Evidence map›Paper›PMID 19570871›Full record

ArticleJournal of virology2009

A simian immunodeficiency virus-infected macaque model to study viral reservoirs that persist during highly active antiretroviral therapy.

Jason B Dinoso, S Alireza Rabi, Joel N Blankson, Lucio Gama, Joseph L Mankowski, Robert F Siliciano, M Christine Zink, Janice E Clements

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

108 citing papers in PubMed, 157 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Article
  8. Review
  9. Review
  10. Engaging innate immunity in HIV-1 cure strategies.Nature reviews. Immunology · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. μ-Lat: A mouse model to evaluate human immunodeficiency virus eradication strategies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  17. Review
  18. Article
  19. Article
  20. Article

48 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

8 authors at 3 institutions in 1 country.

Jason B DinosoDepartment of Pharmacology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
S Alireza Rabi
Joel N Blankson
Lucio Gama
Joseph L Mankowski
Robert F Siliciano
M Christine Zink
Janice E Clements
Johns Hopkins Medicine · USJohns Hopkins University · USHoward Hughes Medical Institute · US

Funding

Project 4: Intracellular mechanism of virus persistence in astrocytes/macrophagesP01MH070306 · NIMH · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2004 to 2015
$16.0M
Minocycline Inhibits Immune Reactivation of CNS SIVR01NS055648 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE E · 2007 to 2011
$3.2M
MOLECULAR PATHOGENESIS OF AIDS RELATED CNS DISEASET32NS007392 · NINDS · JOHNS HOPKINS UNIVERSITY · PI CLEMENTS, JANICE ELLEN · 1995 to 2005
$895k
Howard Hughes Medical InstituteNIMH NIH HHS P01 MH 070306NIMH NIH HHS P01 MH070306NINDS NIH HHS R01 NS055648NINDS NIH HHS T32 NS007392PHS HHS R0143222
6 · The paper itself

Abstract

The treatment of human immunodeficiency virus type 1 (HIV-1) infection with highly active antiretroviral therapy (HAART), a combination of three or more antiretroviral drugs, suppresses viremia below the clinical limit of detection (50 HIV-1 RNA copies/ml), but latently infected resting CD4(+) T cells serve as lifelong reservoirs, and low-level viremia can be detected with special assays. Recent studies have provided evidence for additional reservoirs that contribute to residual viremia but are not present in circulating cells. Identification of all the sources of residual viremia in humans may be difficult. These discoveries highlight the need for a tractable model system to identify additional viral reservoirs that could represent barriers to eradication. In this study, simian immunodeficiency virus (SIV)-infected pig-tailed macaques (Macaca nemestrina) were treated with four antiretroviral drugs to develop an animal model for viral suppression during effective HAART. Treatment led to a biphasic decay in viremia and a significant rise in levels of circulating CD4(+) T cells. At terminal infection time points, the frequency of circulating resting CD4(+) T cells harboring replication-competent virus was reduced to a low steady-state level similar to that observed for HIV-infected patients on HAART. The frequencies of resting CD4(+) T cells harboring replication-competent virus in the pooled head lymph nodes, gut lymph nodes, spleen, and peripheral blood were reduced relative to those for untreated SIV-infected animals. These observations closely parallel findings for HIV-infected humans on suppressive HAART and demonstrate the value of this animal model to identify and characterize viral reservoirs persisting in the setting of suppressive antiretroviral drugs.

Indexed as

Virus LatencyAnimalsAntiretroviral Therapy, Highly ActiveCD4-Positive T-LymphocytesDisease Models, AnimalLymph NodesLymphocyte CountMacacaSimian Acquired Immunodeficiency SyndromeSimian Immunodeficiency VirusViremia

Identifiers

PMID19570871
PMCPMC2738256
OpenAlexW2164458439

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.