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 log10 plaque forming units per milliliter, or 4.4 log10 50% tissue culture infective dose per milliliter and 7.5 log10 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.
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 log10 plaque forming units per milliliter, or 4.4 log10 50% tissue culture infective dose per milliliter and 7.5 log10 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.
Authors: Paula Saa; Charles Chiu; Kacie Grimm; Guixia Yu; Richard J Benjamin; Laurence Corash; Susan L Stramer Journal: Transfusion Date: 2019-08-13 Impact factor: 3.157
Authors: A M Hashem; A M Hassan; A M Tolah; M A Alsaadi; Q Abunada; G A Damanhouri; S A El-Kafrawy; M Picard-Maureau; E I Azhar; S I Hindawi Journal: Transfus Med Date: 2019-11-06 Impact factor: 2.019
Authors: Sharad Ambardar; Mark C Howell; Karthick Mayilsamy; Andrew McGill; Ryan Green; Subhra Mohapatra; Dmitri V Voronine; Shyam S Mohapatra Journal: Sci Rep Date: 2022-07-13 Impact factor: 4.996
Authors: Susan L Stramer; Marion C Lanteri; Jaye P Brodsky; Gregory A Foster; David E Krysztof; Jamel A Groves; Rebecca L Townsend; Edward Notari; Sonia Bakkour; Mars Stone; Graham Simmons; Bryan Spencer; Laura Tonnetti; Michael P Busch Journal: Transfusion Date: 2022-06-21 Impact factor: 3.337
Authors: Marion C Lanteri; Felicia Santa-Maria; Andrew Laughhunn; Yvette A Girard; Marcus Picard-Maureau; Jean-Marc Payrat; Johannes Irsch; Adonis Stassinopoulos; Peter Bringmann Journal: Transfusion Date: 2020-04-24 Impact factor: 3.157