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 D 37 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 UV 254 sensitivities (D 37 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 D 37 values were significantly different. We used SnS to estimate the UV 254 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.

Using a model developed for estimating solar inactivation of viruses of biodefense concerns, we calculated the expected inactivation of SARS-CoV-2 virus, cause of COVID-19 pandemic, by artificial UVC and by solar ultraviolet radiation in several cities of the world during different times of the year. The UV sensitivity estimated here for SARS-CoV-2 is compared with those reported for other ssRNA viruses, including influenza A virus. The results indicate that SARS-CoV-2 aerosolized from infected patients and deposited on surfaces could remain infectious outdoors for considerable time during the winter in many temperate-zone cities, with continued risk for re-aerosolization and human infection. Conversely, the presented data indicate that SARS-CoV-2 should be inactivated relatively fast (faster than influenza A) during summer in many populous cities of the world, indicating that sunlight should have a role in the occurrence, spread rate and duration of coronavirus pandemics.

Influenza virus is readily transmitted by aerosols and its inactivation in the environment could play a role in limiting the spread of influenza epidemics. Ultraviolet radiation in sunlight is the primary virucidal agent in the environment but the time that influenza virus remains infectious outside its infected host remains to be established. In this study, we calculated the expected inactivation of influenza A virus by solar ultraviolet radiation in several cities of the world during different times of the year. The inactivation rates reported here indicate that influenza A virions should remain infectious after release from the host for several days during the winter "flu season" in many temperate-zone cities, with continued risk for reaerosolization and human infection. The correlation between low and high solar virucidal radiation and high and low disease prevalence, respectively, suggest that inactivation of viruses in the environment by solar UV radiation plays a role in the seasonal occurrence of influenza pandemics.

Cupric and ferric ions were able to inactivate five enveloped or nonenveloped, singleor double-stranded DNA or RNA viruses. The virucidal effect of these metals was enhanced by the addition of peroxide, particularly for copper(II). Under the conditions of our test, mixtures of copper(II) ions and peroxide were more efficient than glutaraldehyde in inactivating 4X174, T7, +6, Junin, and herpes simplex viruses. The substances described here should be able to inactivate most, if not all, viruses that have been found contaminating medical devices.

Germicidal UV (also known as UVC) provides a means to decontaminate infected environments as well as a measure of viral sensitivity to sunlight. The present study determined UVC inactivation slopes (and derived D(37) values) of viruses dried onto nonporous (glass) surfaces. The data obtained indicate that the UV resistance of Lassa virus is higher than that of Ebola virus. The UV sensitivity of vaccinia virus (a surrogate for variola virus) appeared intermediate between that of the two virulent viruses studied. In addition, the three viruses dried on surfaces showed a relatively small but significant population of virions (from 3 to 10 % of virus in the inoculum) that appeared substantially more protected by their environment from the effect of UV than the majority of virions tested. The findings reported in this study should assist in estimating the threat posed by the persistence of virus in environments contaminated during epidemics or after an accidental or intentional release.