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Exam 4

does the ebola virus have a licensed vaccine? no
what is the name of the vaccine going under trial for ebola ZMapp
what are the ways for pathogens to evade and subverse the immune defense d antigen variation, latency state, resist destruction, exploit immune system , induce immunosuppression
what are the different ways pathogens can use antigen variation to evade the immune system different antigen types, antigen drift and shift, and programmed gene rearrangement
serotypes different antigenic types of a pathogen that help an antigen avoid the immune system because the immune system does not have the specific antibody for that antigen
antigenic drift mutations alter epitopes in hemagglutinin so that neutralizing antibody can no longer bind to the antigen
antigenic shift RNA segments are exchanged between viral strains in secondary host and there is no cross-protective immunity to virus expressing a completely new hemagglutinin
programmed gene rearrangment there are many inactive copies for VSG gene but only one site for expression. inactive genes are copies into expression site by gene conversion changing epitope. keeps happening for each inactive copy so chronic cycles of antigen clearance cause damage
example of a disease that uses antigenic variation Type A influenza
example of a disease that uses programmed gene rearrangement sleeping sickness aka African tyrpanosomiasis
example of a disease that uses antigenic variation pneumonia
latency state initial infection is cleared by effective immune response but residual virus populations persist and can be reactivated. often due to quiescent virus and low level of MHC I
example of a disease that uses latency state herpes simplex virus
how does TB resist destruction it prevents the fusion of phagosomes with lysosomes so they can't be destroyed in macrophages. so bacteria is trapped in granulomas
how does taxoplasmosis (kitty liter parasite) evade destruction it generates its own vesicle which isolates it from the rest of the cell and avoids fusion with other vesicles so no peptides are broken up that can be loaded on self-MHC
how does listeriosis exploit the immune system hijacks actin filaments in macrophages to form vacuoles which spread to to adjacent cells without exposing to extracellular space
syphillis--how does it exploit the immune system it coats its surface with host proteins until it has invaded host tissue
how does lyme disease exploit the immune system coats itself with complementary inhibitory protein factor H made by host
what are the mechanisms to subvert the host immune system inhibition of humoral immunity, inhibition of inflammatory response, blocking of antigen procession and presentation, and immunosuppression of host
how does staphylococcus subvetr the immune system produces a toxins that acts as a superantigen that non-specifically activate a large number of T cells and produce cytokines that toxic shock. stimulated T cells also go AICD leading to immunosuppression
how do the measles subvert the immune system causes long lasting immunosuppression through infection of dendritic cells and reduce T and B cell function
leprosy chronic infection that causes granulomas of nerves, respiratory tract, skin, and eyes results in lack of ability to feel pain and loss of limbs due to repeated injuries
how does leprosy subvert the immune system granulomas cause low or absent T cell responsiveness due to drop in cytokine levels
primary immunodeficiencies cause by inherited mutations in any of genese involved in immune response
common feature of immunodeficiency disease recurrent infections with similar pathogens at young age, other symptoms include allergy, autoimmunity, cancers
secondary immunodeficiencies acquired as a consequence of any other diseases, environmental factors, or side-effects of medical intervention
normal B cell population in blood 0.3 X 10^9 per liter
normal t cell population in blood 1.0 - 2.5 X 10^9 per liter
neutrophil population in blood 3.00-5.5 X 10^9 per liter
eosinophils population in blood .05 - .25 X 10^9 per liter
basophils population in blood .02 X 10^9 per liter
how do you measure of B cell and T cell population in vivo serum Ig levels in response to pokeweed mitogen for B cells and skin test in response to phytohemagglutinin for T cells
SCID severe combined immunodeficiency
X-linked SCID muttion in IL-2R common gamma chain for T and NK cell development
SCID caused by Jak3 mutation Jak3 associated with gamma chain and transduces its signaling
SCID caused by RAG mutation failure of VDJ recombinantion results in arrest of lymphocyte development --- Omenn syndrome
Omen Syndrom SCID caused by RAG mutation
SCID caused by TCR mutation CD3 complex in pre-TCR signaling
SCID caused by defect in thymic ffunction thymus development requires transcription factors such as FOXN1 and TBXI
DiGeorge syndrome SCID by thymic function
MHC Class II deficiency defects in CD4 T cell development
MHC Class 1 deficiency defects in CD8
X linked amgammaglobulinemia XLA mutation in Bruton's tryosine kinase BTK that trasduces signals through pre-BCR. arresting pre-B cell stage
X linked hyper IgM syndrome mutations in CD40 ligand or NEMO, a downstream kinase for CD40
common variable immunodeficiencies CVIDs defects in one or more isotypes of immunoglobulin, such as IgA deficiency and hyper IgE syndrome
X linked hyper IgM syndrome unable to active B-cells fully in CD40L deficiency patients
deficiency in classical complement pathway (C1 and C2 and C4) leads to immune-complex disease such as systemic lupus
deficiency in C3 leads to pyogenic bacteria and sometimes immune complex disase such as pneumonia
problems in phagocyte productions lead to and are caused by congenital neutropenia and widespread pyogneic bacterial infections. cause is ELA2 mutation
problems in phagocyte adhesion lead to and are caused by leukocyte adhesion deficiency and widespread pyogenic bacterial infection. cause is leukocyte integrin CD18 deficiency
problems in phagocyte activation lead to and are caused by TLR signaling defects and severe cold pyogenic bacterial infection.. cause is TLR3 deficiency
problems in phagocyte killing lead to and are caused by chronic granulomatous disease, G6PD deficiency, and myeloperoxidase deficiency leading to intracellular and extracellular infection, defective respiratory burst, and defective intacellular killing. cause can be NADPH oxidase mutation
hematopoietic stem cell transplant one MHC allele is shared between donor and recipient and so donor cells undergo selection of MHC molecules of common allele in recipient thymus that are activated by MHCaxb APC
main difficulties of HSC MHC polymorphisms, hard to find a match
process of HSC transplantation deplete donor graft of mature T cells to avoid attacking host (GVHD) and myeloablative treatment of host to destruct the bone marrow to minimize HVGD
gene therapy somatic gene therapy corrects inherited immune deficiency. isolate HSC, introduce normal gene, and reinfuse back in patient.
challenge of gene therapy target insertion of corrected gene
HIV and AIDS acquired immune deficiency syndrome is caused by infection with human immunodeficiency virus
how does HIV transmit via body fluids via sexual intercourse, contaminated needles, blood products, mother to baby
course of HIV infection acute phase, asymptomatic phase, symptomatic phase, AIDS
what does HIV essentially do kills CD4 T cells, causes apoptosis of CD4 T cells or causes CD8 T cells to kill CD4 T cells
HIV structure enveloped retrovirus. contains viral envelope, RNA genome, reverse transcriptase, integrase, and protease, core and matrix proteins
HIV genome 9 genes with overlap reading frames
major genes of HIV gag:structure protein, pol:enzymes, env: envelope glycoproteins
HIV infection of CD4 T cells?for gp120 receptor of gp120 (envelope protein) is CD4 causing CD4, dendritic, and macrophages trget cells
what is the coreceptor for HIV CCR5 and CXCR4
adhesion of HIV to target cells gp120 ginds to CD$ and then gp41 causes fusion of envelope with cell plasma membrane
HIV infection of dendritic cells receptors of DC bind to gp120, along with CD 206, CD 207, and CD 209 causing DC-SIGN and HIV is transferred from DC to CD4 T cells
genetic deficiency of what confers to resistance to HIV CCR5. 32 base pair deletion from coding region puts individuals at risk of exposure to HIV but resist toinfection
viral cDNA formation reverse transcriptase makes RNA to DNA
viral integration integrass; provirus and latent infection, integrates viral DNA into DNA
where does binding of viral DNA happening HIV genome has 9 genes flankes by long terminal repeats LTRs that are the binding sites for gene regultory proteins
regulatory proteins of HIV Tat: transcription regulation, Rev: export viral RNA
replication of HIV T cell activation leads to HIV replication. NFkB binds to LTR and initiates the transcription of viral RNA by host RNA pol II. Tat enhances and amplifies transcription. Rev helps viral RNA export from nucleus
HIV strategy to escape immunity antigenic variation (mutations) and latency (provirus)
Vif induces degradation of APOBEC (aolipoprotein B mRNA editing enzyme, catalytic polypeptide-like), a natural cytidine deaminase that causes extensive mutations in viral cDNA
Nef downregulation of MHCI and II as well as CD4
immune response to HIV controls but does not eliminate. CD8 T cells kill infected cells, Antibodies against envelope proteins and core proteins, CD4 T cells prlofierate reponses, cytokines CCL3-5 compete with HIV to bind to CCR5, APOBEC causes extensive mutations in viral cDNA
destiny of HIV infection cell-mediated immunity is lost, causing opportunistic infections, tumors, and death
HAART: Highly Active Antiretroviral Therapy combination therapy with cocktail inhibitors targeting both reverse transcriptase (nucleoside analogs such as AZT) and viral protease. reduces HIV circulating in blood d
viral protease cleaves viral polyproteins to produce envelopes and enzymes
disadvantages of HAART ineffective at HIV eradication, side effects (mitochondiral DNA synthesis) and high cost
viral entry inhibitors target gp120, gp41, CCR5
viral integrase inhibitors target p32
AIDS treatment challenges durg resistance: rapid replication and mutations. therapeutic vaccines: mutations and latency, prophylactic vaccine:diversity among HIV strains and ethics
allergic reaction harmful immunologically mediated hypersensitivity reactions in response to harmless/innocuous antigens (allergens)
Ig-E mediated allergic reactions Type I hypersensitivity reactions are allergies due to production of IgE against allergens
signals for IgE production 1. differentiation to Th2 cells (IL-4, IL-3) antigen across a mucosal epithelium and needs very low dose of antigen. 2. class switching of B cells, IL4 to IL4R and STAT6, CD40 ligand interacts with CD40
amplification of IgE production of mast cells IgE secreted by plasma cells binds to high affinity Fc receptor FceRI on mast cells that activate them. mast cells then contact and secrete signals to B cells to stimulate IgE production
IgE mediated allergy induced by dust mites (allergen protein Der p 1 - cystein protease) Der p 1 cleaves occludin in tight junctions and enters mucosa. Der p 1 taken up by APC and Th2 priming causing B cell switch to IgE production in lymph node. plasma takes IgE Ab to mucosa and IgE binds to FceRI on mast cell causing granulation
neherton's syndrome characterized by chronic skin inflammation and itch. disrupted skin barrier is susceptible to infection and allergy, leading to development of reddish skin similar to atopic dermatitis
cause of neherton's syndrome lack of protease inhibitor SPINK5
atopy predisposition to become IgE sensitized to environmental allergens
chromosome 11q12-13 encodes the beta subunit of IgE receptor FceRI
chromosome 5q31-33 encodes cytokins IL4, IL 13
hygiene hypothesis reduced exposure to microorganism as a cause for allergy
counter-regulation hypothesis infections drive the production of IL-10 and TGF-beta which downregulate both Th1 and Th2 responses
mast cells are rich in histamine, heparin, protease, and cytokines
connective tissue mast cell associated with vascularized connective tissue
mucosal mast cells submucosal layers of gut and respiratory tract
enzymes in allergy reaction tryptase, chymase, carthepsin G, carboxypeptidease
toxic mediator in allergy reaction histamine, heparin
cytokines in allergy reaction IL4 and IL13
eotaxins chemokines that are particularly imporant for attracting eosinphils from circulation into tissue such as CCL11 CCCL2 and CCL26
immediate reaction of allergic reaction local wheel and falre reaction. histamine
late phase reaction of allergic reaction wide spread edema, calcitonin gene related peptide CGRP and vascular endothelia grow factor VEGF
chronic allergic inflammation of allergic reaction recruitment of Th2 cells and eosinophils, persistent edema and tissue remodeling
anaphylaxis serious allergic reaction that is rapid onset and may cause death. causes a number of symptoms including itchy rash, throat swelling, and low bloody pressure
penicillin allergy beta lactam ring, binds with self proteins and provokes Th2 reponse
what happens if allergen enters intravenously general release of histamine which acts on blood vessels to increase permeability leading to systemic anaphylaxic shock
what happens if allergens entere subcutaneous local release of histamin causes wheal-and-flare reaction. airborne allergens penetrating skin can also cause atopic edema
what happens if allergens enters through inhalation allergic rhinitis caused by increased mucus production and nasal irritation. asthma due to contraction of bronchial smooth muscle and increased mucus secretion
what happens if allergens enter through ingestion contraction of intestinal smooth muscle induced vomiting. outflow of fluid into gut causes diarrhea. antigen diffuses into blood vessels and is widely disseminated causing hives and anaphylaxia or atopic edema
allergic rhinitis and asthma acute response in allergic asthma leads to Th2 mediated chronic inflammation of airways. two features: recruitment and chronic activation of inflammatory cells, mainly Th2 cells and eosinophils and tissue remodeling
chronic inflammation in allergic rhinitis and asthma epithelial cells release CCL5 and CCL11 to induce infiltration of Th cells and leukocytes like eosinophils and neutrophils through CCR3
tissue remodeling in allergic rhinitis and asthma Th2 cytokines induce epithelial cell death and hypertrophy of smooth muscle (thickening of airway walls)
atopic eczema/dermatitis crhonic dermatitis, an inflammotry relapsing, non-contagious, itchy skin disorder.
filaggrin mutations increased the risk for atopic dermatitis. Filaggrin is a protein that binds to keratin fibers in epidermal cells contributing to physical barrier of skin surface
desentization immunotherapy to restore tolerance to allergen by reducing its tendency to induce IgE production; inject escalating dose of allergen
passive immunotherapy anti-IgE antibodies (omalizumab)to prevent IgE binding to FceRI. reduced circulating IgE levels
autoimmunity responses to self antigens or antigens associated with commensal microbiota
autoimmune diseases characterized by tissue damage resembling the immune response to pathogens
self-tolerance condition in which immune system does not attack the self body because lymphocytes that have affinity for self antigens are removed or inactivated via variety of mechanisms
self tolerance mechanisms central tolerance, peripheral tolerance, antigen segregation
central tolerance recognition of self-antigen by immature lymphocytes leads to a negative signal triggering the cell death. happens during B and T cell development
peripheral tolerance tolerance induced in mature lymphocytes once cells have left central lymphoid organs. peripheral anergy, supression by T reg cells ad induction of T reg cells and activation induced cell death
antigen segregation self-antigens are sequestered in certain organs not accessible to immune system, such as thyroid, pancrease, and immunologically privileged sites
AIRE autoimmune regulator control peripheral genes from specialized tissues that are also expressed in thymus
defect of AIRE gene causes inherited form of autoimmunity: APECED autoimmune ployendocrinopathy-candidiasis-ectodermal dystrophy
anergy generation of hyporesponsiveness in lympocytes which encounter antigen in absence of co-stimulatory signals that accompany inflammation or in presence of co-inhibitory signals
systemic lupus erythematosus SLE autoantibodies against DNA, chromatin proteins, and ribonucleoproteins
how is peripheral anergy induced via inactivation of B or T cells by self antigens in secondary lymphoid tissues
regulatory T cells suppress immune responses of other cells and maintain tolerance to self-antigens and abrogating autoimmune disease
natural T reg cells developed in thymus
induced T reg cells developed in peripheral tissues
supression mechanisms of T reg cells IL 10 TGF beta
t reg cell markers CD$ CD25 FoxP3
FoxP3 mutation causes x linked recessive autoimmune syndrome IPEX
colitis inflammatory bowel disease
what cells inhibit colitis CD4 and CD25 Treg
immunologically privileged sites tissue grafts do not elicit immune responses and rejection via physical barrier, inhibitory cytokines, expression of Fas ligand
sympathetic opthalamia bilateral diffuse inflammation and blindness of both eyes following trauma to one eye
mutliple sclerosis chronic inflammatory demyelinating disease due to brain autoantigens for myelin proteins
pathogenic mechanisms of autoimmune diseases autoantibodies (cell surface proteins, extracellular matrix, intracellular antigens) and effector T cells (CD8 and CD4)
myasthenia gravis autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatigue. first noticeable symptome is eye muscles
what causes myasthenia gravis autoantibody inhibits acetylcholine receptor function
Grave's disease autoimmune disease causes thryoid to enlarge and become overactive with hyperthyroid symptoms such as increased heartbeat, muscle, disturbed sleep, and irritability and bulging eyes
what causes grave's disease autoantibody stimulates TSH receptor
transplacental antibody transfer transmission of disease from affected mother to infants via placenta
autoimmune hemolytic anemia occurs when antibodies directed against person's own RBC cause them to lyse leading to insufficient plasma concentration (anemia)
autoimmune thrombocytopenic purpura occurs when antibodies directed against the platelet surface antigen cause a depletion of platelet (thrombocytopenic), which in turn cause hemorrhage
Goodpasture's syndrome rare autoimmune disease in which autoantibodies (against membrane collagen) attack the lungs and kidneys. it may quickly result in permanent lungs and kidney damage, often leading to death
treatment of purpura and anemia removal of spleen, intravenous immunoglobulin
treatment for for goodpasture's syndrome immunosuppression, plasmapheresis
systemic lupus erythematosus (SLE) or lupus system autoimmune disease that immune system attacks the body's cells and tissue, resulting in inflammation and tissue damage in many parts of the body
autoantibodies of lupus attack what chromatin, DNA, rubonucleoprotein complex
Type 1 diabetes form of diabetes melitus that results from the autoimmune destruction of the insulin-producing beta cells in pancreas
symptoms of Type 1 diabetes lack of insulin leads to increased blood and urine glucose, causing polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger) and weight loss
symptoms of multiple sclerosis loss of sensitivity, muscle weakness, ataxia, speed or visual problems
how is it proven that it is effector CD4 T cells that are attacking healthy cell in MS EAE
EAE- experimental autoimmune encephalomyelitis mouse model of MS by deliberately immunizing mice with myelin proteins
rheumatoid arthritis autoimmune disease that results in chronic systemic inflammatory disorder that may affect many tissues and organs but principally attacks flexible (synovial) joins, followed by erosion of bone
therapeutic antibodies for RA attack what TNF alpha
Crohn's disease type of inflammatory bowel disease that may affect any part of the gastrointestinal tract from mouth to anus causing wide variety of symptoms such as abdominal pain, diarrhea, vomiting
where are the antigens derived for Crohn's commensal microbiota
Crohn's disease attacks homeostatic mechanisms of mucus by goblet cells, tight junctions, antimicrobial peptides, regulatory T cells
what causes Crohn's disease NOD2 mutations which is for intracellular receptor for peptide derived from bacteria. the downstream signal is NFkB that induces release of antimicrobial peptides
immunosuppressive durgs exert broad inhibition of immune system and so opportunistic infection is common complication
immunosupressive antibodies target specific proteins expressed/secreted by immune cells to inhibit immune system. requires mechanissm involve lymphocyte depletion, inactivation, preventing, migration, and a neutralizing inflammatory cytokines
corticosteroids derivatives of glucocorticoid family of steroid hormones. can cross plasma membrane and bind to nuclear receptors interacting with transcription factors to regulate 20% gene expression in leukocytes
cyclosporin A, tacrolimus (FK506) inhibits calcineurina Ca2+ dependent phosphatase binding to immunophilin. calcineurin activates a transcription factor NFAT which is important for IL-2 production
raamycin inhibits a serine/threonine kinase mTOR which is important for cell proliferation and growth
RAPTOR regulatory associated protein of mTOR
RICTOR rapamycin-insensitive companion of mTOR
humanization since most antibodies are most readily made using mouse cells that cause immune reaction in human, antibody engineering to decrease immunogenicity but to maintain specificity
lymphocyte depletion antibodies immunosuppressive monoclonal antibodies that trigger lymphocyte desturction
mechanism of lymphocyte depletion of antibodies phagocytosis, membrane attack complex
muromomab targets CD3 and inhibits T cell receptor signaling
Daclizumab targets CD25 (subunit of IL2) and inhibits IL2 receptor signaling
natalizumab targets alpha4 integrin that binds to VCAM 1 on endothelium for leukocyte infiltration implicated in MS and Crohn's disease
cancer broad group of disease with unregulated cell growth, forming malignant tumors, which may invade nearby parts of body or spread to more distant parts of body through lympatic system or blood stream
risker factors for cancer tobacco use, dietary factors, certain infections, exposure to radiation, lack of physical activity, obesity, and environmental pollutants
risker factors can damage what genes
chemotherapy treatment of cancer with cytotoxic drugs that act by killing cells that divide rapidly
radiation therapy ionizing radiation that damages DNA of cancerous cells
immunotherapy cell-based, antibody therapy, cytokine therapy, and vaccination
tumor rejection antigens are specific to individual tumors
cancer immune surveillance theory that immune cells act as sentinels in recognizing and eliminating continuously arising, nascent transformed tumor cells
immunoediting dynamic process that consists of immunosurveillance and tumor progression. characterized by changes in ummunogenicity of tumors due to anti-tumor response of immune system, resulting in emergence of immune-resistant variants
3 phases of immunoediting elimination, equilibrium, and escape
evidence supporting immune surveillance/immunoediting knockout mice lacking perforin, RAG, or STAT1 develop lymphomas,gut epithelial and breast cancer. development of melanoma in patients transplanted kidneys from donor treated with melanoma. post transplant lymphoproliferative disorder to immunosuppression
mechanisms tumors avoid immune recognition low immunogenecity (no peptide MHC ligand, no adhesion molecules, no co-stim molecules), tumor treated as self antigen, antigenic modulation leading to antigen-loss variants , tumor induced immune supression, tumoe induced privileged site
antigenic modulation antibody against tumor cell surface antigens can induce endocytosis and degradation of the antigen, immune selection of antigen-loss variants
what molecules to tumors release to escape the immune system TGF beta for immunosupression and Treg cell induction. PD-L1 for induction of T-cell death, collagen to produce physical barrier
oncogenic antigens there are strictly tumor specific antigens that result from point mutations or gene rearrangements during oncogenesis
what molecules come from melanomas CdK4 and Beta catenin
cancer testis antigens the proteins are encoded by genes that are normally expressed only in male germ cells in testis. abnormal activation of genes encoding cancer-testis antigens in tumor cells
differentiation antigens proteins are encoded by genes that are normally expressed only in particular type of tissue. tyrosinase expressed by melanoma is important for melanin synthesis
oxerexpression antigens antigens that are strongly overexpressed in tumor tissue. HER-2/neu is a receptor tyrosine kinase.
what do they target to treat breast cancer HER-2/neu
oncoviral antigens protein is critical for oncogenic process by virus infection a
human papiloma virus HPV proteins is highly expressed in cervical carcinoma. vaccine made to target HPV proteins for cervical cancer
adoptive T-cell therapy form of passive immunization by the transfusion of T-cells. T-cells specific to tumor antigen can either by removed from tumor sample or genetically engineered. activation and expansion follow.then transfusion. no approved therapy yet
dendritic cell therapy provokes anti-tumor response by causing dendritic cells to present tumor antigens. 1) activate DC ex vivo in presence of tumor antigens then put back and provoke immune response
first only based cell therapy? for what? Sipuleucel-T for prostate cancer
antibody therapy currently the most successful form of immunotherapy. cell surface receptor are common targets and include the EGF receptor and HER2.
what drug targets HER-2 for breast cancer Trastuzumab
cytokine therapy use of cytokines to provoke immune response against tumor. use especially interferons, interleukins
interferon alpha is used in what treatment hariy cell leukemia, AIDS-related Kaposi's sarcoma, folicular lymphoma, chronic myeloid leukemia, and malignant melanoma
interleukin-2 used in treatment of what malignanat melanoma and renal cell carcinoma
vaccination therapy tumor specific antigens in principle the best approach for cancer immunotherapy. difficult to develop due to complexity of antigens expressed by tumors
Gardasil vaccine to protect women against cervical cancer
vaccination administration of antigenic material to stimulate an individual's immune system to develop adaptive immunity to a pathogen
traditional vaccines attenuated pathogens and killed organisms. pathogenic virus isolated, grown in human culture, infect monkey cells, virus acquires mutation in monkey cells allowing i grow, virus no longer grows well in human cells
attentuation selecting for growth in nonhuman cells
polio, measles,mumps, rubella, varicella are what type of vaccines attenuated viral vaccines
BCG vaccines for TB is what type of vaccines attentuated bacterial
pros of attenuated vaccines very potent response, CD4 T cells and CD8 T cells,
cons of attenuated vaccines reversion of vaccine to virulent strain; risks to immunosuppressed patient/infants
modern vaccine using rational approaches based on detailed molecular understanding of microbial pathogenicity and analysis of protective host response and so are genetically-attenuated and acellular
how can attenuation be achieved recombinant DNA technique
genetically attenuated influenza vaccine introduce series of mutations into or deletion of gene encoding a viral polymerase protein PB2
advantage to genetically atteenuated influenza impossible for engineered virus to revert to wild type virulent virus
whole cell vaccine still cause side effects, typically redness pain and swelling
acellular vaccines including conjugate vaccine, peptide vaccine, and DNA vaccine are safer but less potent and more expensive
bacteria with capsule of polysaccharide when conjugated with protein carriers convert from; to from T-cell independent to T cell dependent antibody response
conjugate vaccine conjugates polysaccharide capsule of bacteria with protein carriers
peptide-base vaccine identify T cell peptide epitopes that stimulate protective immunity
what are the two ways to identify epitopes for peptide-base vaccine immunogenic protein peptides are synthesized and tested and reverse immunogenetic approach is endogenous peptides are eluted from MHC binding groove and their sequence determined by mass spectrometry
DNA-based vaccine injection of stretch of microbial DNA leads to deveelopment antibody response and cytotoxic T cells against whole microbiota
mechanisms for DNA-based vaccine DNA transfects host cells and express proteins as antigens
how do you enhance immunogenicity for DNA-based vaccine mix DNA with plasmids that encode cytokines and include genes expressing co-stimulatory molecules
methods of enhancing effectiveness of vaccine adjuvants, inorganic aluminum salts, pertussis toxoid
adjuvants substances that enhance the immunogenicity of antigens
inorganic aluminum salts stimulates NLRP3, bacterial sensor mechanisms of innate immune system, only one approved by FDA
pertussis toxoid together diphtheria and tetanus toxoid that make up DTP triple vaaccine
Created by: LittleD331