Evidence map›Paper›PMID 16140752›Full record

ArticleJournal of virology2005

Rab9 GTPase is required for replication of human immunodeficiency virus type 1, filoviruses, and measles virus.

James L Murray, Manos Mavrakis, Natalie J McDonald, Mamadi Yilla, Jinsong Sheng, William J Bellini, Lijun Zhao, Joseph M Le Doux, Michael W Shaw, Chi-Cheng Luo and 4 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 4% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

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28 more citing papers are in PubMed but not listed here.

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

14 authors at 8 institutions in 1 country.

James L MurrayNational Center for HIV, STD, and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Manos Mavrakis
Natalie J McDonald
Mamadi Yilla
Jinsong Sheng
William J Bellini
Lijun Zhao
Joseph M Le Doux
Michael W Shaw
Chi-Cheng Luo
Jennifer Lippincott-Schwartz
Anthony Sanchez
Donald H Rubin
Thomas W Hodge
National Center for Infectious Diseases · USCenters for Disease Control and Prevention · USNational Institutes of Health · USVanderbilt University · USHudsonAlpha Institute for Biotechnology · USNational Center for HIV/AIDS Viral Hepatitis STD and TB Prevention · USThe Wallace H. Coulter Department of Biomedical Engineering · USUniversity of Georgia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rab proteins and their effectors facilitate vesicular transport by tethering donor vesicles to their respective target membranes. By using gene trap insertional mutagenesis, we identified Rab9, which mediates late-endosome-to-trans-Golgi-network trafficking, among several candidate host genes whose disruption allowed the survival of Marburg virus-infected cells, suggesting that Rab9 is utilized in Marburg replication. Although Rab9 has not been implicated in human immunodeficiency virus (HIV) replication, previous reports suggested that the late endosome is an initiation site for HIV assembly and that TIP47-dependent trafficking out of the late endosome to the trans-Golgi network facilitates the sorting of HIV Env into virions budding at the plasma membrane. We examined the role of Rab9 in the life cycles of HIV and several unrelated viruses, using small interfering RNA (siRNA) to silence Rab9 expression before viral infection. Silencing Rab9 expression dramatically inhibited HIV replication, as did silencing the host genes encoding TIP47, p40, and PIKfyve, which also facilitate late-endosome-to-trans-Golgi vesicular transport. In addition, silencing studies revealed that HIV replication was dependent on the expression of Rab11A, which mediates trans-Golgi-to-plasma-membrane transport, and that increased HIV Gag was sequestered in a CD63+ endocytic compartment in a cell line stably expressing Rab9 siRNA. Replication of the enveloped Ebola, Marburg, and measles viruses was inhibited with Rab9 siRNA, although the non-enveloped reovirus was insensitive to Rab9 silencing. These results suggest that Rab9 is an important cellular target for inhibiting diverse viruses and help to define a late-endosome-to-plasma-membrane vesicular transport pathway important in viral assembly.

Indexed as

AnimalsCell LineChlorocebus aethiopsDogsEbolavirusFiloviridaeGene Products, gagHIV-1HumansMarburgvirusMeasles virusModels, BiologicalMutagenesisrab GTP-Binding ProteinsRatsRNA, MessengerGene Products, gagrab GTP-Binding ProteinsRNA, MessengerRNA, Small InterferingRNA, Viral

Identifiers

PMID16140752
PMCPMC1212642
OpenAlexW2058283168

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.