Evidence map›Paper›PMID 35332385›Full record

ReviewCurrent topics in microbiology and immunology2023

Modulation of MHC and MHC-Like Molecules by Varicella Zoster Virus.

Allison Abendroth, Barry Slobedman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current topics in microbiology and immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. 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

2 authors.

Allison AbendrothInfection, Immunity and Inflammation, School of Medical Sciences, Faculty of Medicine and Health, Charles Perkins Centre, The University of Sydney, Level 5 (East) D17, Camperdown, NSW, 2006, Australia. allison.abendroth@sydney.edu.au.
Barry SlobedmanInfection, Immunity and Inflammation, School of Medical Sciences, Faculty of Medicine and Health, Charles Perkins Centre, The University of Sydney, Level 5 (East) D17, Camperdown, NSW, 2006, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Varicella zoster virus (VZV) is a medically important human herpesvirus that has co-evolved with the human host to become a highly successful and ubiquitous pathogen. Whilst it is clear the innate and adaptive arms of the immune response play key roles in controlling this virus during both primary and reactivated infections, it is also apparent that VZV "fights back" by encoding multiple functions that impair a wide range of immune molecules. This capacity to manipulate the immune response is likely to be important in underpinning the success of VZV as a human pathogen. In this review, we will focus on the plethora of mechanisms that VZV has evolved to prevent and/or delay immune functions via regulating the expression of major histocompatibility complex (MHC) class I and MHC class II molecules, as well as several MHC-like molecules. In doing so, we will highlight both established and newly emerged VZV-encoded immunomodulatory capabilities and provide context to new avenues of research that seek to build the most comprehensive understanding of how this virus interfaces with these aspects of host immunity.

Indexed as

Herpesvirus 3, HumanHistocompatibility Antigens Class IIHistocompatibility Antigens Class IHumansHistocompatibility Antigens Class IHistocompatibility Antigens Class IIImmune evasionMHC class IMHC class IIMHC-like moleculesVaricella zoster virus

Identifiers

PMID35332385

What OpenQuestion holds

Textmetadata
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.