Evidence map›Paper›PMID 38603131›Full record

ArticleProceedings of the Institution of Mechanical Engineers. Part C. Journal of mechanical engineering science2022

A mechanical-thermodynamic model for understanding endocytosis of COVID-19 virus SARS-CoV-2.

Paritosh Mahata, Laxminarsimharao Vennamneni, Soham Chattopadhyay

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the Institution of Mechanical Engineers. Part C. Journal of mechanical engineering science, 2022. 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
0.1field-weighted citation impact, top 59% 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, 3 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

3 authors at 1 institution in 1 country.

Paritosh MahataDepartment of Mechanical Engineering, Birla Institute of Technology, Ranchi, India.ORCID https://orcid.org/0000-0003-2882-5840
Laxminarsimharao VennamneniDepartment of Mechanical Engineering, Gandhi Institute of Technology and Management, Hyderabad, India.
Soham ChattopadhyayDepartment of Bioengineering, Birla Institute of Technology, Ranchi, India.
Birla Institute of Technology, Mesra · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We analyze the endocytosis process of COVID-19 (coronavirus disease 2019) virus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) using a mechanical-thermodynamic model. The virus particle is designed to interface with the cell membrane as a hard sphere. The role of cytoplasmic BAR (Bin/Amphiphysin/RVs) proteins is considered in the endocytosis. Interestingly, the Endophilin N-BAR cytoplasmic proteins show resistance in participating endocytosis, whereas F-BAR, Arfaptin BAR, Amphiphysin N-BAR, and PX-BAR proteins participate in endocytosis. The increase in membrane tension, concentrated force between the cell membrane receptor, and spike glycoprotein present on the surface of virus particle promote the endocytosis. Also, the increase in the bending modulus of membrane leads to the two-phase solution of BAR protein concentration on the interior of cell membrane surface. We observe an unstable region of protein concentration, which may help one to retard the endocytosis process and thus the viral infection. Though the present study is focused on SARS-CoV-2, it can be extended to understand any other viral infections, involving endocytosis process.

Indexed as

BAR proteinCOVID-19endocytosismechanical-thermodynamic modelSARS-CoV-2

Identifiers

PMID38603131
PMCPMC9127454
OpenAlexW4280603799

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.