Evidence map›Paper›PMID 25762730›Full record

ReviewJournal of virology2015

The Road Less Traveled: HIV's Use of Alternative Routes through Cellular Pathways.

Ailie Marx, Akram Alian

Abstract readReview
In one paragraph

Review in Journal of virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. 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.

Ailie MarxFaculty of Biology, Technion-Israel Institute of Technology, Haifa, Israel.
Akram AlianFaculty of Biology, Technion-Israel Institute of Technology, Haifa, Israel alian@tx.technion.ac.il.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathogens such as HIV-1, with their minimalist genomes, must navigate cellular networks and rely on hijacking and manipulating the host machinery for successful replication. Limited overlap of host factors identified as vital for pathogen replication may be explained by considering that pathogens target, rather than specific cellular factors, crucial cellular pathways by targeting different, functionally equivalent, protein-protein interactions within that pathway. The ability to utilize alternative routes through cellular pathways may be essential for pathogen survival when restricted and provide flexibility depending on the viral replication stage and the environment in the infected host. In this minireview, we evaluate evidence supporting this notion, discuss specific HIV-1 examples, and consider the molecular mechanisms which allow pathogens to flexibly exploit different routes.

Indexed as

Active Transport, Cell NucleusAnimalsCytidine DeaminaseHIV-1HIV InfectionsHost-Pathogen InteractionsHumansLentivirusLentivirus InfectionsModels, Biologicalvif Gene Products, Human Immunodeficiency VirusVirus IntegrationVirus ReplicationCytidine Deaminasevif Gene Products, Human Immunodeficiency Virusvif protein, Human immunodeficiency virus 1

Identifiers

PMID25762730
PMCPMC4442546

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.