Editing Antiviral drug (section)

=== Origin of antiviral resistance ===
The genetic makeup of viruses is constantly changing, which can cause a virus to become resistant to currently available treatments.<ref>{{Cite book|last1=Nijhuis|first1=M|last2=van Maarseveen|first2=NM|last3=Boucher|first3=CA|title=Antiviral Strategies|chapter=Antiviral Resistance and Impact on Viral Replication Capacity: Evolution of Viruses Under Antiviral Pressure Occurs in Three Phases|series=Handbook of Experimental Pharmacology|volume=189|date=2009|issue=189|pages=299–320|doi=10.1007/978-3-540-79086-0_11|pmid=19048205|isbn=978-3-540-79085-3}}</ref> Viruses can become resistant through spontaneous or intermittent mechanisms throughout the course of an antiviral treatment.<ref name="CDC"/> Immunocompromised patients, more often than immunocompetent patients, hospitalized with [[pneumonia]] are at the highest risk of developing oseltamivir resistance during treatment.<ref name= CDC/> Subsequent to exposure to someone else with the flu, those who received oseltamivir for "post-exposure prophylaxis" are also at higher risk of resistance.<ref>{{cite web|title=WHO {{!}} Antiviral use and the risk of drug resistance|url=https://www.who.int/csr/disease/swineflu/notes/h1n1_antiviral_use_20090925/en/|archive-url=https://web.archive.org/web/20140901001937/http://www.who.int/csr/disease/swineflu/notes/h1n1_antiviral_use_20090925/en/|archive-date=1 September 2014|website=www.who.int}}</ref>

The mechanisms for antiviral resistance development depend on the type of virus in question. RNA viruses such as hepatitis C and influenza A have high error rates during genome replication because RNA polymerases lack proofreading activity.<ref name="Bookshelf ID: NBK21523">{{cite book |last1=Lodish |first1=H |last2=Berk |first2=A |last3=Zipursky |first3=S |title=Molecular Cell Biology: Viruses – Structure, Function, and Uses |date=2000 |publisher=W. H. Freeman and Company |location=New York, New York |url=https://www.ncbi.nlm.nih.gov/books/NBK21523/ |access-date=1 December 2018}}</ref> RNA viruses also have small genome sizes that are typically less than 30 kb, which allow them to sustain a high frequency of mutations.<ref name="RacanielloRNA">{{cite web |last1=Racaniello |first1=Vincent |title=The error-prone ways of RNA synthesis |url=http://www.virology.ws/2009/05/10/the-error-prone-ways-of-rna-synthesis/ |website=Virology Blog |date=10 May 2009 |access-date=1 December 2018}}</ref> DNA viruses, such as HPV and herpesvirus, hijack host cell replication machinery, which gives them proofreading capabilities during replication. DNA viruses are therefore less error prone, are generally less diverse, and are more slowly evolving than RNA viruses.<ref name="Bookshelf ID: NBK21523" /> In both cases, the likelihood of mutations is exacerbated by the speed with which viruses reproduce, which provides more opportunities for mutations to occur in successive replications. Billions of viruses are produced every day during the course of an infection, with each replication giving another chance for mutations that encode for resistance to occur.<ref name="PMID19906671">{{cite journal |last1=Thebaud |first1=G |last2=Chadeouf |first2=J |last3=Morelli |first3=M |last4=McCauley |first4=J |last5=Haydon |first5=D |title=The relationship between mutation frequency and replication strategy in positive sense single-stranded RNA viruses |journal=Proc. Biol. Sci. |volume=277 |date=2010 |issue=1682 |pages=809–17 |pmid=19906671 |pmc=2842737 |doi=10.1098/rspb.2009.1247 }}</ref>

Multiple strains of one virus can be present in the body at one time, and some of these strains may contain mutations that cause antiviral resistance.<ref name="PMID9728000" /> This effect, called the [[quasispecies model]], results in immense variation in any given sample of virus, and gives the opportunity for natural selection to favor viral strains with the highest fitness every time the virus is spread to a new host.<ref>{{cite journal |title=Viruses are models for embracing diversity |journal=Nature Microbiology |date=2018 |volume=3 |issue=4 |page=389 |doi=10.1038/s41564-018-0145-3 |pmid=29588540 |doi-access=free }}</ref> Recombination, the joining of two different viral variants, and [[reassortment]], the swapping of viral gene segments among viruses in the same cell, also play a role in resistance, especially in influenza.<ref name="RacanielloRNA" />

Antiviral resistance has been reported in antivirals for herpes, HIV, hepatitis B and C, and influenza, but antiviral resistance is a possibility for all viruses.<ref name="PMID9728000" /> Mechanisms of antiviral resistance vary between virus types.{{citation needed|date=October 2023}}