Evidence map›Paper›PMID 32582563›Full record

ReviewFrontiers in cellular and infection microbiology2020

Human Cytomegalovirus Interleukin 10 Homologs: Facing the Immune System.

Emma Poole, Tainan Cerqueira Neves, Martha Trindade Oliveira, John Sinclair, Maria Cristina Carlan da Silva

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
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

39 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  4. Review
  5. Challenges and opportunities in the management of severe pneumonia. Key concepts from the Seventh Annual Meeting of Spanish Experts 2025.Revista espanola de quimioterapia : publicacion oficial de la Sociedad Espanola de Quimioterapia · 2026
    Review
  6. Review
  7. Observational
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
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  17. A vaccine against cytomegalovirus: how close are we?The Journal of clinical investigation · 2025
    Article
  18. Review
  19. Review
  20. Article
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

5 authors at 2 institutions in 2 countries.

Emma PooleDepartment of Medicine, University of Cambridge, Cambridge, United Kingdom.
Tainan Cerqueira NevesCenter for Natural and Humanities Sciences, Federal University of ABC (UFABC), São Bernardo do Campo, Brazil.
Martha Trindade OliveiraCenter for Natural and Humanities Sciences, Federal University of ABC (UFABC), São Bernardo do Campo, Brazil.
John SinclairDepartment of Medicine, University of Cambridge, Cambridge, United Kingdom.
Maria Cristina Carlan da SilvaCenter for Natural and Humanities Sciences, Federal University of ABC (UFABC), São Bernardo do Campo, Brazil.
Universidade Federal do ABC · BRUniversity of Cambridge · GB

Funding

Medical Research Council MR/S00081X/1
6 · The paper itself

Abstract

Human Cytomegalovirus (HCMV) can cause a variety of health disorders that can lead to death in immunocompromised individuals and neonates. The HCMV lifecycle comprises both a lytic (productive) and a latent (non-productive) phase. HCMV lytic infection occurs in a wide range of terminally differentiated cell types. HCMV latency has been less well-studied, but one characterized site of latency is in precursor cells of the myeloid lineage. All known viral genes are expressed during a lytic infection and a subset of these are also transcribed during latency. The UL111A gene which encodes the viral IL-10, a homolog of the human IL-10, is one of these genes. During infection, different transcript isoforms of UL111A are generated by alternative splicing. The most studied of the UL111A isoforms are cmvIL-10 (also termed the "A" transcript) and LAcmvIL-10 (also termed the "B" transcript), the latter being a well-characterized latency associated transcript. Both isoforms can downregulate MHC class II, however they differ in a number of other immunomodulatory properties, such as the ability to bind the IL10 receptor and induce signaling through STAT3. There are also a number of other isoforms which have been identified which are expressed by differential splicing during lytic infection termed C, D, E, F, and G, although these have been less extensively studied. HCMV uses the viral IL-10 proteins to manipulate the immune system during lytic and latent phases of infection. In this review, we will discuss the literature on the viral IL-10 transcripts identified to date, their encoded proteins and the structures of these proteins as well as the functional properties of all the different isoforms of viral IL-10.

Indexed as

CytomegalovirusCytomegalovirus InfectionsHumansImmune SystemInfant, NewbornInterleukin-10Viral ProteinsInterleukin-10Viral ProteinsHCMVHCMV interleukin 10 homologhuman cytomegalovirusIL-10 signalingUL111A

Identifiers

PMID32582563
PMCPMC7296156
OpenAlexW3034502324

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.