How does UVC disinfection work?
As evident by multiple research studies and reports, when biological organisms are exposed to deep UV light in the range of 200 nm to 300 nm it is absorbed by DNA, RNA, and proteins.
Absorption by proteins can lead to rupture of cell walls and death of the organism. Absorption by DNA or RNA (specifically by thymine bases) is known to cause inactivation of the DNA or RNA double helix strands through the formation of thymine dimers. If enough of these dimers are created in DNA, the DNA replication process is disrupted, and the cell cannot replicate.
Cells that cannot replicate, cannot infect.
It is widely accepted that it is not necessary to kill pathogens with UV light, but rather apply enough UV light to prevent the organism from replicating. The UV doses required to prevent replication are orders of magnitude lower than required to kill, making the cost of UV treatment to prevent infection commercially viable.
Ensuring complete inactivation
Generally, in bacteria, a number of different repair mechanisms have evolved to repair these UV-induced lesions. These mechanisms include direct reversal of the damage by a photolyase (photo reactivation), removing of the damaged base by a DNA glycosylase (base excision repair, BER), incision of the DNA adjacent to the damage by an endonuclease (UV-damage endonuclease, UVDE) or removal of a complete oligonucleotide containing the damage (nucleotide excision repair, NER). As a result, the strategy in UV disinfection has been to provide a sufficiently high dosage to ensure that nucleic acid is damaged beyond repair.
