Evidence map›Paper›PMID 9096396›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Development of a novel anti-HIV-1 agent from within: effect of chimeric Vpr-containing protease cleavage site residues on virus replication.

D Serio, T A Rizvi, M Cartas, V S Kalyanaraman, I T Weber, H Koprowski, A Srinivasan

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 34 citations in OpenAlex.

  1. The HIV-1 Vpr Protein: A Multifaceted Target for Therapeutic Intervention.International journal of molecular sciences · 2017
    Review
  2. Review
  3. Nanotechnology-based approaches for the development of diagnostics, therapeutics, and vaccines.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2014
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Gene therapy for HIV infections: Intracellular immunization.The Canadian journal of infectious diseases = Journal canadien des maladies infectieuses · 1999
    Article
  11. HIV-1 Gag shares a signature motif with annexin (Anx7), which is required for virus replication.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  12. Article
  13. 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

7 authors at 1 institution in 1 country.

D SerioDepartment of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
T A Rizvi
M Cartas
V S Kalyanaraman
I T Weber
H Koprowski
A Srinivasan
The University of Texas MD Anderson Cancer Center · US

Funding

FUNCTIONAL STUDIES WITH HYBRID HIVSR01AI029306 · NIAID · WISTAR INSTITUTE · PI SRINIVASAN, ALAGARSAMY · 1990 to 1999
–
NIAID NIH HHS AI29306
6 · The paper itself

Abstract

Effective antiviral agents will be of great value in controlling virus replication and delaying the onset of HIV-1-related disease symptoms. Current therapy involves the use of antiviral agents that target the enzymatic functions of the virus, resulting in the emergence of resistant viruses to these agents, thus lowering their effectiveness. To overcome this problem, we have considered the idea of developing novel agents from within HIV-1 as inhibitors of virus replication. The specificity of the Vpr protein for the HIV-1 virus particle makes it an attractive molecule for the development of antiviral agents targeting the events associated with virus maturation. We have generated chimeric Vpr proteins containing HIV-1-specific sequences added to the C terminus of Vpr. These sequences correspond to nine cleavage sites of the Gag and Gag-Pol precursors of HIV-1. The chimeric Vpr constructs were introduced into HIV-1 proviral DNA to assess their effect on virus infectivity using single- and multiple-round replication assays. The virus particles generated exhibited a variable replication pattern depending on the protease cleavage site used as a fusion partner. Interestingly, the chimeric Vpr containing the cleavage sequences from the junction of p24 and p2, 24/2, completely abolished virus infectivity. These results show that chimeric proteins generated from within HIV-1 have the ability to suppress HIV-1 replication and make ideal agents for gene therapy or intracellular immunization to treat HIV-1 infection.

Indexed as

Anti-HIV AgentsBase SequenceCell LineGene Products, vprHIV-1HIV ProteaseHumansHydrolysisMolecular Sequence DataProtein Sorting SignalsRecombinant Fusion ProteinsVirus Replicationvpr Gene Products, Human Immunodeficiency VirusAnti-HIV AgentsGene Products, vprHIV ProteaseProtein Sorting SignalsRecombinant Fusion Proteinsvpr Gene Products, Human Immunodeficiency Virus

Identifiers

PMID9096396
PMCPMC20372
OpenAlexW2002156682

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.