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Inactivation of Zika virus in platelet components using amotosalen and ultraviolet A illumination
Author(s) -
Santa Maria Felicia,
Laughhunn Andrew,
Lanteri Marion C.,
Aubry Maite,
Musso Didier,
Stassinopoulos Adonis
Publication year - 2017
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1111/trf.14161
Subject(s) - infectivity , platelet , virology , titer , virus , vero cell , zika virus , ultraviolet , ultraviolet light , pathogen , chemistry , biology , photochemistry , microbiology and biotechnology , immunology , materials science , optoelectronics
BACKGROUND Concerned over the risk of Zika virus (ZIKV) transfusion transmission, public health agencies recommended the implementation of mitigation strategies for its prevention. Those strategies included the use of pathogen inactivation for the treatment of plasma and platelets. The efficacy of amotosalen/ultraviolet A to inactivate ZIKV in plasma had been previously demonstrated, and the efficacy of inactivation in platelets with the same technology was assumed. These studies quantify ZIKV inactivation in platelet components using amotosalen/ultraviolet A. STUDY DESIGN AND METHODS Platelet components were spiked with ZIKV, and ZIKV infectious titers and RNA loads were measured by cell culture‐based assays and real‐time polymerase chain reaction in spiked platelet components before and after photochemical treatment using amotosalen/ultraviolet A. RESULTS The mean ZIKV infectivity titers and RNA loads in platelet components before inactivation were either 4.9 log 10 plaque forming units per milliliter, or 4.4 log 10 50% tissue culture infective dose per milliliter and 7.5 log 10 genome equivalents per milliliter, respectively. No infectivity was detected immediately after amotosalen/ultraviolet A treatment. No replicative virus remained after treatment, as demonstrated by multiple passages on Vero cell cultures; and ZIKV RNA was not detected from the first passage after inactivation. Additional experiments in this study demonstrated efficient inactivation to the limit of detection in platelets manufactured in 65% platelet additive solution, 35% plasma, or 100% plasma. CONCLUSION As previously demonstrated for plasma, robust levels of ZIKV inactivation were achieved in platelet components. With inactivation of higher levels of ZIKV than those reported in asymptomatic, RNA‐reactive blood donors, the pathogen‐inactivation system using amotosalen/ultraviolet A offers the potential to mitigate the risk of ZIKV transmission by plasma and platelet transfusion.