continuous Infusion of High Dose Acyclovir Following Hematopoietic Cell Transplantation.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2224-2224
Author(s):  
Janet H. Kim ◽  
Joanna Schaenman ◽  
Dora Y. Ho ◽  
Janice (Wes) M. Brown
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Continuous Infusion ◽  
Cell Transplantation ◽  
Hematopoietic Cell Transplantation ◽  
Conflicts Of Interest ◽  
Hematopoietic Cell ◽  
Myelogenous Leukemia ◽  
High Dose ◽  
Simplex Virus

Abstract Abstract 2224 Poster Board II-201 Although acyclovir (ACV)-resistant herpes simplex virus (HSV) occurs in healthy patients, higher rates have been reported in 7-27% of immunocompromised patients, particularly in the setting of acyclovir prophylaxis. Infection due to ACV-resistant HSV (ACV-R HSV) is frequently severe and poses challenges to treatment, particularly following hematopoietic cell transplantation (HCT). Unfortunately, currently available alternative therapies including foscarnet, cidofovir, and ganciclovir are frequently limited by their toxicity profile. We present a series of five HCT patients from 1997-2008 with severe infections due to ACV-R HSV who were successfully treated with continuous infusion of high dose acyclovir. A Pubmed search of published literature from 1948-2009 confirmed this as the first report of ACV-R HSV in HCT patients treated with this regimen. The characteristics of the patients are summarized in the table. Patients ranged in age from 24 to 55 and had undergone an allogeneic HCT following a myeloablative preparative regimen. All grafts were composed of peripheral blood hematopoietic cells. Underlying diseases included acute myelogenous leukemia, myelodysplastic syndrome, and essential thrombocytosis. Four of the five patients were receiving treatment for GVHD of the skin (grades 2-4), with regimens that included varying doses of prednisone. Infection was due to HSV-1 in three patients and HSV-2 in two. In vitro testing revealed that high median inhibitory concentrations were necessary to inhibit viral replication by 50% (MIC50) for all five isolates consistent with resistance to acyclovir, ganciclovir, and foscarnet. Failed HSV treatment regimens included standard, intermittent doses of acyclovir (5-10 mg/kg IV every eight hours), foscarnet, cidofovir, and/or famciclovir. Adverse reactions to these agents included severe renal insufficiency, hyponatremia, and neutropenia. The doses of ACV administered via continuous infusion ranged from 30 to 50 mg/kg per day, and time to resolution of lesions ranged from 1 week to 2 months. No patients experienced toxicity associated with continuous infusion of high dose acyclovir and therapy could be continued as an outpatient when appropriate. Conclusions: Continuous infusion of high dose acyclovir for acyclovir resistant HSV is an attractive and more tolerable alternative for patients failing standard dose intermittent infusion acyclovir or intolerant of alternative standard therapies such as foscarnet, cidofovir, or ganciclovir. At this time it is not clear how the altered pharmacokinetics that results from continuous infusion of high doses of acyclovir overcomes viral resistance. We are currently investigating the mechanisms by which the sustained levels of ACV provide this therapeutic advantage. Disclosures: No relevant conflicts of interest to declare.

Herpes simplex virus and varicella zoster virus

2015 ◽  
Vol 28 (6) ◽  
pp. 589-595 ◽  
Author(s):  
Surjo K. De ◽  
Jennifer C.L. Hart ◽  
Judith Breuer
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Varicella Zoster Virus ◽  
Varicella Zoster ◽  
Simplex Virus

scholarly journals A Genome-Wide Comparative Evolutionary Analysis of Herpes Simplex Virus Type 1 and Varicella Zoster Virus

PLoS ONE ◽  
2011 ◽  
Vol 6 (7) ◽  
pp. e22527 ◽  
Author(s):  
Peter Norberg ◽  
Shaun Tyler ◽  
Alberto Severini ◽  
Rich Whitley ◽  
Jan-Åke Liljeqvist ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Varicella Zoster Virus ◽  
Herpes Simplex Virus Type ◽  
Evolutionary Analysis ◽  
Varicella Zoster ◽  
Genome Wide ◽  
A Genome ◽  
Simplex Virus

Viable herpes simplex virus type 1 and varicella-zoster virus in the trigeminal ganglia of human cadavers

2013 ◽  
Vol 85 (5) ◽  
pp. 833-838 ◽  
Author(s):  
Hisako Saitoh ◽  
Yuko Momma ◽  
Hiroyuki Inoue ◽  
Daisuke Yajima ◽  
Hirotaro Iwase
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Varicella Zoster Virus ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Trigeminal Ganglia ◽  
Varicella Zoster ◽  
Human Cadavers ◽  
Simplex Virus

Herpesvirus Infections

2018 ◽  
Author(s):  
Martin S. Hirsch
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Varicella Zoster Virus ◽  
Ganglion Cells ◽  
Human Herpesvirus ◽  
Herpes Infection ◽  
Varicella Zoster ◽  
Clinical Syndromes ◽  
Simplex Virus ◽  
Human Herpesviruses

The herpes group of viruses is composed of at least eight human viruses and numerous animal viruses. The human herpesviruses include herpes simplex virus types 1 and 2 (HSV-1 and HSV-2), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human herpesvirus types 6 (HHV-6), 7 (HHV-7), and 8 (HHV-8, also known as Kaposi sarcoma–associated herpesvirus). Human herpesviruses share the properties of latency and reactivation. Members of the group can cause productive lytic infections, in which infectious virus is produced and cells are killed, or nonproductive lytic infections, in which viral DNA persists but complete replication does not occur and cells survive. After acute lytic infections, herpesviruses often persist in a latent form for years; periodic reactivations are followed by recurrent lytic infections. Sites of latency vary: HSV and VZV persist in neural ganglion cells, EBV persists in B cells, and CMV probably remains latent in many cell types. The sites of latency for HHV-6 and HHV-7 have not been identified, although both herpesviruses have been detected in salivary glands. All human herpesviruses have a worldwide distribution. Considerable efforts are being directed toward the development of vaccines and antiviral agents that will be active against herpesviruses. This chapter discusses the epidemiology, pathogenesis, diagnosis, prevention, and treatment of herpes simplex virus and varicella-zoster virus and their clinical syndromes. The descriptions of the clinical syndromes include complications and clinical features, as well as descriptions of symptoms. Tables provide information on chemotherapy for primary genital and mucocutaneous herpes infection, suppression of severe and recurring genital herpes infection, and varicella-zoster infection. Figures provide photographic illustrations of the various clinical syndromes. A sidebar about herpesvirus information on the Internet provides further detail. This review contains 123 references, 4 tables, and 6 highly rendered figures.

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