Evidence map›Paper›PMID 11022787›Full record

ReviewVirus genes2000

Immune escape by hepatitis B viruses.

U Protzer, H Schaller

Abstract readReview
PubMed
In one paragraph

Review in Virus genes, 2000. 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
1.0field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. The underlying mechanisms for the "simultaneous HBsAg and anti-HBs serological profile".European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2011
    Review
  6. Article
  7. Review
  8. Article
  9. 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 at 1 institution in 1 country.

U ProtzerZentrum für Molekulare Biologie (ZMBH), University of Heidelberg. Germany.
H Schaller
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B viruses are DNA viruses characterized by their very small genome size and their unique replication via reverse transcription. The circular genome has been efficiently exploited, thereby limiting genome variation, and leaves no space for genes in addition to those essentially needed during the viral live cycle. Hepatitis B viruses are prototype non-cytopathic viruses causing persistent infection. Human hepatitis B virus (HBV), as well as the closely related animal viruses, most frequently are transmitted vertically from mothers to their offspring. Because infection usually persists for many years, if not lifelong, hepatitis B viruses need efficient mechanisms to hide from the immune response of the host. To escape the immune response, they exploit different strategies. Firstly, they use their structural and non-structural proteins multiplely. One of the purposes is to alter the immune response. Secondly, they replicate by establishing a pool of stable extrachromosomal transcription templates, which allow the virus to react sensitively to changes in its microenvironment by up- or downregulating gene expression. Thirdly, hepatitis B viruses replicate in the liver which is an immunopriviledged site.

Indexed as

AnimalsGenome, ViralHepatitis BHepatitis B virusHumansLiverVirus Replication

Identifiers

PMID11022787
OpenAlexW1543008521

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.