Evidence map›Paper›PMID 34440891›Full record

ReviewCells2021

Innate Immune Responses to Herpesvirus Infection.

Christine M O'Connor, Ganes C Sen

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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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 at 1 institution in 1 country.

Christine M O'ConnorDepartment of Genomic Medicine, Infection Biology Program, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA.ORCID 0000-0003-4943-3774
Ganes C SenDepartment of Inflammation and Immunity, Infection Biology Program, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA.
Cleveland Clinic Lerner College of Medicine · US

Funding

TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA · 1994 to 2020
$35.6M
ANTIVIRAL ACTIONS OF INTERFERONSR01CA068782 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI SEN, GANES C. · 1995 to 2020
$7.6M
Manipulation of host factors that promote HCMV latencyR01AI150931 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI O'CONNOR, CHRISTINE M · 2021 to 2025
$2.4M
NCI NIH HHS P01 CA062220NCI NIH HHS R01 CA068782NIAID NIH HHS R01 AI150931NIH HHS CA062220NIH HHS CA068782
6 · The paper itself

Abstract

Infection of a host cell by an invading viral pathogen triggers a multifaceted antiviral response. One of the most potent defense mechanisms host cells possess is the interferon (IFN) system, which initiates a targeted, coordinated attack against various stages of viral infection. This immediate innate immune response provides the most proximal defense and includes the accumulation of antiviral proteins, such as IFN-stimulated genes (ISGs), as well as a variety of protective cytokines. However, viruses have co-evolved with their hosts, and as such, have devised distinct mechanisms to undermine host innate responses. As large, double-stranded DNA viruses, herpesviruses rely on a multitude of means by which to counter the antiviral attack. Herein, we review the various approaches the human herpesviruses employ as countermeasures to the host innate immune response.

Indexed as

AnimalsHerpesviridae InfectionsHumansImmunity, InnateSignal TransductionVirus Replicationantiviral host responseHCMVherpesvirusHSVinnate immune responseinnate immunityintrinsic immunityKSHV

Identifiers

PMID34440891
PMCPMC8394705
OpenAlexW3195867609

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.