Evidence map›Paper›PMID 21827431›Full record

ReviewInfectious disorders drug targets2011

The genetic basis of human cytomegalovirus resistance and current trends in antiviral resistance analysis.

S H James, M N Prichard

Abstract readReview
In one paragraph

Review in Infectious disorders drug targets, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Discovery ofActa pharmaceutica Sinica. B · 2022
    Article
  3. Review
  4. Article
  5. Review
  6. New inhibitors of cytomegalovirus DNA polymerase.ACS medicinal chemistry letters · 2013
    Article
  7. Article
  8. Review
  9. Observational
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

S H JamesUniversity of Alabama at Birmingham, Birmingham, AL 35233-1711, USA. sjames@peds.uab.edu
M N Prichard

Funding

NIAID NIH HHS N01 AI030049NIAID NIH HHS N01-AI-30049
6 · The paper itself

Abstract

Infections due to resistant human cytomegalovirus (CMV) are an emerging problem, particularly in immunocompromised hosts. When managing such patients, clinicians should be aware of the possibility of developing CMV antiviral resistance, especially while on prolonged therapy or if severe immunosuppression is present. CMV resistance to current antiviral agents is mediated by alterations in either the UL97 kinase or DNA polymerase, encoded by the UL97 and UL54 genes, respectively. UL97 mutations are capable of conferring resistance to ganciclovir, while UL54 mutations can impart resistance to ganciclovir, cidofovir, and foscarnet. If treatment failure is suspected to be due to antiviral resistance, CMV resistance analysis should be obtained. Phenotypic resistance assays performed on clinical isolates measure antiviral susceptibilities directly, but are laborious and time-consuming. Therefore, genotypic resistance analysis has become the more common means of diagnosing CMV resistance. Mutations in UL97 or UL54 may be clinically associated with resistance, but their effect on antiviral susceptibility must be confirmed by marker transfer techniques such as recombinant phenotyping.

Indexed as

AnimalsAntiviral AgentsCytomegalovirusCytomegalovirus InfectionsDNA-Directed DNA PolymeraseDrug Resistance, ViralHumansImmunocompromised HostMutationPhosphotransferases (Alcohol Group Acceptor)Viral ProteinsAntiviral AgentsDNA-Directed DNA Polymeraseganciclovir kinasePhosphotransferases (Alcohol Group Acceptor)UL54 protein, Human herpesvirus 5Viral Proteins

Identifiers

PMID21827431
PMCPMC3773841

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.