Evidence map›Paper›PMID 7494257›Full record

ArticleJournal of virology1995

Naturally occurring accessory gene mutations lead to persistent human immunodeficiency virus type 1 infection of CD4-positive T cells.

M Kishi, Y H Zheng, M K Bahmani, K Tokunaga, H Takahashi, M Kakinuma, P K Lai, M Nonoyama, R B Luftig, K Ikuta

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact, top 98% 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

10 citing papers in PubMed, 0 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

10 authors at 1 institution in 1 country.

M KishiSection of Serology, Hokkaido University, Sapporo, Japan.
Y H Zheng
M K Bahmani
K Tokunaga
H Takahashi
M Kakinuma
P K Lai
M Nonoyama
R B Luftig
K Ikuta
Hokkaido University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proviral DNA from cells surviving severe but transient cytopathic effects, mediated by infection with recombinant human immunodeficiency virus type 1 (HIV-1) carrying a single gene mutation at vif, vpr, or vpu, was characterized by use of HIV-1-specific primer pairs in a two-step PCR. Deletion mutations were detected in a region that spanned the vif and vpr open reading frames. Cloning and sequencing of the amplified DNA from this region revealed frequent large deletions in a limited number of nucleotide positions. Analyses of the deletions suggested that (i) genetic recombination, (ii) template-primer slippage, and (iii) misalignment of the growing point during reverse transcription of the HIV-1 genome might be the mechanisms that generated the mutations. Apart from the large deletions, smaller deletions that gave frameshift mutations in vif and/or vpr prevailed. In addition, cells infected with a triple mutant defective in vif, vpr, and vpu did not show any cytopathic effect. Thus, mutations generating multiple accessory gene defects during HIV-1 replication correlate with viral persistence and loss of cytopathogenicity.

Indexed as

Genes, vifGenes, vprGenes, vpuMutationBase SequenceCD4-Positive T-LymphocytesCell Line, TransformedDefective VirusesDNA PrimersDNA, ViralFrameshift MutationGenome, ViralHIV-1HumansKineticsMolecular Sequence DataDNA PrimersDNA, ViralOligonucleotide Probes

Identifiers

PMID7494257
PMCPMC189689
OpenAlexW1520662317

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.