Evidence map›Paper›PMID 25331717›Full record

ArticleBMC research notes2014

A comparison of elasticities of viral levels to specific immune response mechanisms in human immunodeficiency virus infection.

Sarudzai P Showa, Farai Nyabadza, Senelani D Hove-Musekwa, Gesham Magombedze

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC research notes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 52% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

4 authors at 3 institutions in 3 countries.

Sarudzai P ShowaDepartment of Applied Mathematics, National University of Science and Technology, P,O, Box AC 939 Ascot, Bulawayo, Zimbabwe. showa.sarudzai@gmail.com.
Farai Nyabadza
Senelani D Hove-Musekwa
Gesham Magombedze
Stellenbosch University · ZANational Institute for Mathematical and Biological Synthesis · USNational University of Science and Technology · ZW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe presence of an asymptomatic phase in an HIV infection indicates that the immune system can partially control the infection. Determining the immune mechanisms that contribute significantly to the partial control of the infection enhance the HIV infection intervention strategies and is important in vaccine development. Towards this goal, a discrete time HIV model, which incorporates the life cycle aspects of the virus, the antibody (humoral) response and the cell-mediated immune response is formulated to determine immune system components that are most efficient in controlling viral levels. Ecological relationships are used to model the interplay between the immune system components and the HIV pathogen. Model simulations and transient elasticity analysis of the viral levels to immune response parameters are used to compare the different immune mechanisms.

resultsIt is shown that cell-mediated immune response is more effective in controlling the viral levels than the antibody response. Killing of infected cells is shown to be crucial in controlling the viral levels. Our results show a negative correlation between the antibody response and the viral levels in the early stages of the infection, but we predicted this immune mechanism to be positively correlated with the viral levels in the late stage of the infection. A result that suggests lack of relevance of antibody response with infection progression. On the contrary, we predicted the cell-mediated immune response to be always negatively correlated with viral levels.

conclusionNeutralizing antibodies can only control the viral levels in the early days of the HIV infection whereas cell-mediated immune response is beneficial during all the stages of the infection. This study predicts that vaccine design efforts should also focus on stimulating killer T cells that target infected cells.

Indexed as

Immunity, CellularAntibodies, NeutralizingAsymptomatic DiseasesComputer SimulationHIVHIV InfectionsHost-Pathogen InteractionsHumansImmunity, HumoralModels, ImmunologicalNumerical Analysis, Computer-AssistedTime FactorsViral LoadVirus ReplicationAntibodies, Neutralizing

Identifiers

PMID25331717
PMCPMC4221687
OpenAlexW1994504006

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.