Photochemical Inactivation of Chikungunya Virus in Human Apheresis Platelet Components by Amotosalen and UVA Light

Konstantin A. Tsetsarkin Department of Pathology, University of Texas Medical Branch, Galveston, Texas; Cerus Corporation, Concord, California; Biosecurity Research Institute, Kansas State University, Manhattan, Kansas

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Adam Sampson-Johannes Department of Pathology, University of Texas Medical Branch, Galveston, Texas; Cerus Corporation, Concord, California; Biosecurity Research Institute, Kansas State University, Manhattan, Kansas

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Lynette Sawyer Department of Pathology, University of Texas Medical Branch, Galveston, Texas; Cerus Corporation, Concord, California; Biosecurity Research Institute, Kansas State University, Manhattan, Kansas

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John Kinsey Department of Pathology, University of Texas Medical Branch, Galveston, Texas; Cerus Corporation, Concord, California; Biosecurity Research Institute, Kansas State University, Manhattan, Kansas

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Stephen Higgs Department of Pathology, University of Texas Medical Branch, Galveston, Texas; Cerus Corporation, Concord, California; Biosecurity Research Institute, Kansas State University, Manhattan, Kansas

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Dana L. Vanlandingham Department of Pathology, University of Texas Medical Branch, Galveston, Texas; Cerus Corporation, Concord, California; Biosecurity Research Institute, Kansas State University, Manhattan, Kansas

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Chikungunya virus (CHIKV) is a mosquito-borne alphavirus that recently re-emerged in Africa and rapidly spread into countries of the Indian Ocean basin and South-East Asia. The mean viremic blood donation risk for CHIKV on La Réunion reached 1.5% at the height of the 2005–2006 outbreaks, highlighting the need for development of safety measures to prevent transfusion-transmitted infections. We describe successful inactivation of CHIKV in human platelets and plasma using photochemical treatment with amotosalen and long wavelength UVA illumination. Platelet components in additive solution and plasma units were inoculated with two different strains of high titer CHIKV stock (6.0–8.0 logs/mL), and then treated with amotosalen and exposure to 1.0–3.0 J/cm2 UVA. Based on in vitro assays of infectious virus pre- and post-treatment to identify endpoint dilutions where virus was not detectable, mean viral titers could effectively be reduced by > 6.4 ± 0.6 log10 TCID50/mL in platelets and ≥ 7.6 ± 1.4 logs in plasma, indicating this treatment has the capacity to prevent CHIKV transmission in human blood components collected from infected donors in or traveling from areas of CHIKV transmission.

Author Notes

* Address correspondence to Dana L. Vanlandingham, Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, 1800 Denison Ave., Manhattan, KS 66506. E-mail: dlvanlan@vet.k-state.edu

Financial support: Funding for this study was provided by Cerus Corporation.

Authors' addresses: Konstantin A. Tsetsarkin, National Institutes of Allergy and Infectious Diseases, Neurotropic Flaviviruses Section, Bethesda, MD, E-mail: tsetsarkinka@niaid.nih.gov. Adam Sampson-Johannes, Lynette Sawyer, and John Kinsey, Cerus Corporation, Concord, CA, E-mails: Dna.3@sbcglobal.net, LSawyer@cerus.com, and shotokando@aol.com. Stephen Higgs, Biosecurity Research Institute, Kansas State University, Manhattan, KS, E-mail: shiggs@k-state.edu. Dana L. Vanlandingham, Department of Diagnostic Medicine and Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS, E-mail: dlvanlan@vet.k-state.edu.

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