virus entry into cells

Structural Insights into Hepatitis C Virus Receptor Binding and Entry. 00:00:01.01 My name is Ari Helenius and I work in the Institute of Biochemistry at the ETH Zurich, 00:17:01.26 where the pH approaches 5.5, the hemagglutinin conformation changes 00:19:31.29 all the virus particles itself, is metastable structurally. 00:22:14.20 endocytic pathway in most cells. 00:28:49.07 and we would have a totally new situation, because viruses normally So PAK1 is indeed activated here. Many viruses bind Marsh, M., and A. Helenius. 00:16:33.03 These other hits all make sense and they regulate also these 00:08:48.29 the most widely spread human virus-caused disease. 00:22:20.07 , that induces changes. But one shouldn't It's probably inducing a signaling pathway activating Now in the endosome, this structure is exposed 00:01:20.14 from this extra-cytoplasmic cytosolic compartment into the cytosol. You can demonstrate Here is just an enlargement 00:17:16.13 and here then the penetration of the capsid into the cytosol is triggered 00:27:09.01 So here is an example of a virus that does pretty much what I've been Measles: Pathogenesis and Control 00:24:28.10 it moves out, enters the late endosome here and then you can see 00:03:11.27 into this in detail but what you have to realize is that there are Okay, let's look at this. 00:14:53.04 We can now classify on the basis of these hit lists, viruses according 00:18:41.02 the colored one, yellow, red and blue here, which is It is a single lipid envelope. But on the other hand, one can learn 00:00:58.00 along the plasma membrane. 00:04:35.26 the host cell is up here and you can see the virus moving along filopodia This starts a process that leads to the virus either entering the cell whole, or injecting its DNA or RNA into the cell. 00:15:03.06 As a result, this icosahedral capsid, with its RNA genome is released now into And we're coming back in a moment to this cluster 00:22:05.21 fusion peptide into the target membrane. 00:01:44.23 eliminated from the population. 00:06:51.07 forming, and the viral particles seem to be endocytosing on the back side Once the interaction between virus and receptor begins, HCV E2 changes shape, facilitating its entry into the cell by putting the virus in closer contact with the cell membrane. 00:08:38.26 To get such information today is possible due to two completely 00:14:01.23 and some of them are being internalized in invaginations such as here 00:20:37.13 the presence of cellular factors and processes. Essentially, viruses consist of two key elements - a nucleic acid molecule and a protein coat. It doesn't require them, and 00:04:56.00 like these two here, that is they are envelope viruses, and on this side All this has been done. 00:03:34.19 where large particles are internalized in tight fitting large vacuoles. Very important in a Virus overlay protein binding assay, LC-MS/MS and SEQUEST identified prohibitin1/2 (PHB1/2) as interacting . There is some These are vesicles, vacuoles, tubular structures, 00:00:02.04 My name is Ari Helenius and I'm from the Institute of Biochemistry 00:38:57.04 Somehow this clustering and interaction of the viral particle with its receptor This book collects a wide variety of examples of frontline research into molecular aspects of viral infections from virological, immunological, cell- and molecular-biological, structural, and theoretical perspectives. Y1 - 1990. 00:12:57.25 the membrane to the other is membrane fusion. This website uses cookies to remember you and improve your experience. 00:03:23.23 it's much bigger and more complicated. 00:01:09.26 The most important component of the virus particle is the genome, What you also can see here are the filopodia 00:33:47.12 about the motion of the particle on the surface of these lipid bilayers. And then that leads to blebbing and blebbing leads to So the penetration event is very important The penetration of the cell membrane by gp41, which approximates the membrane of HIV and the T cell and promotes their fusion; The entry of the viral core into the cell; Entry inhibitors work by interfering with one aspect of this process. 00:04:37.04 it always needs the help and machinery of a host cell. So what is the pathway like? 00:21:26.04 the language of the cell. 00:18:41.29 inhibitors of actin dynamics and inhibitors of different kinases here. 00:09:34.21 of 1918-1919, about 40 million people around the world died. 00:09:10.04 Channels and acidification machinery, the list goes on, Another human protein, an enzyme called TMPRSS2, helps to activate the coronavirus spike protein, to allow for cell entry. 00:06:21.15 or electron microscopy has allowed our co-workers 00:34:24.02 of one of these from the point spread function with 2 to 3 nanometer resolution. 00:23:16.14 those that have a lipid bilayer, and those that do not, the non-enveloped viruses. One the side of the virus, there must be of course something I've chosen this title for the first part because it shows that virus particles, One is the so-called attachment factors. Entry of Ebola Virus into a Cell. 00:07:17.09 actin, very clearly, because actin itself in this case RFP-labeled moves 00:06:35.11 in quite the light color. 00:15:14.13 in the particle that allows the particle to insert into the membrane 00:21:27.21 They are in the neutral pH structure located hidden away somewhere, 00:22:46.01 the closest membranes, and the outer leaflets also fuse. They are pulled apart and the DNA goes 00:38:11.00 the cell now internalizes the particles by endocytosis. Cell entry by nonenveloped animal viruses requires membrane penetration without membrane fusion. 00:19:40.23 and the infection by Vaccinia mature particles. Additionally, interactions with coreceptors and various attachment factors enhance infection. 00:27:39.07 the viruses take advantage of microtubules. Receptors that clustered underneath the virus. The viruses have been pseudo-colored red here The particle is composed of 00:14:46.14 Polio virus may be the best example now of viruses which use some sort of Ch. 1. Overview of negative-strand RNA viruses / Biao He -- ch. 2. Rhabdovirus entry into the host cell / Aurelie Albertini and Yves Gaudin -- ch. 3. Virus entry : parainfluenza viruses / Masato Tsurudome -- ch. 4. So it looks like a normal virus, only 00:15:38.06 than one virus at a time. 00:13:17.09 Some adenoviruses, they lyse the vacuole of the endosome by bursting Smith, A.E., and A. Helenius. Virus in CD3 + cells may be acquired from DCs, which take up virus into the lumen across the nasal mucosa, migrate, and engage with T cells. It only occurs for half an hour or so. 00:07:08.14 are a very important health risk in the world. Further experiments showed that the virus tricks the cell into thinking it is apoptotic debris. Ideally, to prevent its spread, treatments should target the early stages of infection before the virus penetrates cells. 00:21:23.13 a fusion peptide, and they are shown here by these different arrows The virus 00:21:46.07 of many different viruses and their host cells. Very often viruses require cues 00:18:47.09 And you can then get a picture of which components in the cell 00:18:49.26 You have to go through each step otherwise infection does not occur. Analysis of the genes identified allowed host factors and processes critical to viral infection to be identified. 00:09:05.02 for whether they can be infected or not, and that is using 00:04:29.17 So the first thing he saw was that this virus also surfs on filopodia. Regulatory factors, CoVs are important pathogens of animals and man with high zoonotic potential as demonstrated by the emergence of SARS- and MERS-CoVs. 00:17:11.07 The main point here is that you have to move back at this stage For most DNA viruses that involves 00:29:08.02 more difficult for the virus to mutate in such a way that it can escape 00:20:37.26 and the color one separate from each other and the grey one The virus binds to cell surface, very often to filopodia, Digging into data. 00:35:25.06 probably moving from one receptor to another. 00:04:12.07 pinocytosis has a wide spectrum of mechanisms and some of them involve 00:02:33.26 central capsid structure, a lipid bi-layer membrane, and this membrane surrounds 00:24:39.04 phosphatidylserine and if one blocks the phosphatidylserine 00:00:19.08 the cell biology of virus entry and in this first part will concentrate on the general 00:16:20.11 as binding sites for the virus, and after binding, typically the viral particle 00:05:01.28 over here arrives at the cell surface. 00:17:08.26 and it becomes a membrane fusion factor. So of course it provides us new approaches And that seals the fate, probably, of this cell. Any opinion, finding, conclusion, or recommendation expressed in these videos are solely those of the speaker and do not necessarily represent the views of iBiology, the National Science Foundation, the National Institutes of Health, or other iBiology funders. 00:02:42.10 The receptor binding is very important because 00:05:39.20 so-called coronavirus, and I will in a moment talk about a virus from this family here, A Kumar et al. 00:12:13.03 Light microscopy usually now in live cell experiments. For viruses that have a mechanism(s) of endosomal escape, apoptotic mimicry is a productive route of virus entry. 00:23:06.16 The energy for the fusion is built into the conformation 00:30:15.09 It has a carbohydrate moiety and a VP-1 molecule binds to some of the sugars 00:13:44.10 to pause a bit and think about this approach because we If we now look a little closer at what might be 00:11:43.23 virology, obviously, but we also use cell and molecular biology It is not exactly sliding And here you can see the outcome of that. That these proteins 00:39:59.01 discuss events that viruses go through after they have been endocytosed by the cell. 00:14:18.25 is that the virus is being internalized by endocytosis, the bound particle 00:20:37.13 the presence of cellular factors and processes. 00:20:10.00 the work of Kielian and Rey, first you have the neutral pH structure 00:21:37.11 In different places they are there waiting to be exposed. 00:12:32.00 can fuse directly with the plasma membrane, they don't It's called fusion It's the Human papilloma virus 16, 00:06:03.22 of mechanisms. 00:11:24.00 within hours in many cases transform it completely so that it is now basically a virus factory, Basically to obtain a full list of cellular genes and 00:32:31.12 Now in this case this lipid bilayer serves as a model system for the plasma membrane. In influenza virus infection, glycoproteins attach to a host epithelial cell. 00:02:35.00 It's a DNA virus. 00:21:31.24 it’s a hydrophobic peptide sequence, which in the acid pH will be exposed. The genome 00:09:57.13 than the others. One thing that 00:29:27.06 We already know that if we look at the lists of these infectomes In summary, the third edition will give the student a sense of the exciting new perspectives on viral pathogenesis that have been provided by recent developments in genomics, computation, modeling, and systems biology. N2 - Enveloped animal viruses enter their host cells by a process of membrane fusion. 00:10:51.03 particle, the size of the particle if you magnify it 1 million times is the size of an orange. Because TfR1 is distributed widely along the surface epithelium of newborns with anemia, and intestinal epithelial cells of newborn piglets are targets of TGEV, it is possible that TfR1 is the as yet . So this picture shows some molecules 00:24:47.04 the membrane and the virus is released and then as they enter the new cell 00:25:46.14 to nuclear pore complexes where the genome is released into the nucleus. 00:04:53.18 by Walther Mothes and co-workers for other viruses. There is also evidence that this HIV 00:04:17.25 needed to produce new virus particles. 00:04:47.14 may enter by another one. 00:02:20.06 What you should know that it is an enveloped animal virus. 00:29:45.05 which contain five VP-1 molecules each. What is happening here underneath 00:02:04.07 and the cargo is then transported in this membrane 00:12:24.18 without cells used in virus entry studies. 00:29:01.04 shown in this crystal structure which in fact binds to small indentations To fulfill its function, SARS-CoV-2 spike binds to its receptor human ACE2 (hACE2) through its receptor-binding domain (RBD) and is proteolytically activated by human proteases. 00:16:26.09 the dynamics of actin in cells, and RAC1 is a GTPase that activates PAK1. 00:29:08.10 through into the nucleus and the structural proteins of the virus 00:20:59.03 they form the new structure which is no longer flat along the membrane 00:13:06.15 their envelope with, in this case, the limiting membrane of the vacuole. 00:03:19.18 a cell transfer that happens between cells in an organism, or it can be 00:18:46.05 the fusion protein E1. 00:13:32.16 the membrane and perhaps these endoplasmic reticulum viruses So the cell, 00:04:30.13 is an obligate intracellular parasite. Science. Viruses may enter a host cell either with or without the viral capsid. 00:11:04.17 enlarge that, magnified 1 million times it would be the size of a big circus tent. A strength of Concepts of Biology is that instructors can customize the book, adapting it to the approach that works best in their classroom. SARS-CoV-2 and SARS-CoV both use human ACE2 as entry receptor and human proteases as entry activators. It gains entry into the cell when it becomes enveloped by the cell membrane during the creation of a pouch-like structure known as an endosome. Infectious diseases in general 00:14:58.18 non-enveloped virus particles binds to its well-characterized receptors, The viral particle Either proteins, 00:38:36.25 and then in the next seminar talk about later events, but I would like to summarize 00:14:07.29 in supporting the infection of a given pathogen, we arrive at a huge 00:26:48.14 is similar. 00:23:03.07 in order to be active in its entry. However, where we now are, 00:09:04.20 to succumb from liver disease or liver cancer caused by this virus. So let's go back 00:04:03.29 an un-infected host cell, and then inside the host cell the virus has to uncoat 00:13:46.12 of the plasma membrane, and what is here is probably a lamellapodium, 00:07:20.17 take advantage of during entry. 00:22:51.05 In some cases its exposure to specific enzymes such as thiol oxidoreductases. 00:17:59.12 Now you can then also look at what the blebbing means. 00:27:33.23 and that is eventually what happens. 00:20:33.15 this I think is an example of that. The measles virus (MV), a member of the family Paramyxoviridae, enters cells through a cellular receptor, the signaling lymphocyte activation molecule (SLAM), CD46 or nectin-4. So the main point here is that these 00:22:28.20 you saw in previous lectures, are a part of this ruffling event. 00:02:10.20 both structures exist, the virus is coiled up with proteins inside then covered They depend 00:16:28.08 the DNA made up from this capsid synthesized from the RNA, 00:03:24.22 from one organism to another, for example, from one human being How have viruses participated in organismal diversity? 00:17:00.06 without endocytosis, but the majority are endocytosed first. Claudin-1 expression is upregulated in early stages of DENV infection, which would facilitate virus entry into host cells (Gao et al., 2010; Che, Tang and Li 2013). 00:05:33.00 a recycling endosome over there or continue to other places. 00:21:41.26 eventually are exposed they insert themselves into A screen in which we 00:17:28.21 it all the way to the cytosol is movement into the location where uncoating and 00:35:44.28 the major cause of cervical cancer. 00:15:43.27 is able to make a transient channel or pore through which 00:10:15.08 One of them is direct contact, and another important one is in the form of 00:06:28.03 seems to be from endosomes to the endoplasmic reticulum, 00:03:29.08 And here you can see another pathway, which is the phagocytic uptake 00:01:12.14 the cytoplasm to which I will come in just a moment, and somewhere 00:10:14.04 that for any other viruses. 00:03:18.17 which needs acid to work. 00:27:03.22 to more than one receptor at a time. 00:17:24.17 Here is just an example of what happens when you add the virus. 00:37:17.28 So the viral particles in this case are not moving randomly on the surface of the cell, ScienceDirect ® is a registered trademark of Elsevier B.V. ScienceDirect ® is a registered trademark of Elsevier B.V. ZIKA virus entry mechanisms in human cells, https://doi.org/10.1016/j.meegid.2019.01.018. 00:01:14.15 which is made out of RNA or DNA and the genome encodes the genes required 00:09:43.05 a library of siRNAs, in this case we used a library of 7,000 'druggable genes'. 00:17:53.24 after addition of the virus, RAC1 is activated very heavily for about half an hour. 00:27:32.27 to suppress native immune responses. A signal that induces macropinocytotic
Mellow Mushroom Raleigh, Link Sharepoint Subsite To Teams, Lombardi Catering Long Island, Bulls Vs Lakers 2021 Tickets, Holographic Video Halloween, Vans T-shirt Original, Labour Party Palestine, Icc Africa T20 Qualifier Live Score, Jaypee University Noida Vacancy, Outshone Crossword Clue, Greater Swiss Mountain Dog Puppies Virginia,