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Journal of Virology, November 2005, p. 14244-14252, Vol. 79, No. 22
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.22.14244-14252.2005

Predicted Inactivation of Viruses of Relevance to Biodefense by Solar Radiation

C. David Lytle and Jose-Luis Sagripanti^*

Research and Technology Directorate, Edgewood Chemical Biological Center, U.S. Army, Aberdeen Proving Ground, Maryland 21010-5424

Received 27 June 2005/ Accepted 22 August 2005

UV radiation from the sun is the primary germicide in the environment. The goal of this study was to estimate inactivation of viruses by solar exposure. We reviewed published reports on 254-nm UV inactivation and tabulated the sensitivities of a wide variety of viruses, including those with double-stranded DNA, single-stranded DNA, double-stranded RNA, or single-stranded RNA genomes. We calculated D₃₇ values (fluence producing on average one lethal hit per virion and reducing viable virus to 37%) from all available data. We defined "size-normalized sensitivity" (SnS) by multiplying UV₂₅₄ sensitivities (D₃₇ values) by the genome size, and SnS values were relatively constant for viruses with similar genetic composition. In addition, SnS values were similar for complete virions and their defective particles, even when the corresponding D₃₇ values were significantly different. We used SnS to estimate the UV₂₅₄ sensitivities of viruses for which the genome composition and size were known but no UV inactivation data were available, including smallpox virus, Ebola, Marburg, Crimean-Congo, Junin, and other hemorrhagic viruses, and Venezuelan equine encephalitis and other encephalitis viruses. We compiled available data on virus inactivation as a function of wavelength and calculated a composite action spectrum that allowed extrapolation from the 254-nm data to solar UV. We combined our estimates of virus sensitivity with solar measurements at different geographical locations to predict virus inactivation. Our predictions agreed with the available experimental data. This work should be a useful step to understanding and eventually predicting the survival of viruses after their release in the environment.

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* Corresponding author. Mailing address: U.S. Army Research Development and Engineering Command, Edgewood Chemical Biological Center, Attn: AMSRD-ECB-RT, Aberdeen Proving Ground, MD 21010-5424. Phone: (410) 436-3431. Fax: (410) 436-2081. E-mail: joseluis.sagripanti{at}us.army.mil.

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Journal of Virology, November 2005, p. 14244-14252, Vol. 79, No. 22
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.22.14244-14252.2005

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