Viricidal Activity of Biocides

Viricidal Activity Of Biocides   

It is generally accepted that viruses can be divided into two groups according to their susceptibility to biocides. Lipophilic viruses that possess a viral envelope derived from their host (e.g. HIV, herpes simplex virus, influenza virus) are the most susceptible to biocides. The hydrophilic viruses comprise all the non-enveloped viruses and differ tremendously in size and structure. Among these, the small non-enveloped viruses such as the picornaviruses (e.g. poliovirus, hepatitis A virus, foot-and-mouth disease virus) are often considered to be the least susceptible to biocide exposure, although some larger viruses such as adenoviruses and rotaviruses can also be quite resilient. Overall, the viricidal activity of biocides has been little studied and often conflicting information can be found in the peer-reviewed literature. Discrepancies in reported viricidal activity often can be traced to the difference in efficacy test methodology used, and notably the lack of an appropriate neutralizer to quench the activity of the biocides. In general terms if the membrane-active biocides such as biguanides, phenolics, QACs and alcohols have a good efficacy against enveloped viruses, their activity against non-enveloped viruses is limited. A recent study, however, indicated that the limitation in activity of the biguanide PHMB was caused by the formation of viral aggregates.

One of the biggest challenges for biocide activity against viruses is that viruses on surfaces are often associated with soiling and fomites. Such an association allows viral survival (notably for enveloped viruses) on surfaces for long periods of time, as fomites/soiling appear to protect viruses from desiccation. In addition, these organic materials can protect viruses from detrimental chemical agents such as biocides. Viricidal tests do not always consider viruses embedded in an organic load.

In terms of mechanisms of action, the goal of a viricide should be the destruction of the viral nucleic acid. In reality, very few biocides have been shown to affect the viral genome; cationic biocides and alcohols damage the viral envelope releasing an intact viral capsid and genome, although they have been shown to affect the capsid in some instances, but not the viral genome. Biocides that have been shown to interact and break open the capsid (e.g. chlorine-releasing agents) might not have a damaging effect on the viral nucleic acid. To date, only a few biocides (i.e. mainly oxidizing agents) have been observed to damage the viral nucleic acid within the capsid.

The main mechanism of viral resistance to biocides is the formation of viral aggregates before or during biocide exposure. These clumps protect some viruses from the damaging effect of biocides that fail to penetrate deep within these clumps. Chlorine-releasing agents (e.g. hypochlorite) and PHMB have been shown to produce viral aggregates, limiting their viricidal efficacy. To some extent a change in capsid configuration has been shown to alter the susceptibility of viruses to a lower concentration of biocides (e.g. glutaraldehyde). Finally, multiplicity reactivation, a process that has been observed only in vitro, concerns the reassembly of intact viruses that have been structurally damaged by a biocide intervention, but where the genome remains intact. This process, together with the suggestion that the viral genome of certain viruses (e.g. hepatitis B virus) can remain infectious, emphasizes the importance for viricides to destroy the viral nucleic acid.