⛸️ Spike Pada Virus Tersusun Atas Protein Dan Karbohidrat Yang Disebut Like attentively would read, but has not understood

When the TGEV spike protein binds to EGFR, it sets in motion the microfilaments’ polymerization by activating an intracellular signaling pathway that involves phosphoinositide-3 kinase and Rac1/Cdc42 GTPases as well as the ERK MAPK Pathogenic Coronaviruses of Humans and Animals, 2023Natural Protein FibersC. Viney, in Encyclopedia of Materials Science and Technology, Viral Spike ProteinThe structural characteristics of virus coats capsids are highly relevant to virus propagation, and are therefore the subject of intensive study. The coat must contain and protect the nucleic acid genetic contents, be resilient against impact, be capable of broaching the outer wall of a target cell, and provide a secure pathway for conducting nucleic acid into the target. Hollow spikes on the capsid fulfill the latter two roles, from which it has been deduced that they must have unusually high strength and stiffness in axial compression. Because compressive strength and stiffness have been a long-term but elusive goal of polymer science, the hierarchical structure of spike proteins deserves careful attention.a Cross-β-sheetsViral spike protein contains several repeats of relatively short β-strand-forming amino acid sequences. The chain folds back and forth to assemble a β-sheet, stabilized by intramolecular hydrogen bonds Fig. 2. Because the long axis of the sheet is transverse rather than parallel to the molecular backbone, the structure in this case is known as a cross-β-sheet. Some silks, the egg stalks of green lacewing flies, are also reinforced by cross-β-sheet crystals.b Higher-order structureThe structure varies significantly between different virus types. For both rotavirus and human adenovirus, there is evidence that three cross-β-sheets interact to form a hollow trimeric box beam that resists buckling in compression. Structural characterization is hampered by the small size of individual spikes length⩽30 nm and width⩽5 nm. Hydrophobic bonding is presumed to be important in stabilizing their structure, since 70% of the amino acid residues are hydrophobic in representative engineered model polymers, based on multiple consecutive copies of the principal repeated sequence in native adenovirus spike protein, can self-assemble into a liquid crystalline phase in solution. However, trimeric box beams have not been found in the hierarchical microstructure of fibers spun from this phase. The spun fibers are formed under significantly off-equilibrium conditions, and should not be expected to have the same internal structure as the native spikes.c PropertiesIn tensile tests conducted on dry fiber, the breaking strength is ∼ GPa, the stiffness ∼4 GPa, and the elongation to failure ∼ 30%. Given the evidence that the native spikes rely on hydrophobic bonding to maintain their structure, the properties of analog fibers as measured in air are likely to be inferior compared to results obtained in water—even if the detailed microstructure of the native material could be reproduced. In other words, the natural material is designed to work in an aqueous medium, and attempts to mimic its properties must take this reality into full chapterURL nanomaterials for infectious diseasesArchita Jha, Yashwant Pathak, in Nanotheranostics for Treatment and Diagnosis of Infectious Diseases, HydrogelThe SARS-CoV-2 Virus spike proteins contain a receptor-binding domain RBD for attachment and entry into the host cell. Recombinant RBD can induce a neutralizing antibody response that can bind to the SARS-Cov-2 RBD thus inhibiting the infection cycle [70]. Being cost-effective and amenable to large-scale manufacturing, subunit vaccines containing the recombinant RBD antigen provide beneficial value in global vaccine distribution efforts. Injectable polymer-nanoparticle PNP hydrogel structures with de-risked adjuvants CpG and Alum provide efficient vaccine delivery methods with enhanced immunogenicity of RBD. The hydrogel along with alum is beneficial and allows for a controlled and slow release of the vaccine over a span of 10–18 days, eliminating the need for booster shots. Additionally, polymer-nanoparticles hydrogels allow for the loading of various components of the vaccine such as the RBD, alum, and CpG to be co-delivered. The IgG antibody titers, utilized as markers for the immune response by RBD and adjuvants in PNP hydrogels, were 60 times greater than utilizing other adjuvants or RBD by itself [71]. Overall, hydrogels utilized for subunit vaccines have displayed promising results and ensured widespread vaccine full chapterURL Methods in Protein Biochemistry Part AMax Meyrath, ... on behalf of the CON-VINCE Consortium, in Methods in Enzymology, 20222 Before you beginThis virus-free assay uses two cell lines expressing respectively the viral spike and host cell receptor ACE2 on their surface and builds on the principle that cell membranes merge upon spike-ACE2 interaction. Each cell line additionally expresses one part of the NanoLuc luciferase HiBiT or LgBiT that on their own do not emit light, but when brought together, quickly self-complement due to their high affinity for each other to reconstitute a fully functional NanoLuc HiBiT technology, Promega. When co-incubated, these two cell lines are able to form syncytia through their cell membrane fusion facilitated by the spike-ACE2 interaction, in turn allowing rapid and spontaneous complementation of the cytoplasmic NanoLuc fragments and giving rise to ultra-bright bioluminescence in the presence of a specific substrate Fig. 1. Similar to classical viral neutralization assays, pre-incubation with neutralizing antibodies blocking the spike-ACE2 interaction prevents syncytia formation, which can be titrated and quantified by measuring the reduced light emission in comparison to cells that were not treated with neutralizing antibodies Fig. 1A and C.Fig. 1. Cell fusion assay based on high-affinity NanoLuc complementation HiBiT A Schematic representation of the assay set-up. LgBiT and spike-expressing HEK293T cells are mixed with HiBiT- and ACE2-expressing Vero E6 cells and co-incubated overnight. Upon spike interaction with ACE2, cell membranes merge, forming a multinucleated syncytium and enabling complementation of both NanoLuc fragments, eventually leading to light emission upon substrate addition. Pre-incubation of spike-expressing cells with neutralizing antibodies will prevent the spike–ACE2 interaction and limit syncytia formation. Multiple sera can be tested simultaneously in 96- or 384-well format, enabling high-throughput screening of samples. B Representative microscopy pictures, illustrating syncytium formation between Vero E6 cells expressing an mKOrange-tagged membrane marker and HEK293T cells expressing a NeonGreen cytoplasmic marker. DAPI-stained nuclei are depicted in blue. C Representative picture of a 96-well plate after substrate addition taken with an ordinary mobile phone camera Huawei p20 Pro. The intense blue bioluminescent signal emitted by the NanoLuc is well visible even with the naked eye. No light is emitted from wells where cells did not efficiently form syncytia, indicative of the presence of neutralizing A Figure was created using the material, vectors and protocols described below, this “SARScytium” assay can easily and reproducibly be performed using transiently transfected cells, where one cell line is transfected with viral spike and LgBiT, whereas the other cell line is transfected with HiBiT and ACE2 Fig. 1A. The approach using transient transfections allows for high versatility and flexibility of the assay with easy and fast adaptability to spike variants. This can be of particular interest given that the antibody neutralization profile considerably varies between the different spike variants and the high probability of emergence of new variants Duarte et al., 2022; Harvey et al., 2021. Alternatively, cells stably expressing the required proteins can be used. This accounts especially for ACE2, where a variety of cells stably expressing ACE2 are commercially available, such as Vero E6 cells that endogenously express ACE2, or HEK or HeLa cells exogenously overexpressing ACE2 together or not with the protease TMPRSS2 that serves as a co-factor for SARS-CoV-2 infection and is implicated in spike priming on the full chapterURL coronavirus infections of the lower respiratory tract and their preventionN. Petrovsky, in The Microbiology of Respiratory System Infections, 20163 Recombinant spike protein vaccinesA major advance in vaccine development was the identification that the SARS virus spike S protein mediates cell entry via its ability to bind angiotensin-converting enzyme 2 and CD209L, thereby triggering virus endocytosis into target A human monoclonal antibody binding the S protein N-terminal domain was shown to be able to block infection, thereby identifying S protein as a major target of SARS virus neutralizing Consistent with this, monkeys could be protected against SARS infection by intranasal immunization with a S protein-encoding live parainfluenza S protein was also shown to be the target of CD4 and CD8 T cell responses suggesting these may also be important to SARS A recombinant S protein vaccine was manufactured using an insect cell expression system but was found to be considerably less immunogenic that inactivated whole virus vaccine, requiring ∼100 times more antigen to achieve the same level of Attempts to improve the immunogenicity of S protein vaccine by formulation with alum adjuvant again resulted in severe lung eosinophilic immunopathology in response to SARS virus infection, marking this as another potentially unsafe This confirmed that the problem of lung eosinophilic immunopathology was not just confined to inactivated or nucleocapsid protein vaccines but was a more general problem of vaccines made from any SARS virus full chapterURL in respiratory systemMd Bashir Uddin, ... Syed Sayeem Uddin Ahmed, in Recent Advancements in Microbial Diversity, SARS virusesACE2 angiotensin-converting enzyme 2 acts as the SARS viral spike glycoprotein binding receptor, allowing the virus to adhere to host cells and then internalize and replicate Hoffmann et al., 2020; Liu et al., 2020; Yan et al., 2020. However, respiratory tract macrophages and DCs, all essential immune system cells, express ACE2 Keidar et al., 2005. As shown by the influenza, herpes, and Zika viruses, viral infections induce monocytic-enhanced proinflammatory signaling molecules and antiviral responses Nikitina, Larionova, Choinzonov, & Kzhyshkowska, 2018. It has recently been suggested that increased development of proinflammatory macrophages in a subset of COVID-19 patients contributes to an increase in the production of inflammatory cytokines and chemokines, like CXCL10, which causes cytokine storms. This has been found mostly in subjects with a low prognosis Vaninov, 2020; Yang et al., 2020. In general, short-lived monocytes/macrophages will significantly restrict viral replication. Nevertheless, this does not rule out the likelihood of these cells acting as a permissive mechanism and/or a viral reservoir Nikitina et al., 2018. The fact that these cells are the first line of protection against viral infection lends credence to this theory. However, viral infection has the potential to transform these cells into long-living macrophages M and facilitate their migration into tissues where they become infected resident cells. Finally, since SARS viruses, like SARS-CoV-2, use ACE2 as a tight, high-affinity binding site Hoffmann et al., 2020; Liu et al., 2020; Yan et al., 2020. ACE2-expressing pulmonary macrophages can permeate pulmonary invasion during SARS infection. Indeed, we previously demonstrated that monocytes and macrophages release ACE2 Keidar et al., 2005.Interestingly, macrophages also release furin and TMPRSS2, two enzymes implicated in the interaction of the SARS virus’s attachment and effusion sites Bertram et al., 2010; Gagnon et al., 2013 and ADAM 17, which acts as sheddase of ACE2 Nikolaidis et al., 2010. In the presence of both viral binding and activation components, the virus will potentially replicate in human macrophages and DCs, causing abnormal development of proinflammatory cytokines/chemokines, as is the case with MERS-CoV Zhou, Chu, Chan, & Yuen, 2015. Some experiments, on the other hand, have ruled out SARS-CoV viral replication in human macrophages Yilla et al., 2005. Despite abortive infection, which is described as infection without replication, SARS-CoV infection of human macrophages resulted in the expression of proinflammatory chemokines but not antiviral cytokine output Lee et al., 2009; Tseng, Perrone, Zhu, Makino, & Peters, 2005. COVID-19 morbidity and mortality are markedly amplified in definite populations, namely aged and diabetic patients with COPD or congestive heart failure CHF Perico, Benigni, & Remuzzi, 2020, and perhaps among patients on inhibitors of the renin-angiotensin aldosterone system RAAS Fang, Karakiulakis, & Roth, 2020; Perico et al., 2020. These explanations might be related with bigger numbers of AMs in such patients or alterations in the AM phenotype. Indeed, increased numbers of AM in bronchoalveolar lavage BAL were noticed in humans with COPD in proportion to their disease severity Agustí & Hogg, 2019.Read full chapterURL VaccinesJaap W. Back, Johannes Langedijk, in Advances in Immunology, 20122 Stabilizing AntigensThe detailed structural knowledge on many neutralization sites, the location of some conserved exposed surfaces on the native viral spike, and the general architecture and dynamics of the labile structure reveals some clues of how to stabilize the spike in order to induce such broadly neutralizing way of using the structural knowledge for a recombinant protein-based vaccine is to engineer, modify, or stabilize the labile spike in such a way that the recombinant soluble protein mimics the prefusion native trimer that can cross-react with all the broadly neutralizing antibodies and remains stable in a vaccine adjuvant. Several approaches have been applied successfully to stabilize the case the immunogen is based on the soluble envelope protein, the deletion of the membrane anchor destabilizes the trimer which can be compensated by inclusion of heterologous trimerization domains Yang et al., 2000. Additionally, the prefusion conformation can be stabilized by preventing the FP from swinging out and the gp120 head to detach. A straightforward solution to fix the FP in its prefusion position and obstruct the refolding of gp41 into the stable postfusion conformation is to prevent the cleavage of the precursor gp160 into mature gp120–gp41 heterodimer Yang et al., 2000. Alternatively, to increase the chance of maintaining the FP in its native, probably buried, position, gp120 and gp41 can be covalently linked by the introduction of an intermolecular disulfide bridge Binley et al., 2000; Yang et al., 2000. Although it has been possible to engineer a disulfide with trial and error, high-resolution detail of the structure would permit rational introduction of stabilizing disulfide bonds that connect the heterodimer. Disulfide bridges have also been used for the intramolecular stabilization of the flexible regions within the subunits Dey et al., 2009; Zhou et al., 2007. Constructing a heat-stable foot-and-mouth disease vaccine by disulfide engineering came within reach when the crystal structure of the viral capsid was solved Mateo et al., 2008 and also the atomic-level resolution of the complete prefusion spike of HIV will undoubtedly contribute to structure-based design of inter- and intramolecular disulfides without going through the arduous path of trial and full chapterURL Cellular Phagocytosis and Its Impact on Pathogen ControlStefan S. Weber, Annette Oxenius, in Antibody Fc, 2014Targeting of Viruses to FcRsViral infection of target cells in the absence of virus-specific antibodies is in general dependent on the interaction between viral spike proteins and corresponding receptors on target cells, thereby conferring a specific tropism of individual viruses to their target cells. Antibody-opsonized virus particles, however, may gain access to additional FcR-expressing target cells. Uptake of opsonized virus particles into FcR-bearing phagocytes via FcR-dependent phagocytosis may have different outcomes for the infection process and for the ensuing spread and control of the virus infection. While very little is known about the exact intracellular fate of opsonized virus particles and how this relates to their infectivity in phagocytes, most available data indicate that FcR-mediated uptake into phagocytes does not interfere with intracellular viral replication. However, in situations when opsonizing antibodies have direct neutralizing effects on the fusion or uncoating process of the virus, and when this property is maintained under acidic conditions as present in late phagosomes/lysosomes,106–108 FcR-mediated uptake of opsonized viruses might restrict replication within phagocytes. In cases where the infected phagocyte does not support the requirements of a specific viral life cycle, FcR-mediated uptake of opsonized viruses may also lead to enhanced control of viral full chapterURL Treatment and Prevention of Virus InfectionsGuangdi Li, ... Erik De Clercq, in Encyclopedia of Virology Fourth Edition, 2021HIV GP41GP41 is a transmembrane protein encoded by the env gene. As a key structure protein, HIV GP41 binds with GP120 to form HIV spike trimers on the surface of HIV particles Mao et al., 2012. During the viral entry, the N-heptad repeat NHR and C-heptad repeat CHR of GP41 switch to a six-helix bundle 6-HB structure which binds to the human cell membrane and drives the viral fusion into the human cells. Many antiviral agents have been developed to target the hydrophobic pocket within the NHR trimer, therefore preventing viral entry Mostashari Rad et al., 2018.As the only GP41 inhibitor approved by the US FDA, enfuvirtide is a fusion peptide inhibitor that mimics the N-heptad repeat and prevents the formation of the six-helix bundle structure of GP41. Clinical use of enfuvirtide requires twice-daily subcutaneous injection 90 mg/Kg for adults, 2 mg/Kg for children aged 6–16 years Kitchen et al., 2008. Enfuvirtide is not commonly used in clinical practice because of its side effects eosinophilia, neutropenia, increased risk of bacterial pneumonia, its short half-life, and lack of oral availability Reust, 2011. Although many attempts have been made, the development of GP41 inhibitors remains difficult due to the emerging mutations and structural dynamics of HIV full chapterURL repurposing existing vaccines and antibiotics help to control the COVID-19 pandemic?Kajal Rathod, ... Buddolla Viswanath, in Pandemic Outbreaks in the 21st Century, Therapeutic targets•Coronaviruses inhibit antiviral immunity, allowing interferons IFNs to sustain an antiviral state.•The virus moves into the cell by fusing viral spike proteins with the cellular ACE2 receptor, which causes ACE2 to be downregulated. Angiotensin receptor blockers and angiotensin-converting enzyme inhibitors and statins increase ACE2 expression, thereby having better efficacy.•The virus is then endocytosed, with low endosomal pH assisting in the lysis of viral structural proteins. The antiviral action of diprotic bases like chloroquine and hydroxychloroquine may disrupt the acidic environment.•Nucleic acid NA is released into the cytoplasm.•Translation of viral proteins with help of the host ribosomes.•Viral protease enzyme undergoes proteolysis to form functional proteins, for example, RDRP. Inhibitors such as lopinavir, ritonavir, and darunavir may thus be effective against the virus by inhibiting the key protease enzyme.•The replication and transcription of viruses are dependent on the presence of RDRP. Coronaviruses may be prone to RDRP inhibitors including remdesivir, favipiravir, ribavirin, and arbidol. Virions are formed after subsequent translation, proteolysis, and packaging of proteins, which are then exocytosed out of the full chapterURL 2Saul O. Lugo Reyes, Armando Partida Gaytán, in Allergic and Immunologic Diseases, 2022COVID-19 vaccines as gene therapiesSome vaccines to prevent SARS-CoV-2 infection or disease employ messenger RNA Pfizer-BioNTech, Moderna delivered by NPs to transmit our cells the transcript code to manufacture the infamous spike viral glycoprotein or its receptor-binding domain RBD. Other vaccines Oxford-AstraZeneca, Beth Israel-Johnson&Johnson employ a nonreplicating adenoviral vector, from a virus that normally infects chimpanzees, with good results [35]. Some scholars consider these to be gene therapies, even though these vaccines cannot alter human DNA or change our genes. Messenger RNA will not enter the nucleus but will instead stop at the cell ribosomes to deliver the message. No hematologic malignant transformations are expected to occur for the same reason. NP-delivered mRNA and adenoviral vectors are simply clever ways to develop vaccines using gene therapy-based principles or techniques [36].Nevertheless, as for any vaccines and any drugs or injectable biologic agents, safety trials are underway to assess any long-term adverse effects. Given the circumstances of the pandemic, all four vaccines were “fast-tracked” and approved for emergency use, but only after they completed all the safety and efficacy full chapterURL

^{c Virus yang isi tubuhnya terdiri atas RNA, protein, dan banyak lipida, contohnya virus cacar. Tubuh virus tersusun atas senyawa-senyawa berikut: 1) Asam nukleat, asam deoksiribonukleat (DNA) atau asam ribonukleat (RNA) sebagai bagian inti. Asam nukleat pada virus diselubangi kapsid sehingga disebut nukleokapsid.}

Virusmerupakan partikel ultra mikroskopis yang hanya hidup di dalam sel. Virus tersusun dari asam nukleat dan protein. Asam nukleat berfungsi sebagai pembawa informasi genetik virus sedangkan protein berfungsi sebagai pelindung yang menyelubungi asam nukleat. Virus memiliki ukuran yang cukup bervariasi yaitu antara 20 nanometer hingga 300

Virustersusun atas materi inti yang mengandung asam nukleat. Coronavirus Disease Covid-19 Tubuh tersusun dari asam nukleat b. Spike pada virus tersusun atas protein dan karbohidrat yang disebut. Soal dan pembahasan

KlasifikasiKarbohidrat: 1. Monosakarida: terdiri atas 3-6 atom C dan zat ini tidak dapat lagi dihidrolisis oleh larutan asam dalam air menjadi karbohidrat yang lebih sederhana. berikut macam-macam monosakarida : dengan ciri utamanya memiliki jumlah atom C berbeda-beda : triosa (C3), tetrosa (C4), pentosa (C5), heksosa (C6), heptosa (C7). Membransel tersusun atas lemak dan protein disebut dengan lipoprotein. Selain itu membran sel tersusun atas karbohidrat yang disebut dengan glikoprotein yaitu glikogen yang menempel pada protein dan berperan sebagai reseptor hormon dan neurotransmitter, glikolipid yaitu glikogen yang menempel pada fosfolipid berperan untuk menstabilkan membran.

Proteinmerupakan senyawa utama penyusun capsid (ind: kapsid) yang membungkus asam nukleat pada tubuh virus. Kapsid yang tersusun dari protein ini bila terisi asam nukleat (DNA atau RNA) disebut dengan nukleokapsid (nucleocapsid) Lipid yang ada pada virus merupakan jenis fosfolipid, gikolipid, kolestrol dan beberapa lemak alami yang lain. Lemak merupakan komponen utama penyusun envelope (selubung). Senyawa-senyawa lain yang belum diketahui. Jenis-jenis virus | Photo by U.S. federal

Amplopatau selubung virus. Ini merupakan lapisan terluar pada virus saat tahapan daur hidupnya berada pada sel inang. Virus yang berselubung juga memiliki protein yang disebut kapsid antara selubung dan genomnya. Selubung virus ini diturunkan sebagian dari membran sel inang (fosfolipid dan protein), dan dapat pula menyertakan glikoprotein virus.

Proteinintegral yang menembus di antara lapisan fosfolipid,

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spike pada virus tersusun atas protein dan karbohidrat yang disebut