Sunlight inactivation of human viruses and bacteriophages in coastal waters containing natural photosensitizers.

Sunlight inactivation of poliovirus type 3 (PV3), adenovirus type 2 (HAdV2), and two bacteriophage (MS2 and PRD1) was investigated in an array of coastal waters to better understand solar inactivation mechanisms and the effect of natural water constituents on observed inactivation rates (k(obs)). Reactor scale inactivation experiments were conducted using a solar simulator, and k(obs) for each virus was measured in a sensitizer-free control and five unfiltered surface water samples collected from different sources. k(obs) values varied between viruses in the same water matrix, and for each virus in different matrices, with PV3 having the fastest and MS2 the slowest k(obs) in all waters. When exposed to full-spectrum sunlight, the presence of photosensitizers increased k(obs) of HAdV2, PRD1 and MS2, but not PV3, which provides evidence that the exogenous sunlight inactivation mechanism, involving damage by exogenously produced reactive intermediates, played a greater role for these viruses. While PV3 inactivation was observed to be dominated by endogenous mechanisms, this may be due to a masking of exogenous k(obs) by significantly faster endogenous k(obs). Results illustrate that differences in water composition can shift absolute and relative inactivation rates of viruses, which has important implications for natural wastewater treatment systems, solar disinfection (SODIS), and the use of indicator organisms for monitoring water quality.

Simulated sunlight action spectra for inactivation of MS2 and PRD1 bacteriophages in clear water.

Action spectra for simulated sunlight were measured in clear water for two viruses: PRD1, a double-stranded DNA bacteriophage, and MS2, a single-stranded RNA bacteriophage. Viruses were diluted into phosphate buffered saline (20 mM PBS, pH 7.5) and exposed for 22 h to simulated sunlight either directly or through one of six glass filters with 50% cutoff wavelengths ranging from 280 to 350 nm. Virus survival was measured using the double agar layer plaque method. Both UVA (320-400 nm) and UVB (280-320 nm) light were found to contribute to PRD1 inactivation, while only UVB inactivated MS2. A computational model was developed for interpreting these action spectra with 3-nm resolution. Using these methods, we provide detailed estimates of the sensitivity of MS2 and PRD1 to photoinactivation from 285 to 345 nm. The resulting sensitivity coefficients can be combined with solar spectra to estimate inactivation rates in clear water under different sunlight conditions. This approach will be useful for modeling the inactivation of viruses and other microorganisms in sunlit natural and engineered systems.