Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2010 Jun;24(2):413-37.
doi: 10.1016/j.idc.2010.01.001.

Antiviral drug resistance: mechanisms and clinical implications

Lynne Strasfeld  1 , Sunwen Chou
Affiliations
Review

Antiviral drug resistance: mechanisms and clinical implications

Lynne Strasfeld et al. Infect Dis Clin North Am. 2010 Jun.

Corrected and republished in

Abstract

Antiviral drug resistance is an increasing concern in immunocompromised patient populations, where ongoing viral replication and prolonged drug exposure lead to the selection of resistant strains. Rapid diagnosis of resistance can be made by associating characteristic viral mutations with resistance to various drugs as determined by phenotypic assays. Management of drug resistance includes optimization of host factors and drug delivery, selection of alternative therapies based on knowledge of mechanisms of resistance, and the development of new antivirals. This article discusses drug resistance in herpesviruses and hepatitis B.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Map of CMV UL97 gene functional domains and resistance mutations. Ganciclovir resistance (GCVr) mutations are clustered at codons 460, 520 and 590–607. In the latter region mutations A594V, L595S, C592G and C603W are some of the most common, but a variety of point and in-frame deletion mutations are known to confer varying degrees of GCV resistance. Not all sequence changes at codons 590–607 confer ganciclovir resistance.
Figure 2
Figure 2
Map of CMV DNA polymerase functional domains, resistance mutations, and associated phenotypes. All listed mutations have been found in clinical isolates and validated by recombinant phenotyping. Shaded regions indicate where resistance mutations are clustered, with associated phenotypes indicated below. Updated from [92]. GCVr = ganciclovir resistance. CDVr = cidofovir resistance. FOSr = foscarnet resistance.
Figure 3
Figure 3
Map of HBV polymerase gene functional domains (terminal protein, spacer, Pol/rt = polymerase/reverse transcriptase, RNaseH), catalytic subdomains (A–G), and resistance mutations.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Elion GB, Furman PA, Fyfe JA, et al. The selectivity of action of an antiherpetic agent, 9-(2-hydroxyethoxymethyl) guanine. Reproduced from Proc Natl Acad Sci USA. 1977;74:5716–5720. - PubMed
    2. Rev Med Virol. 1999;9(3):147–52. discussion 52–3. - PubMed
    1. Elion GB. Acyclovir: discovery, mechanism of action, and selectivity. J Med Virol. 1993;(Suppl 1):2–6. - PubMed
    1. Gilbert C, Bestman-Smith J, Boivin G. Resistance of herpesviruses to antiviral drugs: clinical impacts and molecular mechanisms. Drug Resist Updat. 2002;5(2):88–114. - PubMed
    1. Wagstaff AJ, Faulds D, Goa KL. Aciclovir. A reappraisal of its antiviral activity, pharmacokinetic properties and therapeutic efficacy. Drugs. 1994;47(1):153–205. - PubMed
    1. Haefeli WE, Schoenenberger RA, Weiss P, et al. Acyclovir-induced neurotoxicity: concentration-side effect relationship in acyclovir overdose. Am J Med. 1993;94(2):212–5. - PubMed

Publication types

Substances

-