virus entry
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Viruses ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 160
Author(s):  
Hirohito Ogawa ◽  
Daisuke Fujikura ◽  
Hikaru Namba ◽  
Nobuko Yamashita ◽  
Tomoyuki Honda ◽  
...  

Human herpesvirus 6B (HHV-6B) is a T-lymphotropic virus and the etiological agent of exanthem subitum. HHV-6B is present in a latent or persistent form after primary infection and is produced in the salivary glands or transmitted to this organ. Infected individuals continue to secrete the virus in their saliva, which is thus considered a source for virus transmission. HHV-6B primarily propagates in T cells because its entry receptor, CD134, is mainly expressed by activated T cells. The virus then spreads to the host’s organs, including the salivary glands, nervous system, and liver. However, CD134 expression is not detected in these organs. Therefore, HHV-6B may be entering cells via a currently unidentified cell surface molecule, but the mechanisms for this have not yet been investigated. In this study, we investigated a CD134-independent virus entry mechanism in the parotid-derived cell line HSY. First, we confirmed viral infection in CD134-membrane unanchored HSY cells. We then determined that nectin cell adhesion molecule 2 (nectin-2) mediated virus entry and that HHV-6B-insensitive T-cells transduced with nectin-2 were transformed into virus-permissive cells. We also found that virus entry was significantly reduced in nectin-2 knockout parotid-derived cells. Furthermore, we showed that HHV-6B glycoprotein B (gB) interacted with the nectin-2 V-set domain. The results suggest that nectin-2 acts as an HHV-6B entry-mediated protein.


2022 ◽  
Author(s):  
Bo Tang ◽  
En-Ze Sun ◽  
Zhi-Ling Zhang ◽  
Shu-Lin Liu ◽  
Jia Liu ◽  
...  

Influenza A virus (IAV) is a global health threat. The cellular endocytic machineries harnessed by IAV remain elusive. Here, by tracking single IAV particles and quantifying the internalized IAV, we found that the sphingomyelin (SM)-sequestered cholesterol, but not the accessible cholesterol, is essential for the clathrin-mediated endocytosis (CME) of IAV. The clathrin-independent endocytosis of IAV is cholesterol-independent. Whereas, the CME of transferrin depends on SM-sequestered cholesterol and accessible cholesterol. Furthermore, three-color single-virus tracking and electron microscopy showed that the SM-cholesterol complex nanodomain is recruited to the IAV-containing clathrin-coated structure (CCS) and facilitates neck constriction of the IAV-containing CCS. Meanwhile, formin-binding protein 17 (FBP17), a membrane-bending protein which activates actin nucleation, is recruited to IAV-CCS complex in a manner dependent on the SM-cholesterol complex. We propose that the SM-cholesterol nanodomain at the neck of CCS recruits FBP17 to induce neck constriction by activating actin assembly. These results unequivocally show the physiological importance of the SM-cholesterol complex in IAV entry. Importance: IAV infects the cells by harnessing cellular endocytic machineries. Better understanding of the cellular machineries used for its entry might lead to the development of antiviral strategies, and would also provide important insights into physiological endocytic processes. This work demonstrated that a special pool of cholesterol in plasma membrane, SM-sequestered cholesterol, recruits FBP17 for the constriction of clathrin-coated pits in IAV entry. Meanwhile, the clathrin-independent cell entry of IAV is cholesterol-independent. The internalization of transferrin, the gold-standard cargo endocytosed solely via CME, is much less dependent on the SM-cholesterol complex. These results would provide new insights into IAV infection and pathway/cargo-specific involvement of cholesterol pool(s).


Author(s):  
Mojtaba Bakhtiari ◽  
Kamyar Asadipooya

Abstract: A new coronavirus pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2], has been on the rise. This virus is fatal for broad groups of populations, including elderly, men, and patients with comorbidities among which obesity is a possible risk factor. The pathophysiologic connections between obesity/metainflammation and COVID-19 may be directly related to increasing soluble ACE2 (angiotensin-converting enzyme 2] levels which potentiates the viral entrance into the host cells, or indirectly related to dysregulation of immune system, microvascular injury and hypercoagulability. The SARS-CoV-2 S-glycoprotein interacts mainly with ACE2 or possibly DDP4 receptors to enter into the host cells. The host proteases, especially TMPRSS2 (transmembrane protease serine 2], support the fusion process and virus entry. While membranous ACE2 is considered a port of entry to the cell for SARS-CoV-2, it seems that soluble ACE2 retains its virus binding capability and enhances its entry into the cells. Interestingly, ACE2 on cell membrane may have protective roles by diminishing cytokine storm-related injuries to the organs. Applying medications that can reduce soluble ACE2 levels, antagonizing TMPRSS2 or blocking DDP4 can improve the outcomes of COVID-19. Metformin and statins through immunomodulatory activities, Orlistat by reducing viral replication, and thiazolidinediones by upregulating ACE2 expression have potential beneficial effects against COVID-19. However, the combination of dipeptidyl peptidase-4 (DDP4] inhibitors and spironolactone/eplerenone seems to be more effective by reducing soluble ACE2 level, antagonizing TMPRSS2, maintaining ACE2 on cell membrane and reducing risk of viral entry into the cells.


2022 ◽  
pp. 55-72
Author(s):  
Lahcen Tamegart ◽  
Mjid Oukhrib ◽  
Hafida El Ghachi ◽  
Abdelali Ben Maloui ◽  
Abdelaati El Khiat ◽  
...  

Coronavirus disease 2019 (COVID-19) is an emerging infectious disease caused by a dangerous virus named SARS-CoV-2. The most important symptoms are fever, cough, fatigue, and breathing problems. In the most serious forms of the disease, the appearance of an acute respiratory distress syndrome caused by the virus can be deadly, especially when people are fragile due to their age or in case of comorbidities. The exacerbated innate immune response could be another deadly complication. Different strategies of treatments are proposed for COVID-19 such as inhibition of virus entry by blocking ACE2 receptor used by COVID-19, inhibition of virus replication by using replication inhibitors, immunomodulatory agents to stimulate a strong immune response against COVID-19, and by using vaccines as an effective method for a long-term strategy for prevention of COVID-19.


2022 ◽  
pp. 127-140
Author(s):  
Aaron Lelo Pambu ◽  
Abdellah Zinedine

The current outbreak of the novel coronavirus, SARS-CoV-2 (coronavirus disease 2019; previously 2019- nCoV), epi-centered in Hubei Province of the People's Republic of China, has spread to many other countries caused an extreme burden for healthcare systems globally. Coronaviruses are traditionally considered nonlethal pathogens to humans, mainly causing approximately 15% of common colds. In this century, we have encountered highly pathogenic human CoVs twice. In this chapter, the authors propose to focus the gastrointestinal physiopathology of the infection of SARS-Cov2. This chapter will develop subject like the gastrointestinal manifestations of the infection to SARS-Cov2. The second part of this chapter will develop the role of the gut microbiome in the SARS-Cov2 diseases susceptibilities. And then the authors will show the etiopathogenesis of SARS-Cov2 associated diarrhea. As reported by previous studies, the SARS-Cov virus entry into host cell is mediated by the interaction between the envelop-anchored viral spike protein and the host receptor named angiotensin-converting enzyme 2 (ACE2).


2021 ◽  
Vol 12 (3) ◽  
pp. 580-586
Author(s):  
Anbu Clemensis Johnson

The spread of Covid-19 has been rampant across the globe, and studies have indicated a connection between the spike in infection and air pollution. The literature review has shown that the link between the SARS-CoV-2 virus causing the disease and air pollutants is still inconclusive. Current evidence from the studies point out two main contributing mechanisms for the spread of the virus: (1) the weakening of the human natural defence mechanism by the air pollutants facilitates virus entry and replication; (2) particulate matter facilitates the airborne transport of vectors. Meteorological parameters also play a significant role in the transmission of the virus. Ultraviolet radiation was negatively correlated with the number of COVID-19 cases, while wind speed was positively correlated. Temperature and humidity increases were associated with a decrease in the number of infections. Some studies have also shown no relationship between humidity and COVID-19 case numbers. Similarly, rainfall predominantly showed no significant correlation. More studies in this area are suggested to further understand the air pollutants effect on the virus, its interaction and the influence of meteorological parameters.


Viruses ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2460
Author(s):  
Snježana Mikuličić ◽  
Johannes Strunk ◽  
Luise Florin

During initial infection, human papillomaviruses (HPV) take an unusual trafficking pathway through their host cell. It begins with a long period on the cell surface, during which the capsid is primed and a virus entry platform is formed. A specific type of clathrin-independent endocytosis and subsequent retrograde trafficking to the trans-Golgi network follow this. Cellular reorganization processes, which take place during mitosis, enable further virus transport and the establishment of infection while evading intrinsic cellular immune defenses. First, the fragmentation of the Golgi allows the release of membrane-encased virions, which are partially protected from cytoplasmic restriction factors. Second, the nuclear envelope breakdown opens the gate for these virus–vesicles to the cell nucleus. Third, the dis- and re-assembly of the PML nuclear bodies leads to the formation of modified virus-associated PML subnuclear structures, enabling viral transcription and replication. While remnants of the major capsid protein L1 and the viral DNA remain in a transport vesicle, the viral capsid protein L2 plays a crucial role during virus entry, as it adopts a membrane-spanning conformation for interaction with various cellular proteins to establish a successful infection. In this review, we follow the oncogenic HPV type 16 during its long journey into the nucleus, and contrast pro- and antiviral processes.


2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Svetlana P. Chapoval ◽  
Achsah D. Keegan

AbstractSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel type b coronavirus responsible for the COVID-19 pandemic. With over 224 million confirmed infections with this virus and more than 4.6 million people dead because of it, it is critically important to define the immunological processes occurring in the human response to this virus and pathogenetic mechanisms of its deadly manifestation. This perspective focuses on the contribution of the recently discovered interaction of SARS-CoV-2 Spike protein with neuropilin 1 (NRP1) receptor, NRP1 as a virus entry receptor for SARS-CoV-2, its role in different physiologic and pathologic conditions, and the potential to target the Spike–NRP1 interaction to combat virus infectivity and severe disease manifestations.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Xiao-Tao Zeng ◽  
Xiao-Ti Yu ◽  
Wei Cheng

Abstract Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike (S) protein determines virus entry and the palmitoylation of S protein affects virus infection. An acyltransferase complex ZDHHC5/GOGAL7 that interacts with S protein was detected by affinity purification mass spectrometry (AP-MS). However, the palmitoylated cysteine residues of S protein, the effects of ZDHHC5 or GOLGA7 knockout on S protein’s subcellular localization, palmitoylation, pseudovirus entry and the enzyme for depalmitoylation of S protein are not clear. Methods The palmitoylated cysteine residues of S protein were identified by acyl-biotin exchange (ABE) assays. The interactions between S protein and host proteins were analyzed by co-immunoprecipitation (co-IP) assays. Subcellular localizations of S protein and host proteins were analyzed by fluorescence microscopy. ZDHHC5 or GOGAL7 gene was edited by CRISPR-Cas9. The entry efficiencies of SARS-CoV-2 pseudovirus into A549 and Hela cells were analyzed by measuring the activity of Renilla luciferase. Results In this investigation, all ten cysteine residues in the endodomain of S protein were palmitoylated. The interaction of S protein with ZDHHC5 or GOLGA7 was confirmed. The interaction and colocalization of S protein with ZDHHC5 or GOLGA7 were independent of the ten cysteine residues in the endodomain of S protein. The interaction between S protein and ZDHHC5 was independent of the enzymatic activity and the PDZ-binding domain of ZDHHC5. Three cell lines HEK293T, A549 and Hela lacking ZDHHC5 or GOLGA7 were constructed. Furthermore, S proteins still interacted with one host protein in HEK293T cells lacking the other. ZDHHC5 or GOLGA7 knockout had no significant effect on S protein’s subcellular localization or palmitoylation, but significantly decreased the entry efficiencies of SARS-CoV-2 pseudovirus into A549 and Hela cells, while varying degrees of entry efficiencies may be linked to the cell types. Additionally, the S protein interacted with the depalmitoylase APT2. Conclusions ZDHHC5 and GOLGA7 played important roles in SARS-CoV-2 pseudovirus entry, but the reason why the two host proteins affected pseudovirus entry remains to be further explored. This study extends the knowledge about the interactions between SARS-CoV-2 S protein and host proteins and probably provides a reference for the corresponding antiviral methods.


2021 ◽  
Vol 161 ◽  
pp. 105278
Author(s):  
Ruihan Shi ◽  
Lei Hou ◽  
Li Wei ◽  
Jue Liu
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