Knowledge Articles

A Genomic Model for the Prediction of Ultraviolet Inactivation Rate Constants for RNA and DNA Viruses

Wladyslaw J. Kowalski1, William P. Bahnfleth2, Mark T. Hernandez3

1 Immune Building Systems, Inc., 575 Madison Ave., 10thFloor, New York, NY10022, [email protected]

2 The Pennsylvania State University, Department of Architectural Engineering, University Park, PA 16802

3 University of Colorado, UCB 428, Department of Civil, Environmental, and Architectural Engineering,

1111 Engineering Drive #441, Boulder, CO 80309


mathematical model is presented to explain the ultraviolet susceptibility of viruses in terms of genomic sequences that have a high potential for photodimerization. The specific sequences with high dimerization potential include doublets of thymine (TT), thymine-cytosine (TC), cytosine (CC), and triplets composed of single purines combined with pyrimidine doublets. The complete genomes of 49 animal viruses and bacteriophages were evaluated using base-counting software to establish the frequencies of dimerizable doublets and triplets. The model also accounts for the effects of ultraviolet scattering. Constants defining the relative lethality of the four dimer types were determined via curve-fitting. A total 77 water-based UV rate constant data sets were used to represent 22 DNA viruses. A total of 70 data sets were used to represent 27 RNA viruses. Predictions are provided for dozens of viruses of importance to human health that have not previously been tested for UV susceptibility.


Ultraviolet susceptibility, UV rate constants, D90 values, photodimerization, genomic modeling, pyrimidine dimers, viruses, ultraviolet germicidal irradiation, water disinfection, air disinfection, Z values, bioweapons, UVGI.


          Bacterial and fungal contamination of heating, ventilation and air-conditioning (HVAC) cooling coils is a widespread phenomenon which leads to poor indoor air quality (IAQ) (Huegenholtz 1992; Levitin et al., 2001; Apter 1994) and Hospital Acquired Infections (HAIs) (Walter 1969; Ryan et al., 2011). The downstream or supply side of the cooing coil is typically where the highest concentration of microorganisms exist, typically in concentrations of 105 – 106 colony forming units (CFU) of microorganisms per cm² of coil urface area (Hugenholtz and Fuerst 1992; Ryan et al., 2011; Leach and Scheir 2014). In addition to poor IAQ the biofilms growing on cooling coils can lead to underperforming HVAC systems often resulting in reduced airflow, increased pressure differential and uneven airflow uniformity (ASHRAE 2013; Kowalski 2011; Sigel and Nazaroff 2002).
          Ultraviolet Germicidal Irradiation (UVGI) is recognized as an effective tool to treat biofilms growing on HVAC surfaces (ASHRAE 2015; ASHRAE 2016; Leach and Scheir 2014; Ryan et al., 2011). The ASHRAE Handbook for HVAC Applications suggests 50-100μW/cm² (0.394 in²) of UVC intensity, at the coil’s surface, can be an effective coil treatment. However, the document does not quantify the effectiveness nor does it address the UVC intensity required for coil penetration dependent upon fin spacing or coil depth. This paper will present data from laboratory modeling and measurements of the UVC intensities at the surface of typical HVAC coils. Additional analysis is presented to demonstrate the effective UVC penetration of the coil’s interstitial spaces and theoretical microbial reduction on coil surfaces.
          There are two alternative verification methods to test the effectiveness of coil cleaning and disinfection are: A.) sampling for bacteria and fungi pre versus post coil treatment or B.) determining if the coil performance characteristics are returned to design conditions (Kowalski 2011). This paper demonstrates results using both verification methods and will conclude with presentation of field data from case studies of two tertiary care hospitals. The two hospitals were experiencing severely underperforming HVAC systems after repeated chemical coil treatments. Both hospitals were able to mitigate the coil’s biofilm and restore optimum performance by applying a minimum UVGI intensity at the ccoil’s surface of ≥1,000 μW/cm². Contamination from coils was analyzed pre and post UVGI installation. Based upon these data, standards can be established for minimum coil UVC intensities to effectively treat varying coil depths and fin spacing.

UV rate constants and D90 values, as well as other terms defining UV susceptibility, have been determined in laboratory experiments and cataloged for decades, but as yet no one has produced a definitive theoretical model that can predict the ultraviolet susceptibility of microbes. The subject of virus UV susceptibility has been extensively studied and the processes that occur at the molecular level have been quantified to an extraordinary degree, but the complexities of these processes seem to have precluded development of a complete quantitative model of virus inactivation. The pieces to this complex puzzle have, in fact, been available in the literature for some time, particularly in the works of Setlow and Carrier (1966), Smith and Hanawalt (1969), Becker and Wang (1989), and others, but what was unavailable was specific knowledge about the genomes. Through the efforts and industry of molecular biologists, this gap has been filled over the previous two decades and a large number of viruses have had their genomes sequenced and published. This paper applies the basic inactivation models originally proposed by various researchers to an assortment of viral genomes from the NCBI database (NCBI 2009) and statistically evaluates the correlation with known UV D90 values. With some enhancements of the basic model and adjustments to the parameters, a new model is developed herein that provides fairly accurate predictions for both RNA and DNA viruses. This model also includes a new ultraviolet scattering model developed by the authors that contributes to the overall accuracy of the DNA model.

Rate Constant Determinants

Various intrinsic factors determine the sensitivity of a virus to UV exposure under any set of constant ambient conditions of temperature and humidity. These include, but may not be limited to, the following species-dependent properties:

• Physical size
• Molecular weight of DNA or RNA
• DNA Conformation (A or B)
• Presence of chromophores or UV absorbers
• Propensity for clumping or agglutination
• Presence of repair enzymes or dark/light repair mechanisms
• Hydrophilic surface properties
• Relative Index of Refraction
• Specific UV spectrum (broad band UVC/UVB vs. narrow band UVC)
• G+C% and T+A%
• % of Potential Pyrimidine or Purine Dimers

          The physical size of a virus bears no clear relationship with UV susceptibility, except that for the largest viruses, as size increases, the UV rate constant tends to decrease slightly (which is likely the result of UV scattering as discussed later). It might be expected that physical size would confer photoprotection through thickness alone, but it appears that the protein composition of the capsid, not its thickness, is a more important determinant due to the presence of UV-absorbing chromophores (Webb 1965).

         Molecular weight has sometimes been cited as a factor in UV susceptibility (David 1973). However, it has been demonstrated that shearing DNA molecules to half size and then irradiating them does not alter the number of pyrimidine dimers or viral DNA inactivation, and this could be considered evidence that UV-induced damage to DNA is independent of molecular weight (Scholes et al 1967). Figure 1 illustrates this effect for a large number of viruses

– there is no clear relationship between molecular weight (or genome size) and the D90 values for any of the virus types – double-stranded DNA, single-stranded RNA, double-stranded RNA, or single-stranded DNA.


          Other suspected determinants can be dismissed because of their relatively minor or insignificant effect, such as the specific UV spectrum, the presence of repair enzymes, and hydrophilic surface properties. The DNA conformation is apparently a factor, but in this paper DNA viruses (in water – B conformation) are treated separately from RNA viruses (A-conformation). The matter of chromophore content and the relative index of refraction cannot be fully resolved at present and although they might be major factors, they are left for future research. Similarly, the propensity for clumping, which has been noted to be a protective factor, cannot be resolved due to a lack of detailed knowledge regarding chromophore content of envelopes and nucleocapsids.

          One criteria worth examining in detail is the genomic G+C or T+A content. The genomic GC content of RNA viruses varies from about 30-60%, while that of DNA viruses varies from about 30-75%. One study on UVB irradiation of bacteria reports a strong correlation between the formation of cytosine-containing photoproducts with increasing GC content (Matallana-Surget 2008). Since an increased thymine content will likely result in a proportional increase in photodimers of the TT and CT variety, it could be expected that there must be some statistical relationship between G+C% (or conversely with T+A%) and UV susceptibility. Figure 2 shows the results of this comparison for 27 double stranded DNA viruses and Figure 3 shows the same for 28 single-stranded DNA viruses irradiated in water. These comparison represent average UV rate constants for virus species where there are more than one data set. The DNA viruses show no significant correlation. The RNA viruses, however, show a fairly good correlation with an R2 of about 45%. This latter result, however promising, represents the limits of GC% content as a predictor of UV susceptibility, since it only provides an indicator of the presence of thymine doublets and triplets rather than an exact accounting of the potential dimers in any genome.


The UV Scattering Model


Viruses, which are about 0.02 microns and larger, are subject to ultraviolet scattering effects due to the fact that their size is very near the wavelength of ultraviolet light. The effect of scattering is to reduce the effective irradiance to which the microbe is exposed, and it is necessary to account for this attenuation before proceeding with the genomic model. The interaction between ultraviolet wavelengths and the particle is a function of the relative size of the particle compared with the wavelength, as defined by the size parameter:

The scattering of light is due to differences in the refractive indices between the medium and the particle (Modest 1993, Garcia-Lopez et al 2006). The scattering properties of a spherical particle in any medium are defined by the complex index of refraction:

where n = real refractive index

κ = imaginary refractive index (absorptive index or absorption coefficient) The process of independent Mie scattering is also governed by the relative refractive index, defined as follows:

         The refractive index of microbes in visible light has been studied by several researchers. Balch et al (2000) found the median refractive index of four viruses to be 1.06, with a range of 1.03-1.26. Stramski and Kiefer (1991) assumed viruses to have a refractive index of 1.05. Biological cells were assumed by Mullaney and Dean (1970) to have relative refractive indices of about 1.05 in visible light. Klenin (1965) found S. aureus to have a refractive index in the range 1.05-1.12. Petukhov (1964) gives the refractive index of certain bacteria in the limits of 1.37-1.4. There are no studies that address the real refractive index of bacteria or viruses at UV wavelengths except Hoyle ans Wickramasinghe (1983) who suggest ns = 1.43 as a reasonable choice for coliform bacteria. Water has a refractive index of nm = 1.4 in the ultraviolet range. If we scaled the refractive index of viruses (Balch’s value) to that of water (from visible to UV), the estimated real refractive index would be 1.06(1.4/1.33) = 1.12. Garcia-Lopez et al (2006) state that for soft-bodied biological particles n is between 1.04-1.45. All things considered, we choose n = ns = 1.12 for the real refractive index of viruses under UV exposure. In fact, any value in the range 1.03-1.45 seems to have very little net impact on the fraction of scattered UV irradiation as was verified by multiple trials.

          For the imaginary refractive index (the absorptive index) in the UV range no information is available. Per Garcia-Lopez et al (2006), hemoglobin has a κ of 0.01-0.15, while polystyrene has a κ of 0.01-0.82. However, we can reasonably assume a value comparable to that of water, k=1.4, or any value in the range of the real refractive indices given above as they have even less overall impact than the choice of the real refractive index. These values were used as input to a Mie Scattering program (Prahl 2009) to estimate the effects of UV scattering at the wavelength of 253.7 nm, and with negligible concentrations (0.000001 spheres/μm3).


          Table 1 below summarizes the primary parameters computed by the Mie Scattering program in the first eight columns (Prahl 2001), including the scattering efficiency (Qsca), the extinction efficiency (Qext), the absorption efficiency (Qabs), the scattering cross-section (Csca), the extinction cross-section (Cext), and the absorption cross-section (Cabs). The efficiency terms are essentially self-defining but readers may consult the references for detailed definitions and further information on Mie theory (Modest 1993, vandeHulst 1957, Bohren and Huffman 1983). The scattering cross-section represents the area which when multiplied by the incident irradiance gives the power scattered by the particle. The extinction cross-section represents the area which when multiplied by the incident irradiance gives the total power removed from the incident wave by scattering and absorption. The final column shows the computed ratio of the scattering cross-section to the extinction cross-section, which represents the fraction of total irradiance that is scattered away. This fraction is used to reduce the UV exposure dose for the microbes in the genomic model.


           Figure 4 illustrates three parameters from Table 1, the scattering efficiency, the absorption efficiency, and the scattered fraction of incident UV irradiance. The reason that the efficiencies exceed a value of unity is due to the extinction paradox – the fact that in this size range more light can be intercepted than would be by the size of the spherical particle alone. It can be observed that the scattering efficiency increases sharply through the DNA virus size range while the absorption efficiency peaks and then decreases. It can also be seen that the fraction of scattered UV is relatively minor for most RNA viruses, but increases sharply through the DNA virus size range, approaching a limit of about 0.68. The values for UV scatter, last column in Table 1, are hereafter used to decrease the incident UV irradiance (in effect decreasing the UV dose), and may be thought of as correction factors.


          Table 2 shows the diameters of the viruses used in this study and the associated UV scatter correction factors, (which are later applied to the raw D90 values shown in Tables 3 and 4). Virus diameters were obtained from various sources (i.e. Kowalski 2006) and some online databases. Diameters are generally logmean values of the smallest dimension or logmean values of ovoid envelopes, since the logmean value always represents the natural distribution when multiple sizes or a range of sizes occurs. It should be noted that for larger viruses that have an envelope, secondary UV scattering effects may also occur in the nucleocapsid, but these effects are ignored in the current model.


The Genomic UV Susceptibility Model

Double stranded DNA viruses are likely to be the most resistant to UV than single stranded viruses and therefore separate models for ssRNA and dsDNA are appropriate (Gerba et al (2002). Van der Eb and Cohen (1967) demonstrated that the double stranded version of Polyoma virus DNA was four times more resistant to UV inactivation. Capsid structure, as well as nucleic acid size, render double-stranded DNA less susceptible to UV inactivation (Thurston-Enriquez et al 2003). Based on an extensive review of UV rate constants (data not shown), this does appear to be the case, with dsDNA and dsRNA viruses having almost half the UV rate constant of ssRNA and ssDNA viruses.

          The disruption of normal DNA processes occurs as the result of the formation of photodimers, but not all photoproducts appear with the same frequency. Purines are approximately ten times more resistant to photoreaction than pyrimidines (Smith and Hanawalt 1969). Minor products other than CPD dimers, such as interstrand cross-links, chain breaks, and DNA-protein links occur with much less frequency, typically less than 1/1000 of the number of cyclobutane dimers and hydrates may occur at about 1/10 the frequency of cyclobutane dimers (Setlow 1966). Although irradiated vegetating cells produce large amounts of cyclobutane pyrimidine dimers, thymine-containing photoproducts isolated from bacterial spores do not include cyclobutane pyrimidine dimers but include spore photoproducts. Spore photoproducts decrease when the spore transforms to a vegetative state and thymine dimers increase. Spore photoproducts also appear in dry DNA (A conformation) and in RNA, which is in permanent A conformation. For DNA, the thymine dimers decrease under dry conditions (A-DNA) and the spore photoproduct is formed and can become the dominant photoproduct (Rahn and Hosszu 1969). The rate of spore photoproduct formation is unaffected by high concentrations of thymine dimers but high concentrations of spore photoproduct inhibit dimer formation. Wang (1964) first suggested that dimerization is favored when adjacent pyrimidine triplets in ice are suitably oriented and positioned. The effect of base composition can impact the intrinsic sensitivity of DNA to UV irradiation (Smith and Hanwalt 1969). The specific sequence of adjacent base pairs, as well as the frequency of thymines, can de determinants of UV sensitivity. Setlow and Carrier (1966) stated that the probability of photodimerization is approximately proportionally to the nearest-neighbor frequencies of the various pyrimidine sequences. Some 80% of pyrimidines and 45% or purines form UV photoproducts in double-stranded DNA, per studies by Becker and Wang (1989), who also showed that purines only form dimers when adjacent to a pyrimidine doublet. The formation of purine dimers requires transfer of energy in neighboring pyrimidines, and will only occur on the 5’ side of the purine base (50% probability). Becker and Wang (1985) formulated these simple rules for sequence-dependent DNA photoreactivity:

1. Whenever two or more pyrimidine residues are adjacent to one another, photoreactions are observed at both pyrimidines.

2. Non-adjacent pyrimidines, surrounded on both sides by purines, exhibit little or no photoreactivity.

3. The only purines that readily form UV photoproducts are those that are flanked on their 5’ side by two or more contiguous pyrimidine residues.

These rules can be used to extract information from DNA and RNA genomes and will enable computation of the relative probability of photoreactions taking place, a parameter that can be directly compared to UV rate constants as a possible predictor. Table 1 summarizes these rules in terms that can be computed numerically. The doublets and triplets in Table 3 were counted using base counting software written by the author (in C++) and reading from genomes obtained from NCBI (2009). Similar base-counting programs (wordcount programs) are publicly available, such as EMBOSS (Rice et al 2000).

Ignoring the other factors that may determine the UV rate constant, such as the protein coat in viruses and the cell walls of bacteria, about which not enough is known, a function can be written to sum the dimerization probabilities. The probability density map of a spherical genome can be represented by a circular cross-section of the sphere which is subject to a collimated beam of irradiance. The volume of the sphere will be directly proportional to the genome size, since the nucleic acids are essentially packed tight inside a capsid, and because almost all animal viruses of interest are spherical, ovoid, or possess a spherical capsid atop a tail. The size of the model sphere is directly proportional to the base pairs (bp) of the genome cubed, and the area of the cross-section is then the square root of the cube of the base pairs, as illustrated in Figure 4. The dimerization probabilities can be viewed as collapsed onto a circular cross-section exposed to a collimated beam of UV rays. The probability map is illustrative purposes only – the square root of the total dimer probabilities is assumed to be distributed evenly across the cross-sectional area in this model.

Figure 4: The spherical model of DNA has a circular cross-section with a collapsed

dimerization probability density map subject to collimated UV rays.

The square root of the dimer probabilities, counted as per Table 1, is used because it was found on analysis that this produces the best fit overall (for both RNA and DNA), and so without further theoretical justification the dimerization probability equation for ssRNA viruses is written:

Some evidence is available in the literature to allow some starting estimates of the dimer proportionality constants. Per Setlow and Carrier (1966) the average for three bacteria is 1:0.25:0.13. Patrick (1977) suggests ratios of 1:1:1. Unrau (1973) found the ratio was 1:0.5:0.5. Meistrich et al (1970) indicate that in E. coli DNA, the proportions of TT dimers, CT dimers, and CC dimers are in the ratio 1:0.8:0.2, as did Lamola (1973). Table 4 lists 62 of the 70 virus data sets that were used in the ssRNA model, along with the average rate constants and the average D90 values representing 27 single-stranded RNA viruses. These D90 values are not adjusted for UV scatter (per the Table 2 correction factors).

Figure 6: Plot of Dv versus effective UV dose for DNA viruses – the D90 is the effective dose because it has been corrected for UV scattering. The line represents a curve fit (equation shown on graph). A total of 77 data sets were used, weighted in the curve fit of the 22 viruses.

          The lower R2 value may be due to the previously mentioned factor of size – DNA viruses are larger than RNA viruses and may have more innate photoprotection. No available data was omitted from Figure 5 other than a few redundant data sets that were unavailable and the only real outliers are the four Adenovirus sets at about Dv=0.7. Adenovirus is unusually resistant to UV and may have a chromophore-rich envelope to protect the DNA from UV damage or may have robust photorepair mechanisms. Adenoviruses also have hemagglutinins on their outer surfaces that may cause them to clump or aggregate. The aggregation of cells or virions can drastically affect the absorbance through scattering of the incident light (Smith and Hanawalt 1969). Future research on such outliers may provide insight into photoprotection that will lead to improved models of UV susceptibility.

           Table 6 compares the published estimates of the relative proportions of the various dimer types with the values used in the previous models. The factors shown in the table are the three constants in equations (7) and (16). The best fit constants are those that were used in the model in the previous Figures. The zero values assumed for the constants that were not given by the indicated sources did not have any great influence of the R2 value. The hyperchromicity factor was zero for all RNA models, and kept at 0.67 for all DNA models. The results for the DNA model are shown with and without corrections for UV scattering, which make about an 12% difference in the DNA model, but had only a 1% difference on the RNA model, as would be expected from their size. Hyperchromicity had no effect on the RNA model but produced a 1% improvement in the DNA model.




A mathematical model has been presented for the prediction of UV susceptibility of RNA and DNA viruses based on base-counting of potential dimers in the virus genomes. The results correlate well with available data on UV rate constants. This model has been used to estimate the UV rate constants for a range of pathogenic animal viruses and bioweapon agents for which complete genomes were available from the NCBI database and Table 7 summarizes these predictions. Minimum and maximum D90 values are listed that are within the confidence intervals (CIs) of 86% for DNA viruses and 93% for RNA viruses. These CIs represent only the intervals of the data as summarized and do not include any uncertainty in the original 147 data sets, most of which included no error analysis. These rate constant predictions remain to be corroborated by future laboratory testing. Future research will include application of the DNA model to bacteria. Although this genomic model is based on UV rate constants in water it has a direct bearing on airborne UV rate constants as well, since by establishing a theoretical basis for the UV susceptibility of viruses in water, it becomes possible to link them to airborne rate constants – water-based rate constants represent a limit towards which airborne rate constants converge in high humidity (Peccia et al 2001). The variation of UV rate constants with relative humidity (RH) in air is also a function of the DNA conformation which, in turn, determines the relative ratios of pyrimidine dimers, and so a more fundamental understanding of RH effects, and a testable model, may now be possible. Future research into a more complete model of virus inactivation that addresses the photoprotective effects of UV scattering and UV absorption by viral envelopes and nucleocapsids may lead to even greater predictive accuracy. The limits of accuracy of the present model may also be improved as more genomes and data on UV rate constants become available, and as more precise UV experiments are performed using collimated beam systems, and the authors hope that researchers will be inclined to either challenge or confirm the predictions in Table7. If the latter is the case, this model may ultimately enable UV susceptibilities of dangerous pathogens to be determined without the risk of handling them in laboratory tests. The novel approach developed for this research, the use of base-counting software to establish dimerization probabilities, may also have applications in fields unrelated to air and water disinfection, such as ultraviolet photochemistry, mutation research, and solar mutagenesis or skin cancer research.



Aaronson SA. 1970. Effect of ultraviolet irradiation on the survival of simian virus 40 functions in human and mouse cells. J Virol 6(4):393-399.

Abraham G. 1979. The effect of ultraviolet radiation on the primary transcription of Influenza virus messenger RNAs. Virol 97:177-182.

Albrecht T. 1974. Multiplicity reactivation of human cytomegalovirus inactivated by ultra-violet light. Biochim Biophys Acta 905:227-230.

Balch WM, Vaughn J, Novotny J, Drapeau D, Vaillancourt R, Lapierre J, Ashe A. 2000. Light scattering by viral suspensions. Limnol Oceanogr 45(2):492-498.

Battigelli D, Sobsey M, Lobe D. 1993. The inactivation of hepatitis A virus and other model viruses by UV irradiation. Wat Sci Technol 27:339.

Bay PHS, Reichman ME. 1979. UV inactivation of the biological activity of defective interfering particles generated by Vesicular Stomatitis virus. J Virol 32(3):876-884.

Becker MM, Wang Z. 1989. Origin of ultraviolet damage in DNA. J Mol Biol 210:429-438.

Benzer S. 1952. Resistance to ultraviolet light as an index to the reproduction of bacteriophage. J Bact 63:59-72.

Bister K, Varmus HE, Stavnezer E, Hunter E, Vogt PK. 1977. Biological and biochemical studies on the inactivation of Avian Oncoviruses by ultraviolet irradiation. Virol(689-704).

Bockstahler LE, Lytle CD, Stafford JE, Haynes KF. 1976. Ultraviolet enhanced reactivation of a human virus: Effect of delayed infection. Mutat Res 35:189-198.

Bohren C, Huffman D. 1983. Absorption and Scattering of Light by Small Particles. New York: Wiley & Sons. Bohrerova Z, Shemer H, Lantis R, Impellitteri C, Linden K. 2008. Comparative disinfectionefficiency of pulsed and continuous-wave UV irradiation technologies. Wat Res 42:2975-2982.

Bossart W, Nuss DL, Paoletti E. 1978. Effect of UV irradiation on the expression of Vaccinia virus gene products synthesized in a cell-free system coupling transcription and translation. JVirol 26(3):673-680.


Bourre F, Benoit A, Sarasin A. 1989. Respective Roles of Pyrimidine Dimer and Pyrimidine (6-4) Pyrimidone Photoproducts in UV Mutagenesis of Simian Virus 40 DNA in Mammalian Cells. J Virol 63(11):4520-4524.

Butkus MA, Labare MP, Starke JA, Moon K, Talbot M. 2004. Use of aqueous silver to enhance inactivation of coliphage MS-2 by UV disinfection. Appl Environ Microbiol 70(5):2848-2853.

Collier LH, McClean D, Vallet L. 1955. The antigenicity of ultra-violet irradiated vaccinia virus. J Hyg 53(4):513-534.

Cornelis JJ, Su ZZ, Ward DC, Rommelaere J. 1981. Indirect induction of mutagenesis of intact parvovirus H-1 in mammalian cells treated with UV light or with UV-irradiated H-1 or simian virus 40. Proc Natl Acad Sci 78(7):4480-4484.

Danner K, Mayr A. 1979. In vitro studies on Borna virus. II. Properties of the virus. Arch Virol 61:261-271.

Darnell MER, Subbarao K, Feinstone SM, Taylor DR. 2004. Inactivation of the coronavirus that induces severe acute respiratory syndrome, SARS-CoV. J Virol Meth 121:85-91.

David HL. 1973. Response of mycobacteria to ultraviolet radiation. Am Rev Resp Dis 108:1175-1184.

Davidovich IA, Kishchenko GP. 1991. The shape of the survival curves in the inactivation of viruses. Mol Gen, Microb & Virol 6:13-16.

de Roda Husman AM, Bijkerk P, Lodder W, Berg Hvd, Pribil W, Cabaj A, Gehringer P, Sommer R, Duizer E. 2004. Calicivirus Inactivation by Nonionizing (253.7-Nanometer-Wavelength [UV]) and Ionizing (Gamma) Radiation. Appl Environ Microbiol 70(9):5089-5093.

DeFendi V, Jensen F. 1967. Oncogenicity by DNA tumor viruses. Science 157:703-705.

DiStefano R, Burgio G, Ammatuna P, Sinatra A, Chiarini A. 1976. Thermal and ultraviolet inactivation of plaque purified measles virus clones. G Batteriol Virol Immunol 69:3-11.

Dubunin NP, Zasukhina GD, Nesmashnova VA, Lvova GN. 1975. Spontaneous and Induced Mutagenesis in Western Equine Encephalomyelitis Virus in Chick Embryo Cells with Different Repair Activity. Proc Nat Acad Sci 72(1):386-388.

Durance CS, Hoffman R, Andrews RC, Brown M. 2005. Applications of Ultraviolet Light for Inactivation of Adenovirus. : University of Toronto Department of Civil Engineering. Fluke DJ, Pollard EC. 1949. Ultraviolet action spectrum of T1 bacteriophage. Science 110:274-275.

Freeman AG, Schweikart KM, Larcom LL. 1987. Effect of ultraviolet radiation on the Bacillus

subtilis phages SPO2c12, SPP1, and phi 29 and their DNAs. Mut Res 184(3):187-196.

Furuse K, Watanabe I. 1971. Effects of ultraviolet light (UV) irradiation on RNA phage in H2O and in D2O. Virol 46:171-172.

Galasso GJ, Sharp DG. 1965. Effect of particle aggregation on the survival of irradiated Vaccinia virus. J Bact 90(4):1138-1142.

Garcia-Lopez A, Snider A, Garcia-Rubio L. 2006. Rayleigh-Debye-Gans as a model for continuous monitoring of biological particles: Part I, assessment of theoretical limits and approximations. Optics Express 14(19):17. Gerba C, Gramos DM, Nwachuku N. 2002. Comparative inactivation of enteroviruses and adenovirus 2 by UV light. Appl Environ Microbiol 68(10):5167-5169.

Golde A, Latarjet R, Vigier P. 1961. Isotypical interference in vitro by Rous virus inactivated by ultraviolet rays. C R Acad Sci (Paris) 253:2782-2784.

Guillemain B, Mamoun R, Astier T, Duplan J. 1981. Mechanisms of early and late polykaryocytosis induced by the Bovine Leukaemia virus. J Gen Virol 57:227-231.

Gurzadyan GG, Nikogosyan DN, Kryukov PG, Letokhov VS, Balmukhanov TS, Belogurov AA, Zavilgelskij GB. 1981. Mechanism of high power picosecond laser UV inactivation of viruses and bacterial plasmids. Photochem Photobiol 33:835-838.

Harm W. 1968. Effects of dose fractionation on ultraviolet survival of Escherichia coli. Photochem & Photobiol 7:73-86. Havelaar AH. 1987. Virus, bacteriophages and water purification. Vet Q 9(4):356-360.

Helentjaris T, Ehrenfeld E. 1977. Inhibition of host cell protein synthesis by UV-inactivated poliovirus. J Virol 21(1):259-267.

Hill WF, Hamblet FE, Benton WH, Akin EW. 1970. Ultraviolet devitalization of eight selected enteric viruses in estuarine water. Appl Microb 19(5):805-812.

Hollaender A, Oliphant JW. 1944. The inactivating effect of monochromatic ultraviolet radiation on influenza virus. J Bact 48(4):447-454.

Hotz G, Mauser R, Walser R. 1971. Infectious DNA from coliphage T1. 3. The occurrence of single-strand breaks in stored, thermally-treated and UV-irradiated molecules. Int J

Radiat Biol Relat Stud Phys Chem Med 19:519-536.

Hoyle F, Wickramasinghe C. 1983. The ultraviolet absorbance spectrum of coliform bacteria and its relationship to astronomy. Astrophysics and Space Science 95:227-231.

Kariwa H, Fujii N, Takashima I. 2004. Inactivation of SARS coronavirus by means of povidone iodine, physical conditions, and chemical reagents. Jpn J Vet Res 52(3):105-112.

Kelloff G, Aaronson SA, Gilden RV. 1970. Inactivation of Murine Sarcoma and Leukemia viruses by ultra-violet irradiation. Virol 42:1133-1135.

Klein B, Filon AR, vanZeeland AA, vanderEb AJ. 1994. Survival of UV-irradiated vaccinia virus in normal and xeroderma pigmentosum fibroblasts; evidence for repair of UV-damaged viral DNA. Mutat Res 307(1):25-32.

Klenin V. 1965. The problem concerning the scattering of light by suspensions of bacteria. Biofizika 10(2):387-388.

Ko G, Cromenas TL, Sobsey MD. 2005. UV inactivation of adenovirus type 41 measured by cell culture mRNA RT-PCR. Wat Res 39:3643-3649.

Lamola A. 1973. Photochemistry and structure in nucleic acids. Pure Appl Chem 34(2):281-303.

Latarjet R, Cramer R, Montagnier L. 1967. Inactivation, by UV-, X-, and gamma-radiations, of the infecting and transforming capacities of polyoma virus. Virol 33:104-111.

Lee JE, Zoh KD, Ko GP. 2008. Inactivation and UV disinfection of Murine Norovirus with TiO2 under various environmental conditions. Appl Environ Microbiol 74(7):2111-2117.

Levinson W, Rubin R. 1966. Radiation studies of avian tumor viruses and of Newcastle disease virus. Virol 28:533-542.

Linden KG, Thurston J, Schaefer R, Malley JP. 2007. Enhanced UV inactivation of Adenoviruses under polychromatic UV lamps. Appl Environ Microbiol 73(23):7571-7574.

Lovinger GG, Ling HP, Gilden RV, Hatanaka M. 1975. Effect of UV light on RNA directed DNA polymerase activity of murine oncornaviruses. J Virol 15:1273.

Lytle CD. 1971. Host-cell reactivation in mammalian cells. 1. Survival of ultra-violet-irradiated herpes virus in different cell-lines. Int J Radiat Biol Relat Stud Phys Chem Med 19(4):329-337.

Mamane-Gravetz H, Linden KG, Cabaj A, Sommer R. 2005. Spectral sensitivity of Bacillus subtilis spores and MS2 coliphage for validation testing of ultraviolet reactors for water disinfection. Environ Sci Technol 39:7845-7852.

Martin JP, Aubertin AM, Kirn A. 1982. Expression of Frog Virus 3 early genes after ultraviolet irradiation. Virol 122:402-410.

Matallana-Surget S, Meador J, Joux F, Douki T. 2008. Effect of the GC content of DNA on the distribution of UVB-induced bipyrimidine photoproducts. Photochem Photobiol Sci 7:794-801.Meistrich M, Lamola AA, Gabbay E. 1970. Sensitized photoinactivation of bacteriophage T4. Photochem Photobiol 11(3):169-178.

Meng QS, Gerba CP. 1996. Comparative inactivation of enteric Adenoviruses, Poliovirus and coliphages by ultraviolet irradiation. Wat Res 30(11):2665-2668.

Mullaney P, Dean P. 1970. The small angle light scattering fo biological cells. Biophys J 10:764-772

NCBI. 2009. Entrez Genome. : National Center for Biotechnology Information. Nomura S, Bassin RH, Turner W, Haapala DK, Fischinger PJ. 1972. Ultraviolet inactivation of Maloney Leukaemia Virus: Relative target size required for virus replication and rescue of ‘defective’ Murine Sarcoma virus. J Gen Virol 14:213-217.

Nuanualsuwan S, Mariam T, Himathongkham S, Cliver DO. 2002. Ultraviolet inactivation of Feline Calicivirus, Human Enteric Viruses, and coliphages. Photochem Photobiol 76(4):406-410.

Nwachuku N, Gerba CP, Oswald A, Mashadi FD. 2005. Comparative Inactivation of Adenovirus Serotypes by UV Light Disinfection. Appl Environ Microbiol 71(9):5633-5636.

Otaki M, Okuda A, Tajima K, Iwasaki T, Kinoshita S, Ohgaki S. 2003. Inactivation differences of microorganisms by low pressure UV and pulsed xenon lamps. Wat Sci Technol 47(3):185-190.

Owada M, Ihara S, Toyoshima K. 1976. Ultraviolet inactivation of Avian Sarcoma viruses: Biological and Biochemical analysis. Virol 69:710-718.

Patrick MH. 1977. Studies on thymine-derived UV photoproducts in DNA – I. Formation and biological role of pyrimidine adducts in DNA. Photochem Photobiol 25(4):357-372.

Peak MJ, Peak JG. 1978. Action spectra for the ultraviolet and visible light inactivation of phage T7: Effect of host-cell reactivation. Radiat Res 76:325-330.

Peccia J, Werth HM, Miller S, Hernandez M. 2001a. Effects of relative humidity on the ultraviolet induced inactivation of airborne bacteria. Aerosol Sci & Technol 35:728-740.

Petukhov V. 1964. The feasibility of using the Mie theory for the scattering of light from suspensions of spherical bacteria. Biofizika 10(6):993-999.

Rahn RO, Hosszu JL. 1969. Influence of relative humidity on the photochemistry of DNA films. Biochim Biophys Acta 190:126-131.

Rainbow AJ, Mak S. 1970. Functional Heterogeneity of Virions in Human Adenovirus Types 2 and 12. J Vir 5:188-193.

Rainbow AJ, Mak S. 1973. DNA damage and biological function of human adenovirus after U.V. irradiation. Int J Radiat Biol 24(1):59-72.

Rauth AM. 1965. The physical state of viral nucleic acid and the sensitivity of viruses to ultraviolet light. Biophysical Journal 5:257-273.

Rice P, Longden I, Bleasby A. 2000. EMBOSS: The European Molecular Biology Open Software Suite. Trends Genet 16:276-277.

Ronto G, Gaspar S, Berces A. 1992. Phages T7 in biological UV dose measurement. Photochem Photobiol 12:285-294.

Ross LJN, Wildy P, Cameron KR. 1971. Formation of small plaques by Herpes viruses irradiated with ultraviolet light. Virol 45:808-812.

Ryan D, Rainbow A. 1986. Comparative studies of host-cell reactivation, cellular capacity and enahnced reactivation of herpes simplex virus in normal, xeroderma pigmentosum and

Cockayne syndrome fibroblasts. Mut Res 166:99-111.

Sarasin AR, Hanawalt PC. 1978. Carcinogens enhance survival of UV-irradiated simian virus 40 in treated monkey kidney cells: Induction of a recovery pathway? Proc Natl Acad Sci 75(1):356-350.

Scholes CP, Hutchinson F, Hales HB. 1967. Ultraviolet-induced damage to DNA independent of molecular weight. J Mol Biol 24:471-474.

Seemayer NH. 1973. Analysis of minimal functions of Simian virus 40. J Virol 12(6):1265-1271.

Sellers MI, Nakamura R, Tokunaga T. 1970. The effects of ultraviolet irradiation on Mycobacteriophages and their infectious DNAs. J Gen Virol 7(3):233-247.

Selsky C, Weichselbaum R, Little JB. 1978. Defective host-cell reactivation of UV-irradiated Herpes Simplex virus by Bllom’s Syndrome skin fibroblasts. In: Hanawalt PC, Friedberg EC, Cox CF, editors. DNA Repair Mechanisms. New York: Academic Press. Setlow RB, Carrier WL. 1966. Pyrimidine dimers in ultraviolet-irradiated DNA’s. J Mol Biol 17:237-254 (missing 250-254).

Setlow J, Boling M. 1972. Bacteriophage of Haemophilus influenzae – II. Repair of ultraviolet irradiated phage DNA and the capacity of irradiated cells to make phage. J Mol Biol

Shanley JD. 1982. Ultraviolet irradiation of Murine Cytomegalovirus. J Gen Virol 63:251-254.

Shimizu A, Shimizu N, Tanaka A, Jinno-Oue A, Roy B, Shinagawa M, Ishikawa O, Hoshino H.2004 Human T-cell leukaemia virus type 1 is highly sensitive to UV-C light. J Gen Virol


Shin G, Linden KG, Sobsey MD. 2005. Low pressure ultraviolet inactivation of pathogenic enteric viruses and bacteriophages. J Environ Eng Sci 4(Supp 1):S7-S11.

Simonet J, C G. 2006. Inactivation and genome degradation of poliovirus 1 and F-specific RNA phages and degradation of their genomes by UV irradiation at 254 nanometers. Appl
Environ Microbiol 72(12):7671-7677.

Smirnov Y, Kapitulez S, Kaverin N. 1992. Effects of UV-irradiation upon Venezuelan equine encephalomyelitis virus. Virus Res 22(2):151-158.

Smith KC, Hanawalt PC. 1969. Molecular Photobiology: Inactivation and Recovery. New York: Academic Press. Sommer R, Pribil W, Appelt S, Gehringer P, Eschweiler H, Leth H, Cabaj A, Haider T. 2001. Inactivation of bacteriophages in water by means of non-ionizing (UV 253.7nm) and ionizing (gamma) radiation: A comparative approach. Wat Res 35(13):3109-3116.

Stramski D, Keifer D. 1991. Light scattering by microorganisms in the open ocean. Prog Oceanogr 28:343-383.

Templeton MR, Andrews RC, Hofmann R. 2006. Impact of iron particles in groundwater on the UV inactivation of bacteriophages MS2 and T4. J Appl Microbiol 101(3):732-741.

Thurston-Enriquez JA, Haas CN, Jacangelo J, Riley K, Gerba CP. 2003. Inactivation of Feline calicivirus and Adenovirus Type 40 by UV radiation. Appl Environ Microbiol 69(1):577-582.

Unrau P, Wheatcroft R, Cox B, Olive T. 1973. The formation of pyrimidine dimers in the DNA of fungi and bacteria. Biochim Biophys Acta 312:626-632.

van der Eb AJ, Cohen JA. 1967. The effect of UV-irradiation on the plaque-forming ability of single- and double-stranded polyoma virus DNA. Biochem Biophys Res Comm 28(2):284-293.

vandeHulst H. 1957. Light Scattering by Small Particles. New York: Chapman & Hall, Ltd. VonBrodrotti HS, Mahnel H. 1982. Comparative studies on susceptibility of viruses to ultraviolet rays. Zbl Vet Med B 29:129-136.

Wang SY. 1964. The mechanism for frozen aqueous solution irradiation of pyrimidines. Photochem Photobiol 3:395-398.

Wang J, Mauser A, Chao SF, Remington K, Treckmann R, Kaiser K, Pifat D, Hotta J. 2004. Virus inactivation and protein recovery in a novel ultraviolet-C reactor. Vox Sang 86(4):230-238.

Webb SJ. 1965. Bound Water in Biological Integrity. Springfield, IL: Charles C. Thomas. Weidenmann A, Fischer B, Straub U, Wang C-H, Flehmig B, Schoenen D. 1993. Disinfcetion of Hepatitis A virus and MS-2 coliphage in water by ultraviolet irradiation: Comparison of UV-susceptibility. Wat Sci Technol 27(3-4):335-338.

Weigle JJ. 1953. Induction of mutations in a bacterial virus. Proc Natl Acad Sci USA 39:628.

Weiss M, Horzinek MC. 1986. Resistance of Berne virus to physical and chemical treatment. Vet Microbiol 11:41-49.

Wilson B, Roessler P, vanDellen E, Abbaszadegan M, Gerba C. Coliphage MS-2 as a UV water disinfection efficacy test surrogate for bacterial and viral pathogens. In: Association AWW, editor; 1992; Denver, CO. Winkler U, Johns HE, Kellenberger E. 1962. Comparative study of some properties of bacteriophage T4D irradiated with monochromatic ultraviolet light. Virol 18:343-358.

Wolff MH, Schneweis KE. 1973. UV inactivation of herpes simplex viruses, types 1 and 2. Zentralbl Bakteriol 223(4):470-477.

Yoshikura H. 1971. Ultraviolet inactivation of murine leukemia and sarcoma viruses. Int J Cancer 7:131-140.

Yoshikura H. 1989. Thermostability of Human Immunodeficiency virus (HIV-1) in a Liquid Matrix is far higher than that of an ecotropic Murine Leukemia virus. Jpn J Cancer Res 80:1-5.

Zavadova Z, Gresland L, Rosenbergova M. 1968. Inactivation of single- and double-stranded ribonucleic acid of encephalomyocarditis virus by ultraviolet light. Acta Virol 12:515-522.

Zavadova Z, Libikova H. 1975. Comparison of the sensitivity to ultraviolet irradiation of reovirus 3 and some viruses of the Kemerovo group. Acta Virol 19:88-90.



54, 56, 58, 60 Soi Pattanakarn 64, Prawet Sub-district, Prawet District, Bangkok 10250 THAILAND

Call us

Call  :  061-484-8988,
 062-321-5855 (Admin)

Tel : 02-130-6371
FAX : 02-130-6372

Have any questions?