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Immuno/Micro/Viro > Test 2-2 > Flashcards

Test 2-2 Flashcards

1
Q

tumor types:

A
  • carcinomas: epithelial cells - most common
  • sarcomas: muscle cells ,aft cells or fibroblasts
  • lymphomas: solid tumors of lymphoi tissues
  • leukemias: lymphocytes and other hematopoietic cells
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2
Q

benign tumor growth is

A
  • slow relatively
  • somewaht differentiated cells
  • usually encapsulated - doesnt spread
  • not fatal unless at critical site (heart or brain)
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3
Q

malignant tumor growth is

A
  • undifferentited cells
  • readily metastesize
  • usually fatal if untreated
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4
Q

tumor specific antigens (TSA)

A
  • unique to a particular tumor and not present on normal cel types!! good to find cancer cells
  • arise as a result of point mutations or gene rearrangements
  • immune response targets –> may be altered self proteins
  • not commonly seen in human tumors
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5
Q

tumor associated antigens (TAA)

A
  • antigens shared by different tumors - also found on normal tissues EX oncofetal antigens- found on fetal butnot adult tissues
  • alpha fetal protein (AFP)
  • carcinoembryonic antigen (CEA)
  • not therapeutic targets! ONLY detection and monitoring
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6
Q

AFP - alpha fetal protein

A
  • produced by certain liver cancers AND NORMAL TISSUES

- ONLY detection and monitoring

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7
Q

CEA - carcinoembryonic antigen

A
  • increases in colon cancer and smokers AND NORMAL TISSUES

- ONLY detection and monitoring

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8
Q

oncogenic viral antigens

A

Some RNA/DNA viruses that produce tumors and viral antigens on class I MHC

  • EBV (DNA VIRUS) - causes B-cell lymphomas, HPV = cervical carcinoma, HBV = hepatocellular carcinoma
  • HTLV-1 (RNA VIRUS) - causes adult t-cell leukemia/lymphoma (CD4t-cells)
  • Tumors are relatively immunologenic bc seen as foreign
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9
Q

differentiation antigens

A
  • tissue specific antigens
  • aid in diagnosing certain tumosr = reveal the tissue of origin
  • EX) pre b-cell tumors express CD10: T-cell leukemias express CD4, CD8, TCR, or IL2 receptor
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10
Q

antibody for anti-tumor immunity

A

LEAST EFFECTIVE METHOD

  • difficult for immune system to respond to tumors bc 1) rarely inflammation (dont elicit co-stim molecules) 2) many tumors dont express unique antigenic peptides
  • antibodies stimulated by tumor antigens DONT inhibit tumor growth
  • some killing of tumor cells via ADCC by NK or macrophages
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11
Q

CTLs for anti-tumor immunity

A

produced against carcinomas, sarcomas, and virus induced tumors

  • most effective against virus induced tumors
  • tumor infiltrating lymphocytes (TILs) in solid tumors largely composed of anti-tumor CTLs –> for some reason they dont do anything
  • SEE peptides on class I MHC
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12
Q

NK cells for anti-tumor immunity

A
  • lyse tumors of hematopoietic and virus induced origins
  • ADCC may be important also in some tumors
  • activating signal = downreg of class I MHC
  • interferons- TNF-alpha and IL2 enhance NK cells lysis of tumor cells
  • lymphokine activated killer cells (LAK) - enhanced killing of various tumor cell types as well as broadened tumor recognition cpability (malignant melanomas)
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13
Q

macrophages for anti-tumor immunity

A
  • kill tumor cells by ADCC or by release of TNF-alpha
  • TNF-alpha (TUMOR NECROSIS FACTOR) can directly lyse tumor cells possibly by producing free radicals or by causing hemorrhagic necrosis of the tumor blood vessels
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14
Q

tumor evasion strategies

A
  • lack of expression MHC proteins
  • MHC proteins cant bind tumor antigen - no antigen presentation
  • induce tolerance –> no costimulatory molecules
  • sneaking through - small numbers of tumor cells may not be immunogenic = by the time they reach immunogenic numbers mutation have occurred to change antigen specificity
  • selection of poorly immunogenic variants-
  • tumor cells may grow so fast to outdistance immune response-
  • anti-tumor antibodies may act as blocking factors-antibodies that bind tumor cells and immune sysmte then cant see those tumor cells
  • antigens shed by tumor cells may bind to cell surface receptors - antibodies bind and tumor sheds those proteins or cuts antibodies off
  • modulation of tumor antigens masked by mucopolysaccharides
  • immunosuppressive substances released by tumor ex)TGF-beta
  • immunoproviledged sie by encasing themselves in collagen and fibrin
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15
Q

selection of poorly immunogenic variants-

A

difficult to make immune resp against tumor cells - when a tumor cells proliferate and mutate rapidly… the immunogenic tumor cells ARE FOUND AND DESTROYED by the immune system. By the time you diagnose the cancer you only have the poorly immunogenic left which are hard to kill!

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16
Q

tumor treatments - nonimmunogenic

A
  • surgery - reduce tumor load;remove before metastesizes;uses drugs in combo with surgery
  • hyperthermia-destroy tumor cells throuw superheating of body tissues
  • ***radiotherapy- x-rays or cobal 60 =ionizing radiation = destroys rapidly dividing cells; works best on welldefined nonmetastasized tumors;sideeffects=damage to bone marrow and intestinal mucosa;inc susceptibility to infection (destruction of radiosensitive lymphocytes);may induce 2ndary tumor formation because of induce DNA mutations
  • ***chemo-inhibits DNA rep RNA transcription, or protein synth;side effects=immunosuppression can be life threatening& may induce secondary tumors
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17
Q

tumor immunotherapy advantages:

A
  • specifically tailor a response to the tumor
  • fewer side effects that nonspecific therapies
  • more effective against tumor metastisis
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18
Q

tumor vaccines

A

vaccinate with tumor cells treated to inc immunogenicity or dendritic cells that have been loaded with tumor antigens

  • melanoma (MAGE) antigens used in clinical studies to induce CTLs
  • HEP B vaccine has decreased incidence of hepatocellular carcinoma
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19
Q

Antibody therapies

A

1) anti-id antibodies surface immunoglobulin of Bcell lymphomas
2) antibodies directed against growth factor receptors
3) immunoconjugates
4) bi-specific antibodies
5) purging bone marrow of tumor cells
6) adoptive cellular immunotherapy -lymphokine activated cell therapy and umor infiltrating lymphocytes therapy
7) cytokine therapy

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20
Q

bi-specific antibodies

A
  • genetically enginerer antibodies that recognize tumor antigens and immune system cells
  • one arm sees tumor and the other immune cell
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21
Q

immunoconjugates

A

antibodies coupled to a toxic substance

  • bacterial toxins, chemotherapeutic drugs, radioisotopes
  • must chose a tumor specific antigen. cross reactivity is a problem.
  • conjugate must be endocytosed**
  • F9ab’)2 fragments (no Fc reion) used to avoid non-specific binding
  • basically antibodies armed with something to help them better to kill cells
  • very portent
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22
Q

antibodies directed against growth factor receptors

A
  • herceptin (tratuzumab) targets the Her2/Neu factor receptor which is overexpressed on 25% breast cancer
  • bocks receptor/ligand interaction = decrease expression of Her2/Neu
  • over expression of Her2/Neu correlates with a poor er prognosis
  • quite effective
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23
Q

anti-id antibodies surface immunoglobulin of Bcell lymphomas

A
  • cell lysis by ADCC or complement required to decrease tumor burden
  • outgrowth of tumor cell mutants are a problem
  • tends to reoccur
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24
Q

purging bone marrow of tumor cells

A

in bvitro purging of bone marrow tumor cells by anti-tumor antibody and complement could provide a tumor free source of bone marrow
-used with analogous bone marrow transplantation in B-cell lymphoma patients that have received chemotherapy and radiation

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25
Q

adoptive cellular immunotherapy

A

1) lymphokine activated killer cell therapy: (LAK) -peripheral blood NK cells cultered wtih high dose IL2 = LAK cells–> reinfuse into patient=tumoricidal LAK cells kill tumor - most success with renal cell carcinoma and malignant melanoma
2) tumor infiltrating lyphocyte (TIL) therapy: leukocytes from solid tumors cultured with IL2 and given to patient
- LAK cells and tumor specific CTLs are grown up in this qtechnique
- clinical trials being done

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26
Q

cytokine therapy:

A

1) IL2 given to patient to generate LAK cells and activate CTLs
- tumor regression in 20-40% of renal carcinoma and malignant melanoma patients; severe side effects: pulmonary edema and shock
- several deaths in clinical trials
2) TNF-apha: powerful antitumor effects but too toxic at concentrations needed to eliminate tumor cells
3) IFN-alpha=tumor antiproliferative effects: inc NK cell activity and inc class I MHC expression on tumor cells
4) transfection of cytokine genes into patient tumor cells = immune stimulation while decreasing systemic side effects

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27
Q

cyclosporin

A
  • knocks out primary response and not so much secondary.
  • if doing tranplant graft rejection will start out as primary so theres the benefit. It doesnt touch secondary so you retain all of your memory too until steroid treatment which kills them all
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28
Q

immunodef definition

A

lack of a immune system or failure of components of the immune system that increase susceptibility to infection

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29
Q

primary immunodef is

A

congenital

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30
Q

secondary immunodef is and example

A
  • acquried = happens to you later on that affects immune response
  • HIV - AIDS, immunosuppresive drugs, disseminated cancer, splenectomy,malnutrition
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31
Q

immunodef was improved by/discovered

A

antibiotic therapy

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32
Q

general principles of immunodef

A
  • the type of infection defends on what youre lacking
  • no humoral = susceptible to extracellular bac
  • CMI impaired = susceptile to viruses and intra-bac
  • if BOTH = infections with all classes of microorganisms
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33
Q

EBV more susceptible to

A

lymphomas

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34
Q

HPV more susceptible to

A

skin cancers, cervical cancers

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35
Q

T-cell def more susceptible to

A

general increase in risk due to loss of t-cell immunosurveillance role

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36
Q

B-cell deficiency serum Ig levels will be:

A

decreased

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37
Q

t-cell deficiency serum Ig levels will be:

A

normal or reduced

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38
Q

B-cell def skin test reaction

A

normal

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39
Q

T-cell def skin test reaction

A

decreased

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40
Q

b-cell def lymphoid tissue morphology

A

germinal centers decrease or are absent

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41
Q

t-cell def lymphoid tissue morphology

A

normal follicles but decrease in paracortical regions

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42
Q

b-cell def infectious agent susceptibility

A

primarily extracell-bacteria

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43
Q

t-cell def infectious agent susceptibility

A

viruses, intracellul bac and fungi

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44
Q

skin test reactions are dependent on…

A

CELL MEDIATED IMMUNITY

type IV or DTH

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45
Q

defect in B-cells

A

1) x-linked agammaglobulinemia (Bruton’s agammaglobu…)
2) common variable immunodef
3) Selective IgA def
4) hyper IGM syndrome

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46
Q

pre-b-cell blocked to mature into mature b-cell disease is:

A

x-linked agammaglobinemia

Ig secretion is decrease:

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47
Q

mature b-cell blocked maturation into plsama cell disease is:

A

common variable immunodeficiency

Ig secretion is decreased:

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48
Q

diagnosis of x-linked agammaglobulinemia:

A

test for ABSENCE of circulating B-cells after infant is greater than 6-9 mo old

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49
Q

treatment of x-linked agammaglobulinemia

A

controled by monthly injections of pooled gamma globumin + antibiotic therapy
-vaccines cant be used because antibody response will not work

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50
Q

x-linked agammaglobulinemia (Bruton’s agammaglobu…)

A

=recurrent pyogenic bac infections(pneumonia, otitis media, meningitis, spsis

  • absence of mature b-cells=little serum immunoglobulin
  • normal bone marrow pre-b-cells, so block exists in maturation (b-cell dev starts but is BLOCKED due to tyrosine kinase)
  • molecular basis of disease:mutations/deletion in b-cell tyrosine kinase (involves signal transduction
  • x-linked disease=restricted to males. Female carries have other normal X for back up
  • T-cell immmunity is OK so not susceptible to viral or fungal
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51
Q

common variable immunodef

A
  • Mature b-cells cant differentiate into plassma cells=dec antibodies
  • affects males and females equally
  • sincreased recurent bacterial infections
  • progressive insufficiency can occur even with treatment (genetic component?)
  • congenital or sporadic
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52
Q

diagnosis of common variable immunodef

A

normal levels of circulating mature b-cells that cant dif into plasma cells

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53
Q

treatment of common variable immunodef

A
  • monthly gamma globulin shots + antibiotics
  • long lifespam if treated
  • high incidence of autoimmune disease - dont know why (rheumatoid, pernicious anemia, autoimmune hemolytic anemia)
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54
Q

Selective IgA def

A
  • affects B-cels
  • MOST COMMON
  • inherited or aqcuired (embryonic rubella or drug exposure)
  • asymptomatic but some may have inc infections of mucosal sites
  • IgM can compensate for missing IgA = transported across mucosa
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55
Q

issues with selective IgA def

A
  • develop anti-IgA = severe or fatal transfusion reactions if given plasma containing iGA
  • example = breast milk from mother has IgA
  • antigenic stimulus for IgA=IgA in breast milk
  • medical alert bracelet
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56
Q

treatment of selective IgA def

A
  • antibiotics (if needed) but no gamma globulin (contains very small amounts of IgA)
  • No IgA replacement therapy available
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57
Q

diagnosis of selective IgA def

A
  • severly low IgA levels with all others being normal
  • B-cells surface IGA but no dif into plasma cells
  • intrinsic b-celll defects or absence of cytokines that enhance secretion of IgA such as IL5 and TGF-beta
  • t-lymphocyte fucntion intact
  • may have inc allergy,GI tract disease and or autoimmune disease
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58
Q

hyper IGM syndrome=

A

over abundance of IgM antibody AND lack of other antibody isotypes
1) x-linked hyper IgM syndrome = ONLY IGM! inherited DEFICIENCY of CD40L on t–cells==> CD40 not engaged on B-cells==>no isotype switching
-cytokines determine which isotype a b-cell will produce but general isotype switching mech requires Cd40 engagement)
2)hyper IgM type 2 syndrome=inherited MUTATION in the gene activation-induced cytidine deaminase which, for unknown reasons, prevents isotype switching
BOARD QUESTION

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59
Q

IL 4 to produce

A

swithc IgE

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60
Q

IL-5 to produce

A

switch to IgA

61
Q

Di-George Syndrome

A
  • T-cell Defect due to hypoplasia or agenesis of thymus (total loss or partial loss)
  • also=congenital thymic hypoplasia
  • facial features, parathyroid gland, and vessels of the heart affected bc they differentiate from the third and fourth pharyngeal puches during embryogeneseis
  • defective maturation of t-cells = poor CMI against viruses and fungi
  • associated with maternal alcoholism and chromosome 22q11 deletions
  • facial features obscured AND low T-cell count on obs diagnosis
62
Q

diagnosis of Di George syndrome

A
  • immunoglobulin near nromal but t-cells severely decreased
  • in severely affected patients immunoglobulin will be decreased too
  • chest X-ray will show NO thymic shadow
63
Q

treatment of Di George syndrome

A

t-cell function increases with age - extrathymic maturation

-site of extra thymic maturation is not known

64
Q

t-cell deficiency diseases

A

1) Di-george syndrome

2) Swiss type agammaglobulinemia

65
Q

Swiss type agammaglobulinemia (SCID)

A
  • failure of B and t-lymphocytes to develop from bone marrow stem cells: Spleen, lymph nodes, tonsils, appendix NOT populated
  • little or no humoral AND cell mediated immunity
  • indiv die from overwheling infections within first year
  • vaccines are deadly to these people
  • family hisotry of early death from infections might alert a phys
66
Q

forms of SCID

A

1) autosomal-25% cases -d eficiency of ADENOSINE which deaminates adenosine & deoxyadenosine
- deoxyadenosine and deoxy-ATP accumulate = toxic to lymphocytes
- B-T cells less efficient in degrading toxic byproduc tthat other cells
- PURINE NUCLEOTIDE PHOSPHORYLASE=accumulation of toxic nucleotide metabolites
2) X-linked=mutation in gene for common gamma chain cytokine receptors IL2, IL4, IL9, and IL15 ==> lymphocytes cannot develop properly - need signals to develop w/out they die

67
Q

treatment of SCID

A
  • bone marrow transplant
  • gene therapy:common gamma chain engineered into virus – few treated patients dev t-cell tumor linked to protoconco gene being activated
68
Q

phagocyte defects list:

A
  • **1)leukocyte adhesion def = widespread bacterial infections
  • **2) chronic granulomatous disease=intracellular and extracellular infections, ganulomas
    3) G6PD deficincy=defective respiratory burst, chronic infection
  • **4)myeloperoxidase deficinecy = defective intracellular killing, chronic infection
  • **5)chediak0higashi syndrone=intra and extraceulluar infections, granulomas
69
Q

Chronic granulomous disease (CGD)

A
  • recurrent bacterial infections from early childhood
  • defect in NADPH xidase = neutrophils cant produce superoxide anion during respiratory burst
  • USUALLY FATAL even with aggressive antibiotic or gene therapy; interferon gamma therapy can start production of NADPH oxidase
70
Q

myeloperoxidase deficinecy

A

-decrease or adsent myeloperoxidase
-produces hypochlorous acid( HOCl) from H2O2.
HOCl is potent antibacterial and antifungal
-NO INC in succeptibility to infection in these indiv due to compensatory immune mechanisms.
-CAN BE DECREASE ability to ward off fungal infections (yeast)

71
Q

chediak0higashi syndrome

A

-neutrophils granules fuse together and dont work well
-t-cell and NK cell functions are impaired too
-metalic silver hair looking in young children if immuno issue too then you know its this
-multi system disorder –>CNS, hepatosplenomegaly, lymphoreticular cancers
-platelet abnormalities=bleeding tendencies
-defective retinal pigment cells = vision impaired
TREATMENT=bone marrow transplant or else doesnt look good long term for pt

72
Q

leukocyte adhesion def

A

defect in beta chain of LFA-1 and Mac-1 adhesion molecules= neutrophils cant adhere to endothelial cells for extraversion

  • recurrent bacterial and fungal infections of skins lungs and blood
  • would healing probelms since macrophages cant traffic to wound
  • moderate and severe versions based on whether little or no LFA
  • severe version fatal in first year of life due to infections
  • LOOKS likfe leukemia bc neutrophils piled up in blood but its just they cant ge tout of blood
  • DIAGNOSIS=EXTREMELY HIGH LEUKOCYTE COUNT
  • TREAT=aggresive antibiotic;prophyalctic antibiots before dental work; granulocyte transfusion to treat extracellular bacterial infections; bone marrow transplantation is curative
73
Q

wiskott-aldrich syndrome

A
  • -X-linked: defective Cytosolic protein that helps regulate the actin cytoskeleton of bone marrow derived cells= immune sys cells cannot traffic to sites of inflammation and band tcells cannot interact
  • triad: immmunodef, eczema, thrombocytopenia
  • near normal levels of t-and b cells
  • t and b-cells respond poorly to antigen
  • recurrent infections beg at six months
  • predisposition to dev autoimmune
  • TREATMENT=intravenuous gamma globulin and antibiolic can prolong survival
74
Q

immunodeficiency + eczema + thrmobocytopenia ===

A

Triad of symptoms==
WISKOTT ALDRICH SYNDROME

(BOARD QUESTION)

75
Q

ataxia telangiectasia

A
  • abnormal recessive, multisystem dsease = immmune defects and loss of ability to coordinate muscles, vascular lesions and increase incidence of tumors
  • defect in ATM protein = intracellular signalling in response to DNA damage
  • lack of repair of DNA breaks explains inc of cancer
  • immune defects= dec t-cells; defective t-helper cell activity; dec serum levels of IgA IgE, and IgG2
  • thymus remains in embryonic state = immune defects
  • TREAT= broad spec antibiotics; bone marrow transp cures
76
Q

which cytokine accounts for increased neutrophil levels

A

G-CSF (calls neutrophils out of the blood )

77
Q

CGD patients tend to have infections caused by catalase positive microbes bc catalase…

A

breaks down bacterial H2O2 to prevnent the formation of hypochlorous acid

(BOARD QUESTION)

78
Q

catalase neg bacteria produce

A

H2O2 producing -h elps CGD patients who cant produce.

79
Q

NBT dye reduction test

A

NBT compound yellow is reduced in neutrophils undergoing a respiratory burst
-upon reduction yellow turns into BLUE in neutrophils doing respiratory burst

80
Q

HIV and types

A
  • integrates into genome
  • RNA with reverse transcriptase (RETROVIRUS)–patients usually die for opportunistic pathogens or tumors
  • type 1 and 2 in US but mostly type 1
  • type2 more prevalent in africa
81
Q

provirus is

A

[viral] DNA integrated into host DNA

82
Q

stages of HIV in untreated individual – BEFORE SYMPTOMATIC

A

1) acute illness - 2 to 6 weeks after initial infection: like infectious mononucleosis (FLU LIKE) (headache, fever, rash, swollen lymph nodes, sore hroat)
- active virus replication occurs in blood and CSF,
- lymphoid organs seeded with virus
2) Seroconversion - 3-17 weeks after exposure = Window period:patient viemic but all serological tests are negative= making antibodies several weeks later . so they dont test positive for HIV right away
- –>Latent phase - 2-10 years being seropositive
- HIV nearly undetectable in blood but replicating in lymphoid tissue
- not known what triggers latentpahse to active phase

83
Q

stages of HIV in untreated individual – AFTER SYMPTOMATIC

A

3) MAY go into AIDS related complex (ARC) = persistent fevers, night sweats, weight loss, chronic diarrhea, inflammatory skin conditions,a nd persistent generalized lymphadenopathy; SOME INDIV have oral candidiasis and/or chronic mucocutaneous herpes seimplex infection
- —> Active phase - “GO INTO AIDS” (CD4 count LESS THAN 200
- Kaposis sarcoma or non hodgkins lymphoma (herpes virus are known to play a role in dev of these tumors)
- recurrent infections with opportunistic pathogens (KILLING OFF OF CD4 T-cells–> coordination of immune lost)
- progressive wasting syndrome (cachexia) (Tumor Nec F-alpa)
- AIDS induced dimentia

84
Q

AIDS opportunistic infection effect on t-cells

A

CD4 count drops (below 200cells/mm3=

AIDS=death soon)

85
Q

Death from from AIDS=

A
  • infection by protozoan, bacteria or viral opportunistic pathogens
  • malignancies such as kaposis sarcoma or lymphomas
  • fatal pneumonia most common cause of death
86
Q

Infectious process of AIDS

A

1) virus attaches to CD4 tcells or mononuclear phagocytes via GP120
2) when bound gp41 binds chemokine receptors (co-receptors) CXCR4 and CCR5 = fusion with host cell
- CCR5 expressed on CD4 t-cells, macrophages, dendritic cells
- CXCR4 on activated T-
3) once inside=proviral state or viral replication state

87
Q

what triggers cells to go into viral replication process? (HIV)

A
  • **-activation of the cell***
  • –>ACTIVATION MOST LIKELY VIA NFkB transcription factor which binds LONG TERMINAL REPEATS OF HIV
    ex) for t-cells TumorNF-alpha induces viral replication
    ex) for monocytes and macrophages- IL1,3,5,TNF IFN-gamma and GM-CSF triggers change
88
Q

infected monocytes/macrophages vs t-cells

A
  • t-cells can be lysed (READILY KILLED) while macro/monocytes cannot.
  • monophages and macrophages may serves as in-vivo reservoir = transport throughout body
89
Q

macrophage effects on CNS

A

-AIDS dementia complex = loss of memory
-destruction neurons via direct infection of neuron by virus
OR
-mcarophage derived cytokine destruction

90
Q

early infection by HIV on replication

A

-HIV replicated SLOWLY!

91
Q

HIV on CD8 t-cell

A

NO EFFECT

92
Q

Killing of T-cell by HIV mechanisms

A

1) direct lysis by budding HIV ( t-cell loses cytoplasm each time buds so lose too much =death)
2) large quantities of cytoplasmic viral DNA toxic to lymphocytes
3) syncytia formation of infected cells with uninfected cells
4) binding of free gp120 to infected AND uninfected cells = antibody response = ADCC
5) CTL mediated destruction of virus infected cells
6) gp120 crosslinking CD4 = apoptosis

93
Q

Suppression of immune response by HIV or by products

A

1) CD4 on t-cell so that it cant bind class II MHC on APC

2) destruction of follicular dendritic cell network by HIV=alters architecture of lymph nodes and spleen

94
Q

why is immunity NOT protective against HIV?

A
  • HIV integrates into host DNA and remains latent
  • Error prone RT –> mutations to evade antibodies and CTLs
  • seroconversion signals antibody production but CTLs are more important in the decline of virus seen after the intial infection
95
Q

Best route to fight HIV?

A

NEED CTLs - CELL MEDIATED

96
Q

good vaccine for HIV will be

A

induce good cell mediated immunity (and humoral)

97
Q

HIV ressitnat individuals:

A

-inherited CCR5 genes are mutated = ressitance to R5 viruses (CXCR4 or R4 strain stil infects)

98
Q

screening test for HIV after seroconversion

A
  • ELISA
    1) HIV H9 cell line - lining plate
    2) add pt serum
    3) antibodies and enzyme +substrate for color change
99
Q

ELISA test issues and some corrective measure

A
  • frequent false positives for multiparous females and pateints with autoimmune diseases
  • repeat ELISA and if still (+) == do Western blot

Binding something else on H9 cell line antigens that bound to plate as well

HIGH FALSE POSITIVE BUT CHEAP AND QUICK

100
Q

Western Blott of HIV

A

SDS page gel - pt serum run in gel and if you know the molecular weight of HIV and or corect antibody then you can confrim HIV
Need 2 out of 3 protines?

101
Q

Other tests of HIV

A
  • PCR - very sensitive- looking for viral genomes in the DNA

- RT-PCR - detects free virusin bodily fluids - usees reverse transcriptase to convert viral RNA into DNA to PCR

102
Q

detecting HIV in neonates

A
  • infants born to HIV infected mothers cant be diagnosed using techniques to detect antiHIV antibody (due to amternal IgG)
  • MUST use viral antigen detection (ELISA), PCR, or HIV culture
103
Q

most appropriate test to test for baby HIV if mother infected

A

PCR-detect integrated HIV genomes in DNA

104
Q

adult potentially exposed to HIV 2 weeks ago… which test would you use to check for HIV?

A

RT-PCR - bc probably not too many antibodies for HIV produced yet. Need to see if yo ucan find HIV RNA in the guy

105
Q

what gives false positive result to HIV ELISA assay? what other circumstances can induce these antibodies to H9?

A

antibodies to the H9 cell line MHC proteins that contaminate the ELISA asasy

transfusions and/or organ/tissue transplant

106
Q

ideal vaccine

A
  • no undesireable side effects
  • easy to administer
  • highly immunogenic
  • highly protective
  • long term immunity

NO EXISTING IDEAL VACCINE

107
Q

viral vaccines - attenuated

A
  • weakened strains of virus EX) sabin polio, measles,mumps
  • human strain virus put into monkey for prolonged will become better at infecting monkey and when put back into human it will be weaker.(decreased human pathogenicity)
  • generates long lasting immunity bc virus can undergo limited replication = greater antigenic stimulus to immune system

-disadvantages: reversion of attenuated strain to full virulence; contaminating pathogens; often fatal problems for immunocompromised; potential risk to fetus

108
Q

what type of immunity do vaccines produce?

A

HUMORAL IMMUNITY

109
Q

Live attenuated virus vaccines produce what type of response?

A

HUMORAL AND CELL MEDIATED (T-cells=mostly CTLs)

110
Q

viral vaccines - inactivated

A
  • chemical treatment to inactivate virus:
  • EX)influenza, rabies, salk polio
  • advantages: less concern for safety compared to live vaccine, transport and storage is easier
  • disadvantage: dont generate level of protection as do live vaccines
  • NO CELL MEDIATED IMMUNITY - DEAD VIRUSDOESNT REPLICATE
111
Q

Viral vaccines - subunit

A

-consist of a single viral protein EX) Hep B surface antigen

112
Q

bacterial vaccines - inacctivated

A
  • bacteria are heat kiled to provide an antigen source
  • EX) pertussis (part of DTP vaccine diphtheria, tetanus, and pertussis)
  • OLDER VERISON- side effects: convulsions and death
  • NEW VERSIONacellular pertussis vaccine = fewer mild or serious side effects
113
Q

NEW pertussis is what kind of a vaccine?

A

BACTERIAL INACTIVATED ACELLULAR

114
Q

bacterial vaccines - toxioid

A

bacterial toxins can be detoxified without loss of immunogenicity

  • EX) isolating toxins from diphtheria and tetanus (DTaP)
  • in dev countris tetanus vaccine is given toprego women to protect newborn from tetanus at unbilical stump
  • ONLY PRODUCES ANTIBODIES (HUMORAL)
115
Q

if someone who is immunodeficient is given vaccine and they die/dont die what type of vaccine was given:

A

LIVE VACCINE / DEAD VACCINE

116
Q

bacterial vaccines - conjugate

A

-encapsulated bacteria have polysaccharide capsules:
-polysacch capsules alone dont produce high affinity antibody or immunologic memory
-conjugating polysaccharides to protein carrier = high affinity IgG + memory response
EX) hemophius influenzae B, Streptococcus pneumoniae, and Neisseria meningitidis
POLYSACCH ALONE ONLY STIMULATE IGG CABLE CHANNEL BC NOT THYMUS DEPENDENT!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
-B-cell finds it (polysacc and protein) and chops it up to activate t-cell and then that b-cell will make antibodies for it

117
Q

adjuvants

A
  • included in a vaccine to stimulate better immune response
  • convert soluble protein antigens into particlate matter = more readily taken up by APC
  • many vaccines use small amount of bacterial products = APCs express co-stim molecules = better at presenting antigen
118
Q

critical time to give children immunizations to protect against common infectious diseases?

A

birth to two years

119
Q

Hepatitis B Vaccine

A
  • adults= greater risk for infection bt childhood immunization against Hep B is more convenient time to give vaccine (between birth and 2)
  • recombinant proteins grown in years (Hep B surface antigen or HBsAG)
  • intramuscular injection => 3 times
  • serum antibodiy prevents virus from infecting liver
  • infants born to HbsAG+ mothers => vaccine and hep B immune globulin (HBIG) within 12 ours of birth at separate injection sites
120
Q

Diphtheria, tetanus, acellular pertussis vaccine (DTaP)

A
  • formaldehyde treated toxin = D/T toxoids (nontoxic and immunogenic)
  • Acellular vaccine = pertussis exotoxin (five subunits: S1 subunit causes toxic side effects of whole cell vaccine but mutated=nontoxic and immunogenic)
  • so a-pertussis toxin is mutated S1 subunit with 4 native subunits = holotoxoid
  • Boosters every 10 years
121
Q

DTaP will do what to protect you?

A

THESE ARE TOXOID VACCINE! It will neutralize the TOXINS produced by the bacteria. IT WILL NOT ERRADICATE THE BACTERIA –> OTHER HOST MECH WILL GET RID OF THE BACTERIA

122
Q

Hemophilus Influenzae type B vaccine

A

Meningitis fight-capsular polysaccharide proteinconjugate vaccine

  • polysaccharides = non memory response, affinity maturation or isotype switching to IgG (ONLY IgM)
  • conjugating polysaccharide to protein carrier = t-cell dependent immune response WITH ALL THE IMMUNE PERKS
  • conjugated to tetanus toxiod, diphtheria toxoid; group B Neisseria meningitidis outer membrane protein
  • intramuscular injections provides serum antibody to stop attach of CNS
123
Q

meningococcal vaccine

A
  • MCV4 or Menactra -
  • ->POLYSACCHARIDE-CONJUGATED
  • protects against 4 groups of Neisseria meningitidis (meningitis - die from septic shock)
124
Q

Polio vaccine

A
  • 2 vaccines - 1) INactivated Salk polliovirus (IPV) injected s.c and 2) live,attenuated sabin oral poliovirus vaccine (OPV)
  • contains three stereotypes of poliomyelis virus
  • IPV generates serum antibodies to neutralize the virus in the blood before it reaches CNS
  • OPV develops local mucosal immunity in HI to prevent spread into bloodstream
  • OPV may cause vaccine induced paralytisc polio bcit can revert to wild type- NO LONGER GIVEN IN USA
125
Q

Mumps, Measles, Rubella (MMR) vaccine

A
  • mumps = salivary gland swelling
  • measles = red blotchy patter on face and body during third day of rash
  • rubella = cataracts, 3-day rash, some fever and joint paint
  • LIVE attenuated = pretective serum antibodies and CELL MEDIATED
  • vaccination protects FETUS from rubella - thats why to-be-moms get it
126
Q

varicella vaccine

A
  • Live attenuated viral vaccine = protection from chicken pox
  • get antibody and CMI response
  • DOES NOT increase risk for herpes zoster - shingles
  • most people are proctect but a few get a mild form
127
Q

rotavirus vaccine

A
  • most common diarrheal pathogen in children worldwide
  • acute diarrhea among children <2yrs old
  • results in death in developing countries
  • tetravalent rhesus-human reassortant retrovirus (RRV-TV)=attenuated rhesus human virus expressing human virus VP7 antigen; genome of rotavirus is segmented = coinfection with human and rhesus strains allows reassortants to emmerge
128
Q

pneumococcal vaccine

A
  • streptococcus pneumoniae kills more people in US each year than all other vaccine preventable diseases combined
  • leading cause of bacterial meningitis in US
  • causes many middle ear infections in children
  • vaccine composed of S. Pneumoniae polysaccharides conjugated to a carrier protein=protects against 13 strains of pneumococcal bacteria that cause moset of the serious infection and ear infections
  • GIVES ANTIBODY AND HUMORAL?
129
Q

influenza vaccine

A

2 types:

1) live attenuated vaccine (flumist) delivered intranasallay and is recommende for healthy, nonpregnant persons 5-49yrs old without high risk conditions
2) inactivated vaccine (given IM) is approved for people >6mo including those with chronic med conditions

  • Often contains one influenza A (H3N2) virus, one influenza A (H1N1) virus and one influenza B virus.
  • Viruses are grown in eggs
130
Q

HPV vaccine

A
  • genital warts and cancer causing
  • affects cervix, vulva, vagina, anus, or penis
  • Gardasil- prevents type 16 and 18
  • Vaccine = L1 protein expressing virus like particles: L1 is major capsid protein of HPV = neutralizes antibodies =protective; targeted to females and males who are not sexually active
131
Q

4yr old child with x-linked agammaglobinemia is accidentally vaccinated. No adverse effects noticed. What vaccine was given?

A

tetanus vaccine. ITS A TOXOID so not actually disease causing.

132
Q

which vaccines can be administered to a pregnant female?

A

all vaccines except live ones

133
Q

which vaccine prevents disease but does not directly cause the elimination of the infectious agent that causes the disease?

A

TOXOID

diphtheria

134
Q

which type of vaccine is most likely to elicit both humoral and cell-mediated immune responses to the vaccine

A

ATTENUATED VIRUS - LIVE VIRUS

135
Q

Pt diagnosed with diffuse large b-cell lymphoma. A pecific therapy was used to target surface immunoglobulin that was expressed by his tumor cells. The tumor cell immunoglob is a type of _____ antigen.

If an idiotypic antibody was used to treat the lymphoma pt, it would recognize what region of the tumor cell?

A

tumor specific

Fab

136
Q

what is the most dreaded, yet common outcome of the teratment of b-cell lymphomas with antiidiotypic antibodies?

A

tumor variants that dont bind the therapy antibody

137
Q

In an experimental attempt to treat a patient with disseminated colon cancer, cancer cells were transfected with a gene that increased the expression of class I MHC molecules. Which component of the immune response likely would participate in killing of the tumor cells?

A

cytotoxic t-cells

138
Q

A patient had a particularly aggressive cancer. A sample of the patient’s tumor revealed that the cells produced a large amount of IL-10. This likely provided a fair degree of protection from the immune system by shifting the patient immune response toward a _____ type of response.

A

Th2

139
Q

1) A 23-year old woman with a history of double vision, difficulty swallowing and weakness in her upper arms had an uneventful pregnancy and delivered a 6 lb. infant. The newborn appeared limp and had difficulty breathing. The baby was placed on a ventilator and was fed through a nasogastric tube. A blood test confirmed the suspected etiology of the infant’s condition. Within three weeks all symptoms subsided and the baby was sent home. Your diagnosis would be transient neonatal
2) What is the etiology of the disease?
3) What did the confirmatory blood test detect?
4) Why was significant improvement seen in the infant’s condition after several weeks?
5) If the infant was given edrophonium, an acetylcholinesterase inhibitor, what result would you expect?
6) What is the mechanism of action of edrophonium?
7) Would this treatment distinguish between a congenital form of the disease and the transient form?

A

1) myasthenia gravis.
2) Mom’s anti-acetylcholine receptor IgG crossed the placenta to cause symptoms.
3) Serological identification of the antibody
4) IgG antibody was catabolized
5) Substantial improvement
6) By blocking the enzyme, it prolongs the presence of acetylcholine in the synaptic cleft.
7) No

140
Q

Studies have shown that immunosuppressed transplant patients have a higher risk of malignancy. However, this patient population doesn’t develop all type of cancers. The types they are more susceptible to developing are those tumors induced by exposure to

A

certain viruses

141
Q

Why are immunosuppressed transplant patients more susceptible to developing virus-induced cancers?

A

depressed t-cell immunity

142
Q

The _______ of an individual has the best chance of being a good match for a transplant.

A

SIBLING

143
Q

How can antibodies be stimulated that could participate in hyperacute rejection?

A

Anti-ABO antibodies
Blood transfusion
Prior organ transplantation
Pregnancy

144
Q

1) A 9-year old female brought to the ER with airway obstruction due to laryngeal edema and swelling of the lips, tongue, face and trunk. Urticaria (i.e. hives) were absent during these episodes. A 14-year old brother had a similar history of attacks. Physical exam was unremarkable. The patient was treated with epinephrine. Based on the clinical manifestations, what disease do you suspect?
2) The following laboratory results are reported: - Serum IgE levels: Normal - C2 and C4 levels: Significantly decreasedBased on the laboratory results and the patient history, which disease would you now suspect?
3) if the epinephrine had no effect on patients condition then it could be?
4) What is the underlying cause of hereditary angioedema?
5) Why did the epinephrine not reverse the condition?
6) What would give a patient that presents with this clinical manifestation?
7) Why epinephrine?

A

1) anaphylacic shock
2) Familial complement deficiency
3) Hereditary angiedema
4) C1-INH def
5) it was not caused by histamine
6) epinephrine
7) It initally appears similar to anaphylxis which is far more common that HAE

145
Q

1) A 5-year old child is suffering from a virus infection. The child has never had a natural exposure to the virus. No vaccine is available to prevent this virus infection. Which cell type from adaptive immunity would be needed to eradicate the virus?
2) Which cell type from adaptive immunity likely would be involved if the child had prior exposure to the virus?

A

1) cytotoxic t-lymph

2) B-lymph

146
Q

What is the main difference between the ADCC of a virus-infected cell and the opsonization and phagocytosis of an extracellular bacteria?

A

Size of the targeted cell varies

147
Q

Why don’t cytotoxic T lymphocytes (CTL’s) kill infected red blood cells (RBC’s)?

A

RBC’s don’t express class I MHC.

148
Q

NK cells require the absence of class I MHC molecules to become activated. RBC’s don’t express class I MHC molecules. Why don’t peripheral blood NK cells kill RBC’s?

A

RBC’s don’t express activating signals.

Immuno/Micro/Viro (14 decks)

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