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.
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.
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