Evidence map›Paper›PMID 20407278›Full record

ReviewNephron. Experimental nephrology2010

HIV-1 and kidney cells: better understanding of viral interaction.

Joanna Mikulak, Pravin C Singhal

Open access · bronzeAbstract readReview
In one paragraph

Review in Nephron. Experimental nephrology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. COVID-19 and Glomerular Diseases.Kidney international reports · 2023
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. HIV-associated immune complex kidney disease.Nature reviews. Nephrology · 2016
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Renal disease in HIV-infected individuals.Current opinion in HIV and AIDS · 2011
    Review
  19. 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 at 1 institution in 1 country.

Joanna MikulakFeinstein Institute for Medical Research and Long Island Jewish Medical Center, New Hyde Park, NY, USA.
Pravin C Singhal
Northwell Health · US

Funding

p66ShcA in HIV associated NephropathyR01DK083931 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2010 to 2013
$2.5M
Renin Angioensin Aldosterone System in Drub Abuse and HIV-associated NephropathyR01DK084910 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2010 to 2014
$1.7M
NIDDK NIH HHS DK083931NIDDK NIH HHS DK084910NIDDK NIH HHS R01 DK083931NIDDK NIH HHS R01 DK084910
6 · The paper itself

Abstract

HIV-associated nephropathy (HIVAN) is the most common disease affecting untreated seropositive patients of African descent. Besides genetic (African descent) and HIV-1 infection (environmental), specific host factors such as activation of renin-angiotensin-aldosterone system (RAAS) have also been demonstrated to play a role in the manifestation of HIVAN. The recent identification of MYH9 as susceptible allele is a key step forward in our understanding for the pathogenesis of focal glomerulosclerosis in people of African-American descent. HIV-1 transgenic models have significantly advanced our knowledge base in terms of role of HIV-1 genes in general and individual gene in particular in the development of renal lesions mimicking HIVAN. These studies suggest that viral replication is not needed for the development of renal lesions. Renal biopsy data from HIVAN patients suggest that renal epithelial cells express HIV-1 genes and thus it may be sufficient to invoke HIVAN phenotype in the presence of specific host and genetic factors. On the other hand, immune response to infection may be required to induce HIV-1 associated immune complex kidney disease (HIVICK). Since renal cell lack conventional HIV-1 receptors, HIV-1 entry into renal cells has been a mystery. Recently, non-conventional pathways have been demonstrated to facilitate HIV-1 entry into renal cells in in vitro studies. These include presence of DEC-205 receptors in renal tubular cells and lipid rafts in podocytes. However, HIV-1 entry through these pathways only allows non-productive infection. It appears that the presence of specific genetic and host factors in in vivo conditions may be facilitating the development of the productive HIV-1 infection in kidney cells.

Indexed as

Host-Pathogen InteractionsAIDS-Associated NephropathyAnimalsAntigens, CDApolipoproteins EApoptosisBlack or African AmericanCell DivisionChildEndothelial CellsEpithelial CellsGlomerulosclerosis, Focal SegmentalHIV-1Human Immunodeficiency Virus ProteinsHumansKidneyAntigens, CDApolipoproteins EDEC-205 receptorglobotriaosylceramideHuman Immunodeficiency Virus ProteinsLectins, C-TypeMinor Histocompatibility AntigensMolecular Motor ProteinsMYH9 protein, humanMyosin Heavy ChainsReceptors, Cell SurfaceTrihexosylceramides

Identifiers

PMID20407278
PMCPMC2889261
OpenAlexW2020366569

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.