Computational investigation for endocytosis of CoVID-19 virus SARS-CoV-2 in cell membrane

Author(s):  
Soumya Mukherjee ◽  
Paritosh Mahata

CoVID-19 virus SARS-CoV-2 follows the endocytosis process to enter inside a cell to infect it. It is important to study the endocytosis of SARS-CoV-2 in cell membrane to prevent the pandemic of CoVID-19. In this paper we develop a finite element based computational model for endocytosis of SARS-CoV-2 in cell membrane and determine curvature generation on it during the process. The virus SARS-CoV-2 is modeled as a rigid spherical particle and cell membrane as an anisotropic elastic material, while its fluidic nature due to lipid exchange with infinite reservoir is preserved using suitable conditions. With the help of a contact pair created between the virus particle and cell membrane, endocytosis process is computationally studied and the curvature of membrane is evaluated as the time progresses during the endocytosis process. At the tip of the virus particle and half-radius distance from it, the membrane follows the curvature of virus very quickly. However, it takes more time for the membrane point located at a distance equal to the radius of the virus particle. This is compensated by the cytoplasmic peripheral proteins binding onto the inside surface of the cell membrane. The role of cytoplasmic peripheral BAR proteins is investigated by using a linear curvature-coupling model with protein concentrations. It is observed that F-BAR protein is more sensitive to the curvature of virus particle in comparison to the other BAR proteins. The sensitiveness deteriorates as the curvature is increased.

1980 ◽  
Vol 28 (1) ◽  
pp. 45-46 ◽  
Author(s):  
F Jaubert ◽  
S Barbey ◽  
C Nogues ◽  
J P Monnet ◽  
M Grun ◽  
...  

The cell membrane and X bodies of histiocytes X from two cases of eosinophilic granuloma were stained by nonspecific esterase. The results show that histiocytes X possess a cell membrane exoenzyme similar to that of other histiocytes, such as alveolar macrophages, but the role of the X body as related to enzyme activity remains an unknown.


2012 ◽  
Vol 195 (2) ◽  
pp. 359-367 ◽  
Author(s):  
Hirofumi Shimomura ◽  
Kouichi Hosoda ◽  
David J. McGee ◽  
Shunji Hayashi ◽  
Kenji Yokota ◽  
...  

ABSTRACTThe glucosylation of free cholesterol (FC) byHelicobacter pyloricells has various biological significances for the survival of this bacterium.H. pyloricells with glucosylated FC are capable of evading host immune systems, such as phagocytosis by macrophages and activation of antigen-specific T cells, and surviving in the gastric mucosal tissues for long periods. An additional role of cholesterol glucosylation in the survival ofH. pyloriwhich is distinct from the role of escaping the host immune system, however, has yet to be identified. This study demonstrated that 7-dehydrocholesterol (7dFC), an FC precursor, is a toxic compound fatal toH. pyloricells, but the cell membrane ofH. pyloriis capable of absorbing this toxic sterol via glucosylation. In contrast to the case with 7dFC, no toxicity toH. pyloricells was detected from the glucosylated 7dFC. In addition,cgtgene mutantH. pyloricells that cannot glucosylate cholesterols had higher susceptibility to the toxic action of 7dFC than wild-typeH. pyloricells. These results indicate that thecgtgene product ofH. pyloriserves to detoxify the sterol fatal to this bacterium and to permit this toxic sterol as a cell membrane lipid component. In summary, this study defined a novel role of cholesterol glucosylation inH. pylori.


2020 ◽  
Author(s):  
J. Feng ◽  
L. Tang ◽  
Z. Liu ◽  
S. Dong ◽  
L. Zhou ◽  
...  

ABSTRACTThe bleb morphology and its changes are an important mechanism of cell’s amoeboid migration. By releasing bonds between the membrane and the cortex of a cell, the formation of bleb can be observed experimentally, but the mechanism that affects the size and shape of this kind of bleb is waiting for further study. In this paper, a two-dimensional fluid-solid coupling model is established to describe a cell with membrane, cortex and cytoplasm in a solution, and a numerical solving method for the fluid-solid coupling model is developed to simulate the behaviors of cell bleb. The effects of parameters, such as the number of broken bonds, the viscosity coefficient of the cortex, and the cell’s membrane modulus on the size and the shape of the bleb were investigated. Numerical results show that the model is effective to simulate the formation and evolution of cell’s bleb, and derive the contribution of several affecting factors to the bleb shape and size clearly.SIGNIFICANCETo understand the process of cell migration with bleb pseudopods in the amoeba cell migration, it is necessary to study the formation mechanism of cells protruding bleb. In this paper, we propose a reasonable and reliable cell numerical model. With this model we successfully simulate the bleb phenomenon consistent with the experimental phenomenon by changing the key impact factors. The method in this paper is applicable to the cell model of amoeba cell migration pattern, which helps to understand the important role of blebs in the process of cell migration.


Author(s):  
zhihong wang

Dear editor, we read with great interest the well written article by Dr Kerget et al with the main objective of investigating the role of TREM-1/TREM-2 ratio on patients with COVID-19 pneumonia. The article pointed that TREM-1 and TREM-2 have important role in inflammation and TREM-1/TREM-2 ratio was higher in severe COVID-19 patients compared with moderate COVID-19 patients. We have certain comments to understand the conclusions of this article. Firstly, triggering receptor expressed on myeloid cells-1 (TREM-1) is mainly express on neutrophils and monocytes in a cell membrane-bound form. A soluble form of TREM-1(sTREM-1), which lacks the cytoplasmic tail and transmembrane part, were detected in the blood in recent studies. Since you have mentioned “serum TREM-1”, we were confused whether you detected TREM-1 or sTREM-1. Secondly, we wanted to know more about the treatment and the kidney functions of the patients. Thirdly, We are curious to see if high TREM-1/TREM-2 ratio could predict the distribution of ILD. We would be glad to hear the opinion of the author on the points, to get a more convincing conclusion.


Biomedicines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 572
Author(s):  
Ivan Jozic ◽  
Jérémy Chéret ◽  
Beatriz Abdo Abujamra ◽  
Mariya Miteva ◽  
Jennifer Gherardini ◽  
...  

Irreversible destruction of the hair follicle (HF) in primary cicatricial alopecia and its most common variant, frontal fibrosing alopecia (FFA), results from apoptosis and pathological epithelial-mesenchymal transition (EMT) of epithelial HF stem cells (eHFSCs), in conjunction with the collapse of bulge immune privilege (IP) and interferon-gamma-mediated chronic inflammation. The scaffolding protein caveolin-1 (Cav1) is a key component of specialized cell membrane microdomains (caveolae) that regulates multiple signaling events, and even though Cav1 is most prominently expressed in the bulge area of human scalp HFs, it has not been investigated in any cicatricial alopecia context. Interestingly, in mice, Cav1 is involved in the regulation of (1) key HF IP guardians (TGF-β and α-MSH signaling), (2) IP collapse inducers/markers (IFNγ, substance P and MICA), and (3) EMT. Therefore, we hypothesize that Cav1 may be an unrecognized, important player in the pathobiology of cicatricial alopecias, and particularly, in FFA, which is currently considered as the most common type of primary lymphocytic scarring alopecia in the world. We envision that localized therapeutic inhibition of Cav1 in management of FFA (by cholesterol depleting agents, i.e., cyclodextrins/statins), could inhibit and potentially reverse bulge IP collapse and pathological EMT. Moreover, manipulation of HF Cav1 expression/localization would not only be relevant for management of cicatricial alopecia, but FFA could also serve as a model disease for elucidating the role of Cav1 in other stem cell- and/or IP collapse-related pathologies.


1999 ◽  
Vol 39 (7) ◽  
pp. 91-98 ◽  
Author(s):  
Ryan N. Jordan ◽  
Eric P. Nichols ◽  
Alfred B. Cunningham

Bioavailability is herein defined as the accessibility of a substrate by a microorganism. Further, bioavailability is governed by (1) the substrate concentration that the cell membrane “sees,” (i.e., the “directly bioavailable” pool) as well as (2) the rate of mass transfer from potentially bioavailable (e.g., nonaqueous) phases to the directly bioavailable (e.g., aqueous) phase. Mechanisms by which sorbed (bio)surfactants influence these two processes are discussed. We propose the hypothesis that the sorption of (bio)surfactants at the solid-liquid interface is partially responsible for the increased bioavailability of surface-bound nutrients, and offer this as a basis for suggesting the development of engineered in-situ bioremediation technologies that take advantage of low (bio)surfactant concentrations. In addition, other industrial systems where bioavailability phenomena should be considered are addressed.


2020 ◽  
Vol 16 (34) ◽  
pp. 2853-2861
Author(s):  
Yanli Li ◽  
Rui Yang ◽  
Limo Chen ◽  
Sufang Wu

CD38 is a transmembrane glycoprotein that is widely expressed in a variety of human tissues and cells, especially those in the immune system. CD38 protein was previously considered as a cell activation marker, and today monoclonal antibodies targeting CD38 have witnessed great achievements in multiple myeloma and promoted researchers to conduct research on other tumors. In this review, we provide a wide-ranging review of the biology and function of the human molecule outside the field of myeloma. We focus mainly on current research findings to summarize and update the findings gathered from diverse areas of study. Based on these findings, we attempt to extend the role of CD38 in the context of therapy of solid tumors and expand the role of the molecule from a simple marker to an immunomodulator.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yorick Janssens ◽  
Nathan Debunne ◽  
Anton De Spiegeleer ◽  
Evelien Wynendaele ◽  
Marta Planas ◽  
...  

AbstractQuorum sensing peptides (QSPs) are bacterial peptides produced by Gram-positive bacteria to communicate with their peers in a cell-density dependent manner. These peptides do not only act as interbacterial communication signals, but can also have effects on the host. Compelling evidence demonstrates the presence of a gut-brain axis and more specifically, the role of the gut microbiota in microglial functioning. The aim of this study is to investigate microglial activating properties of a selected QSP (PapRIV) which is produced by Bacillus cereus species. PapRIV showed in vitro activating properties of BV-2 microglia cells and was able to cross the in vitro Caco-2 cell model and reach the brain. In vivo peptide presence was also demonstrated in mouse plasma. The peptide caused induction of IL-6, TNFα and ROS expression and increased the fraction of ameboid BV-2 microglia cells in an NF-κB dependent manner. Different metabolites were identified in serum, of which the main metabolite still remained active. PapRIV is thus able to cross the gastro-intestinal tract and the blood–brain barrier and shows in vitro activating properties in BV-2 microglia cells, hereby indicating a potential role of this quorum sensing peptide in gut-brain interaction.


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