Learn about The Nobel Prizes that have been awarded sinceas well as the criteria and nomination process that are used to select the winners. NASA Kids is an excellent site for "kids" of all ages and provides an abundance of information, images, and interesting things to do on astronomy and the space sciences. In this lesson, students learn about sources of high-energy radiation and calculate student exposure to ionizing radiation over the past year.
Launch Tool. The overall goal of this case study is to introduce you to the genetic basis of cancer development. You are introduced to a fictional year-old female who sunburns easily and has several other melanoma risk factors.
One day, she discovers that a mole on her leg has started to itch. The case study follows her actions as she gets the mole checked out by her doctor and learns more about cancer in the process. This case was written specifically for a general education health and wellness class. It is most appropriate for students who have a basic background in genetics. The terminology needed to understand the material presented here is minor and can be integrated into the case presentation itself.
Concepts such as gene, mutation, recessive, and dominant can simply be discussed or defined at appropriate times throughout the case. The case study would be most appropriate for small group work and since the material is presented in distinct parts, the whole class can come together for discussion and review between the sections.
Also, please read the Guidelines to get important information regarding how to use case studies in your classroom. See the Tool. See the Collection. See the Lesson. Not an Old Person's Disease. For Educators This case was written specifically for a general education health and wellness class. Did you find this resource helpful?
All rights reserved.Virus entry is a complex process characterized by a sequence of events. KSHV entry is a complex multistep process involving viral envelope glycoproteins and several cell surface molecules that is utilized by KSHV for its attachment and entry. KSHV has a broad cell tropism and the attachment and receptor engagement on target cells have an important role in determining the cell type-specific mode of entry. KSHV utilizes heparan sulfate, integrins and EphrinA2 molecules as receptors which results in the activation of host cell pre-existing signal pathways that facilitate the subsequent cascade of events resulting in the rapid entry of virus particles, trafficking towards the nucleus followed by viral and host gene expression.
KSHV enters human fibroblast cells by dynamin dependant clathrin mediated endocytosis and by dynamin independent macropinocytosis in dermal endothelial cells. Once internalized into endosomes, fusion of the viral envelope with the endosomal membranes in an acidification dependent manner results in the release of capsids which subsequently reaches the nuclear pore vicinity leading to the delivery of viral DNA into the nucleus. In this review, we discuss the principal mechanisms that enable KSHV to interact with the host cell surface receptors as well as the mechanisms that are required to modulate cell signaling machinery for a successful entry.
Herpesviruses have evolved to engage multiple host cell plasma membrane molecules to penetrate the target cells first line of defense [ 1 ]. KSHV displays a broad cellular tropism as it infects a variety of target cells in vitro and in vivo [ 12 ].
KSHV entry and signal induction is a complex event and greatly varies according to cellular tropism [ 13 ]. KSHV utilizes different combinations of host cell surface receptors, and targets different internalization pathways by selectively inducing specific downstream signal molecules [ 13 ].
Independent studies have shown that multiple KSHV glycoproteins engaging host cell membrane binding and entry receptors induce cascades of signal pathways promoting endocytosis. Subsequent steps include fusion of the viral envelope with endosomal membranes, release of virus capsid in the cytosol, capsid trafficking to the nuclear periphery, and delivery of KSHV DNA into the nucleus [ 13 ]. Therefore, these overlapping phases are essential for KSHV de novo infection, which relies on intricate spatio-temporal dynamics of molecular interplay.
This review summarizes almost two decades of extensive research findings by several groups regarding KSHV receptors, entry pathways, trafficking and early immune modulation during de novo infection of target cells. While advances have been made in our understanding of the entry associated signaling events early during KSHV-cell interaction, information regarding KSHV trafficking and nuclear entry remains incomplete.
Hence, this review also highlights current perspectiveson KSHV early events that several groups have reported over the decades of research in the field of KSHV biology. The envelope glycoproteins of KSHV play an important role in infection as they mediate virus-cell initial attachment, entry, assembly, and egress of the virus. KSHV gB is a key envelope glycoprotein involved in the initiation of entry.
Not an Old Person's Disease
Unlike other herpesviruses, lytic phase associated glycoproteins gpK8. Functionally both gB and gpK8. KSHV glycoproteins gM and gN are N-glycosylated to form a heterodimeric complex and functionally participate in virus penetration and egress.
The entry receptors of KSHV are highly specific and utilized in different combinations which greatly vary according to cellular tropism as well as the entry pathways exploited by the virus. Entry receptor utilization is also a primary step in routing KSHV containing cargo to productive vs non-productive pathways of infection [ 31 ]. Heparan sulfates are ubiquitously expressed cell membrane proteoglycans with charged carbohydrate moieties that interact with several protein ligands and extensively studied in herpesviruses.
HS are known to facilitate KSHV attachment and concentration on the cell surface, enabling possible conformational change s in virus glycoprotein s to gain access to specific adjacent entry receptors [ 17 ]. This initial attachment step by a universal receptor partly explains the broad cellular tropism for KSHV. B cells and cell lines lacking Ext1 enzyme are unable to promote the crucial glycosylation step in HS biosynthesis, and lower expression of HS limits KSHV infectivity in these cells.
Integrins are extracellular cell surface receptors, well known for major extracellular matrix ECM outside-in signaling. KSHV was the first herpesvirus shown to utilize integrins as entry receptors in adherent target cells [ 25 ]. Microscopic evidences also support that integrins form a multimolecular receptor complex during KSHV entry into target cells [ 24 ]. The role of integrins in KSHV entry is also characterized in monocytes [ 35 ].
There are some discrepancies regarding the role of integrin subtype used by KSHV in different target cells [ 3637 ]. However, experimental methodologies utilized in those studies explain the reason behind dissimilar findings.In clonal selection of B cells which substance is responsible for determining which cells will eventually become cloned?
The process whereby neutrophils and other white blood cells are attached to an inflammatory site is called Small molecules that bind with self- proteins to produce antigenic substances are called Which of the following determines what specific foreign substances our adaptive immune system will be able to recognize and resist?
Activated T cells and microphages release to mobilize immune cells and attract other leukocytes into the area. Cancer cels and virus infected body cells can be killed before activation of adaptive immunity by Complete proteins and antibodies coat a microorganism and provide binding sites, enabling macrophages and neutrophils to phagocytize the organism.
This phenomenon is termed Class II MHC molecules appear only on the surface of antigen presenting cells, thymic cells, and T cells that have been activated by exposure to antigens. Active and passive humoral immunity are both mechanisms of adaptive immunity that use antibodies.
After becoming immunocompetent the naive T cells and B cells are exposed to the bone marrow where the encounters with antigens occur. Which immunoglobulin class is attached to the external surface of B cells and acts as an antigen receptor of the B cell? Chapter 21 1. Intact skin and mucouse membranes?Luckys supermarket
First line of defense. Second line of defense. Inflammatory response and skin and mucous membrane. Enables quick and efficient response to secondary exposure to antigen. Absence results in no immune response. Forms antibody producing cells. Kills cancer cells and virus infected body cells. Slows or stops the immune response. Main antibody of both primary and secondary immune response. Protects mucosal barriers. Involved in allergies.
Along with IgM, this is a B cell receptor. First to peak during a primary immune response. Which of the following is characteristic of antibodies? Composed of heavy and light polypeptide chains. Which of the following is associated with passive immunity? Passage of IgG antibodies from a pregnant mother to her fetus. Which of the following is not a type of T cell? B lymphocytes develop immunocompetence in the. Which of the following is not a function of the inflammatory response?
The redness and heat of an inflamed area are due to local hyperemia caused by. The antibody molecule is held together by bonds.
Which of the following statements regarding Nk cells is a false or incorrect statement. Nk cells are a type of neutrophil. Which of the following is the correct sequence of events in phagocytosis?NCBI Bookshelf. Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis.
Cambridge: Cambridge University Press; Benjamin E. GewurzJatin M. Vyasand Hidde L. Authors Benjamin E. Gewurz1 Jatin M. Vyas2 and Hidde L. Ploegh 1. The multiple layers of the human immune response present a challenge to viruses, which must survive and multiply within a host for a sufficient period of time to allow successful transmission to susceptible individuals. Given the large proteomes and comparatively low polymerase error rate of human herpesviruses, antiviral immunity at first glance appear to have the upper hand.
Nonetheless, herpesviruses manage prolonged incubation periods following initial infection, with systemic dissemination and prolonged secretion, often from multiple sites. In contrast to the similarly large poxviruses, the ability to subsequently establish persistent infection is a hallmark of the human herpesviruses. To enable this lifestyle, the herpesviruses devote a significant proportion of their genome coding capacity to the expression of immuno-evasins, a collection of molecules that disrupt normal immune physiology.
Each human herpesvirus studied has evolved elegant cell biological solutions to problems posed by the immune response. Innate immunity, an evolutionarily conserved and relatively non-specific system of pattern recognition molecules hardwired in the genome, cytokines such as interferons, phagocytes and natural killer NK cells, represents the first line deployed against microbial invaders, including herpesviruses Janeway and Medzhitov, The clonal expansion of B- and T- lymphocytes that bear antigen-specific receptors for viral epitopes underlies the adaptive antiviral immune response, laying the groundwork for a highly pathogen-specific defense.
Such specificity comes at a price — lymphocyte proliferation requires time to unfold, and innate immunity, in particular NK-cell activity, limits the initial herpesvirus spread. Indeed, NK cell immune deficiencies result in dramatic infection by several herpesviruses McClain et al.
There is significant cross-talk between the innate and adaptive systems, and preliminary pathogen recognition by the innate immune system directly contributes to the development of adaptive immunity. Further, the eventual adaptive response utilizes branches of the innate system for crucial effector function Medzhitov and Janeway, Innate and adaptive immunity act in concert to allow recovery from acute herpesvirus infection.
Adaptive immunity then allows for lifelong immunological memory, affording both control of persistent herpesvirus infection and protection against reinfection. Through millennia of coevolution, herpesviruses have largely reached a state of equilibrium with their human hosts. At the cost of a large proportion of their coding capacity, herpesviruses perturb adaptive immunity to achieve persistent infection, in general with remarkably little collateral damage to their hosts.
However, lapses in T-cell immunity, such as by immunosuppressive agents or by coinfection with other pathogens such as Human Immunodeficiency Virus, can lead to significant herpesvirus-associated pathology. Human herpesvirus genome size and polymerase fidelity place constraints on epitope mutation, and generally do not allow for antigenic variation as a means to avoid T-cell immunity.
Herpesviruses therefore, have devised a range of mechanisms to subvert adaptive immunity. Generalized T-cell immuno-evasion strategies shared by herpesviruses include latency, restriction of viral gene expression to immunoprivileged sites such as the CNS, interference with complement, cytokines, NK-cell function, and apoptosis, all of which are reviewed in detail in other chapters.
This section will highlight the cell biology that underlies herpesvirus evasion of T-cell immunity. Though sacrificing the host cell, lysis ultimately limits the spread of the viral pathogen Heemels and Ploegh, Peptides are produces more Human herpesvirus immuno-evasins of adaptive T-cell immunity discussed in the chapter.
MCMV appears to achieve this phenotype via its M27 gene-product. EBNA-1 is essential for viral genome persistence during cell division and is a major protein expressed during latency Lee et al.The immune system can be divided into two overlapping mechanisms to destroy pathogens: the innate immune response, which is relatively rapid but nonspecific and thus not always effective, and the adaptive immune response, which is slower in its development during an initial infection with a pathogen, but is highly specific and effective at attacking a wide variety of pathogens see Figure 1.
Figure 1. The innate immune system enhances adaptive immune responses so they can be more effective. The barrier defenses are not a response to infections, but they are continuously working to protect against a broad range of pathogens. The different modes of barrier defenses are associated with the external surfaces of the body, where pathogens may try to enter see Table 1.
The primary barrier to the entrance of microorganisms into the body is the skin. Not only is the skin covered with a layer of dead, keratinized epithelium that is too dry for bacteria in which to grow, but as these cells are continuously sloughed off from the skin, they carry bacteria and other pathogens with them.
Additionally, sweat and other skin secretions may lower pH, contain toxic lipids, and physically wash microbes away.Plasma Membrane
Another barrier is the saliva in the mouth, which is rich in lysozyme—an enzyme that destroys bacteria by digesting their cell walls. The acidic environment of the stomach, which is fatal to many pathogens, is also a barrier.End medical term
Additionally, the mucus layer of the gastrointestinal tract, respiratory tract, reproductive tract, eyes, ears, and nose traps both microbes and debris, and facilitates their removal. In the case of the upper respiratory tract, ciliated epithelial cells move potentially contaminated mucus upwards to the mouth, where it is then swallowed into the digestive tract, ending up in the harsh acidic environment of the stomach.
Considering how often you breathe compared to how often you eat or perform other activities that expose you to pathogens, it is not surprising that multiple barrier mechanisms have evolved to work in concert to protect this vital area. A phagocyte is a cell that is able to surround and engulf a particle or cell, a process called phagocytosis. The phagocytes of the immune system engulf other particles or cells, either to clean an area of debris, old cells, or to kill pathogenic organisms such as bacteria.
Many of the cells of the immune system have a phagocytic ability, at least at some point during their life cycles. Phagocytosis is an important and effective mechanism of destroying pathogens during innate immune responses. The phagocyte takes the organism inside itself as a phagosome, which subsequently fuses with a lysosome and its digestive enzymes, effectively killing many pathogens.
On the other hand, some bacteria including Mycobacteria tuberculosisthe cause of tuberculosis, may be resistant to these enzymes and are therefore much more difficult to clear from the body. Macrophages, neutrophils, and dendritic cells are the major phagocytes of the immune system.Elasticsearch deduplication aggregation
A macrophage is an irregularly shaped phagocyte that is amoeboid in nature and is the most versatile of the phagocytes in the body. Macrophages move through tissues and squeeze through capillary walls using pseudopodia. They not only participate in innate immune responses but have also evolved to cooperate with lymphocytes as part of the adaptive immune response.
Science Biology library Human biology Immunology. Role of phagocytes in innate or nonspecific immunity. Types of immune responses: Innate and adaptive, humoral vs. B lymphocytes B cells. Current timeTotal duration Google Classroom Facebook Twitter.
Video transcript Now that we've touched on all of the major players in the specific immune system, what I thought I would do in this video is do a summary so it all fits together a little bit. So the first person or character we got exposed to was the B cell, which I always do in blue. And what made that interesting is that every B cell has its own specific-- or they have membrane bound antibodies, but for each B cell, the membrane bound antibodies on each specific B cell had its own variable portion.
So this B cell-- it'll be variable right like that. And if I were to draw another B cell right here, I would draw the variable portion a little bit different.
Review of B cells, CD4+ T cells and CD8+ T cells
This is why different actual B cells will respond to different antigens or different pathogens that have entered our system. And a B cell gets activated-- let's talk about what happens when it gets activated or what needs to happen. It needs binding of the pathogen onto one of these membrane bound antibodies. But that's not all. I mean, sometimes that's all you need, but usually you also need to be stimulated by a T cell.
And you might say, where's the helper T cell stimulate this guy?A phospholipid is composed of two fatty acids, a glycerol unit, a phosphate group, and a polar molecule. When placed in water, phospholipids will orient themselves into a bilayer in which the non-polar tail region faces the inner area of the bilayer. The polar head region faces outward and interacts with the liquid.
Phospholipids form a lipid bilayer in which their hydrophillic head areas spontaneously arrange to face the aqueous cytosol and the extracellular fluid, while their hydrophobic tail areas face away from the cytosol and extracellular fluid. Large molecules are selectively permitted entrance into a cell through transmembrane proteins that traverse the lipid bilayer.
Phospholipids are very important molecules as they are a vital component of cell membranes. They help cell membranes and membranes surrounding organelles to be flexible and not stiff. This fluidity allows for vesicle formation, which enables substances to enter or exit a cell through endocytosis and exocytosis. Phospholipids also act as binding sites for proteins that bind to the cell membrane. Phospholipids are important components of tissues and organs including the brain and heart.
They are necessary for the proper functioning of the nervous systemdigestive systemand cardiovascular system. Phospholipids are used in cell to cell communications as they are involved in signal mechanisms that trigger actions such as blood clotting and apoptosis. Not all phospholipids are the same as they differ in size, shape, and chemical makeup. Different classes of phospholipids are determined by the type of molecule that is bound to the phosphate group. Choline is bound to the phosphate head region of the molecule.
PC is important structurally to membranes as it helps to maintain membrane shape. It is the second most abundant cell membrane phospholipid. The small head group size of this molecule makes it easier for proteins to be positioned within the membrane. It also makes membrane fusion and budding processes possible.
Inositol is bound to the phosphate group in this phospholipid. Share Flipboard Email. Regina Bailey. Biology Expert. Regina Bailey is a board-certified registered nurse, science writer and educator. Updated September 12, What Are Amphipathic Molecules?
Definition, Properties, and Functions.
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