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MICROBIO BIOL-160 LEC > Disorders Associated with the Immune System > Flashcards

Disorders Associated with the Immune System Flashcards

1
Q

what happens if we have an OVERACTIVE IMMUNE RESPONSE?

A
  • HYPERSENSITIVITY/ALLERGY
  • AUTOIMMUNITY
  • POSSIBILITY OF TRANSPLANT/GRAFT REJECTION
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2
Q

what happens if we have DEFECTIVE IMMUNE RESPONSE?

A
  • due to OLD AGE
  • can be CONGENITAL
  • can be INFECTION – ex. HIV
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3
Q

describe HYPERSENSITIVITY

A
  • where our IMMUNE RESPONSE goes BEYOND NORMAL
  • have SENSITIZATION; previous exposure is needed for hypersensitivity to occur
  • has ALLERGEN; the ANTIGEN ELICITING RESPONSE
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4
Q

what are our FOUR TYPES OF HYPERSENSITIVITY?

A
  • TYPE I (ANAPHYLACTIC)
  • TYPE II (CYTOXIC)
  • TYPE III (IMMUNE COMPLEX)
  • TYPE IV (DELAYED CELL-MEDIATED)
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5
Q

describe TYPE I - ANAPHYLACTIC REACTION

A
  • around only 2 - 30 min to occur
  • needs SENSITIZATION
  • results in FORMATION of IgE ANTIBODIES–binds to MAST CELLS
  • MAST CELLS - releases HISTAMINE
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6
Q

what are our TWO TYPES OF ANAPHYLACTIC REACTIONS?

A
  1. SYSTEMIC – anaphylactic shock
  2. LOCALIZED – hay fever, asthma, hives
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7
Q

describe HISTAMINES

A
  • pre-stored in GRANULES
  • helps to INCREASE PERMEABILITY & DILATION of CAPILLARIES (can lead to EDEMA and SWELLING)
  • increases MUCUS SECRETION
  • allows for SMOOTH MUSCLE CONTRACTION
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8
Q

describe LEUKOTRIENES + PROSTAGLANDINS

A

LEUKOTRIENES:

  • allows for PROLONGED CONTRACTION OF SMOOTH MUSCLES (ASTHMA)

PROSTAGLANDINS:

  • INCREASES MUCUS SECRETION from smooth muscles of our respiratory system
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9
Q

describe SYSTEMIC ANAPHYLAXIS

A
  • seen in ANAPHYLACTIC SHOCK
  • often commonly caused by INJECTED ANTIGENS
  • needs SENSITIZATION–only a small dose can already cause a massive response
  • treatment; EPINEPHRINE – allows to CONSTRICTS BV (BV dilates in reaction and our BP drops)
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10
Q

describe PENICILLIN ALLERGY

A
  • PENICILLIN combines with CARRIER PROTEIN in SERUM – becomes IMMUNOGENIC
  • around 2% have allergy + tested with SKIN TEST
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11
Q

describe LOCALIZED ANAPHYLAXIS

A
  • often seen in INGESTED or INHALED ANTIGENS
  • using SKIN TESTS to identity allergens
  • symptoms depend on HOW ANTIGEN GETS IN
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12
Q

describe HAY FEVER

A
  • involves MAST CELLS in MUCUS MEMBRANES OF RESPIRATORY TRACT
  • ALLERGENS; pollen, dander, spores, mite feces
  • SYMPTOMS; watery eyes, sneezing, congestion
  • ANTIHISTAMINES; competes with HISTAMINE RECEPTOR SITES (allows for a reduced response)
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13
Q

describe ASTHMA

A
  • in the LOWER RESPIRATORY SYSTEM
  • has WHEEZING + SHORTNESS OF BREATH
  • have CONTRACTION of SMOOTH MUSCLES of the BRONCHIAL TUBES
  • INHALANTS – allows to BLOCK IgE (by blocking – HISTAMINE RELEASE IS NOT INDUCED)
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14
Q

describe INGESTED ANTIGENS

A
  • seen often in FOOD INTOLERANCE–this is NOT AN ALLERGY
  • just means the BODY CANNOT PROCESS FOOD
  • can not be reliably tested by SKIN TEST
  • around RIGHT FOODS cause over 90% of FOOD ALLERGIES
    SYMPTOMS:
  • HIVES
  • GI UPSET
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15
Q

what are the TWO WAYS TO PREVENT ANAPHYLATIC SHOCK?

A
  • SKIN TEST
  • DESENSITIZATION
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16
Q

describe SKIN TEST

A
  • helps to DETERMINE what an INDIVIDUAL is ALLERGIC TO
  • uses a SMALL AMOUNT OF ANTIGEN – inserted under the EPIDERMIS of the SKIN
  • looking for a RAPID INFLAMMATORY RESPONSE
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17
Q

describe DESENSITIZATION

A
  • series of using GRADUAL INCREASING DOSES injected under the skin
  • around 65 - 75% effective VS. INHALED ANTIGENS
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18
Q

describe HYGIENE HYPOTHESIS

A

living conditions might be TOO CLEAN–kids are NOT EXPOSED TO GERMS = NO TRAINING FOR IMMUNE SYSTEM

  • upsets the BALANCE BETWEEN TWO TYPES OF HELPER T CELLS; Th1 & Th2
  • Th1 RESPONSE – helps to DOWN REGULATE Th2-RESPONSE; produces IMMUNOGLOBULIN IgE
  • IgE: important to react to COMMON ALLERGENS
  • lower STIMULATION OF TH1 RESPONSE = NO DAMPENING of OVERACTIVE Th2 RESPONSE
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19
Q

describe TYPE II - CYTOTOXIC REACTION

A
  • have IgG & IgM antibodies interact with ANTIGENIC CELLS
  • looks for FOREIGN CELLS that DISPLAY UNKNOWN/FOREIGN ANTIGENS
  • will LYSE the cell; activates the COMPLEMENT SYSTEM / CYTOTOXIC T CELLS

examples;

  • TRANSFUSION REACTION
  • HEMOLYTIC DISEASE OF NEWBORN
  • DRUG INDUCED CYTOTOXIC REACTIONS
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20
Q

describe ABO BLOOD GROUPS

A
  • determines our BLOOD TYPE
  • looking for ABSENCE or PRESENCE of CARBOHYDRATE ANTIGENS on the CELL SURFACE of RBCs
  • TYPE A – has A TYPE CARBS + ANTI B ANTIBODIES
  • TYPE B – has B TYPE CARBS + ANTI A ANTIBODIES
  • TYPE AB – has both A + B TYPE CARBS + NO ANTI-A or ANTI-B ANTIBODIES
  • TYPE O – has NO A + B TYPE CARBS + HAS BOTH ANTI-A + ANTI-B ANTIBODIES
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21
Q

what happens if we get the WRONG BLOOD TYPE?

A
  • a TRANSFUSION REACTION
  • opposing antibodies of blood begin AGGLUTINATION (clumping) + HEMOLYSIS
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22
Q

describe RH GROUPS

A
  • RH FACTOR: protein that is found on the SURFACE of human RBCs
  • around 85% (are RH+ — have Rh factor + NO ANTI-RH FACTOR)
  • around 15% (have ANTI RH FACTOR ANTIBODY)
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23
Q

what happens if we have a TRANSFUSION with the WRONG RH TYPE CELL?

A
  • needs FIRST-TIME SENSITIZATION
  • creation of RAPID SERIOUS RESPONSE LYSING the TRANSFUSED CELLS (within SECOND EXPOSURE)
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24
Q

How is the RH factor inherited?

A
  • if the DOMININANT GENE (D) – has Rh factor is present vs. the RECESSIVE GENE (d) – does not have Rh factor
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25
Q

what happens if we have an RH- MOTHER that is pregnant with an RH+ fetus?

A
  • causation of HEMOLYTIC DISEASE of the NEWBORN
  • blood of both mother and fetus are CONSTANTLY BEING EXCHANGED
  • RH- MOTHER will receive RH ANTIGENS from RH+ FETUS (will start producing ANTI-RH ANTIBODIES)
  • during SECOND EXPOSURE/BABY (if by chance the second baby is RH+)–the ANTI-RH ANTIBODIES will start to attack the baby
  • this all OCCURS ONCE THE BABY IS BORN –effects of JAUNDICE, ANEMIA, and need of a TRANSFUSION
  • within the UTERUS–BABY IS STILL OK because toxic produces are filters out by the PLACENTA
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26
Q

how do we TREAT HEMOYLTIC DISEASE OF NEWBORNS?

A
  • make sure we PREVENT MOTHER from BUILDING UP ANTI RH ANTIBODIES
  • injection of ANTI-RH ANTIBODIES at TIME OF DELIVERY
  • allows for the BINDING OF THE RH FACTOR – as a RESULT OF DELIVERY = no interaction with mom’s immune system
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27
Q

describe TYPE III - IMMUNE COMPLEX REACTION

A
  • where ANTIBODY-ANTIGEN REACTIONS – cleared RAPIDLY by PHAGOCYTIC CELLS
  • sometimes SMALL AB-ANTIGEN COMPLEXES are able to ESCAPE PHAGOCYTOSIS
  • allows to go through BV ENDOTHELIAL CELLS – attaches to the BASEMENT MEMBRANE OF VESSELS
  • activates the COMPLEMENT; causes INFLAMMATION + ATTRACTION OF NEUTROPHILS
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28
Q

describe GLOMERULONEPHRITIS

A
  • a type of IMMUNE COMPLEX CONDITION
  • due to an INFECTION
  • see DAMAGE to the KIDNEY GLOMERULI + SITE OF BLOOD FILTRATION
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29
Q

describe TYPE IV - DELAYED CELL MEDIATED REACTION

A
  • does NOT INVOLVE ANTIBODIES
  • takes around 2 - 3 days to KICK IN
  • caused by our T CELLS
  • mediated by CYTOTOXIC T CELLS + NK CELLS
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30
Q

what is an EXAMPLE of DELAYED CELL-MEDIATED HYPERSENSITIVITY OF SKIN?

A
  • the TB TEST – looking for Mycobacterium tuberculosis –often seen in MACROPHAGES
  • stimulation of DELAYED CELL-MEDIATED IMMUNE RESPONSE
  • test involves; INJECTION OF PROTEIN COMP. of BACTERIA INTO SKIN
  • if you had a PREVIOUS INFECTION; memory cells will occur = shows 1-2 day INFLAMMATORY RESPONSE
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31
Q

describe AUTOIMMUNE DISEASES

A
  • where our IMMUNE SYSTEM begins to INTERACT with SELF-ANTIGENS causing DAMAGE to OWN TISSUES + ORGANS
  • around 75% of autoimmune cases – affects WOMEN
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32
Q

what CAUSES AUTOIMMUNE DISEASES?

A
  • the LOSS OF SELF TOLERANCE
    **- T CELLS mature in the THYMUS – any cells that start to RECOGNIZE THEIR OWN PROTEINS are removed by THYMIC SELECTION
  • also occurs in B CELLS
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33
Q

what are the THREE TYPES OF AUTOIMMUNE DISEASES?

A
  1. CYTOTOXIC
  2. IMMUNE COMPLEX
  3. CELL MEDIATED IN NATURE
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34
Q

what are our CYTOTOXIC AUTOIMMUNE REACTIONS?

A
  1. GRAVES DISEASE
  2. MYASTHENIA GRAVIS
35
Q

describe GRAVES DISEASE

A
  • stimulation of THYROID GLAND (by TSH) to produce THYROID HORMONES
  • the IMMUNE SYSTEM; starts to CREATE ANTIBODIES that MIMICK TSH – INCREASES THYROID ACTIVITY = INCREASE OF THYROID HORMONES

SYMPTOMS:

  • HEART POUNDING
  • TREMBLING
  • SWEATING
  • SWELLING OF THYROID GLAND
  • BULGING EYES
36
Q

describe MYASTHENIA AGRAVIS

A
  • muscles start to become more PROGESSIVELY WEAKER
  • due to ANTIBODY COATING OF ACETYLCHOLINE RECEPTORS within the NEUROMUSCULAR JUNCTION – starts to BLOCK SIGNAL OF MUSCLES
  • any MUSCLES that CONTROL RIB CAGE or DIAPHRAGM – can FAIL LEADING TO DEATH
37
Q

what are our IMMUNE COMPLEX AUTOIMMUNE REACTIONS?

A
  1. SYSTEMIC LUPUS ERYTHEMATOSUS
  2. RHEUMATOID ARTHRITIS
38
Q

describe SYSTEMIC LUPUS ERYTHEMATOSUS

A
  • mainly AFFECTS WOMEN
  • ETIOLOGY (cause) still NOT UNDERSTOOD
  • production of ANTIBODIES that are DIRECTED AGAINST THEIR OWN COMPONENTS/CELLS/DNA
  • has WORSENING SYMPTOMS over TIME / alternates between mild & severe
39
Q

describe RHEUMATOID ARTHRITIS

A
  • where our IMMUNE COMPLEXES are DEPOSITED in the JOINTS
  • IMMUNE COMPLEXES – known as RHEUMATOID FACTORS
  • causes CHRONIC INFLAMMATION – due to DEPOSITION OF FACTORS
  • damage to JOINTS AND CARTILAGE
40
Q

what are OUR CELL-MEDIATED AUTOIMMUNE REACTIONS?

A
  1. MULTIPLE SCLEROSIS
  2. INSULIN DEPENDENT DIABETES (TYPE 1)
  3. PSORIASIS
41
Q

describe MULTIPLE SCLEROSIS

A
  • women 2x more LIKELY TO GET
  • have the T CELLS + MACROPHAGES ATTACKS THE MYELIN SHEATH OF NERVES
  • has a SLOW PROGRESSION with PERIODS OF REMISSION
  • has EVIDENCE OF GENETIC PREDISPOSITION (of multiple genes)
  • UNKNOWN ETIOLOGY
  • possible is TRIGGERED BY EPSTEIN-BARR VIRUS INFECTION
42
Q

describe INSULIN DEPENDENT DIABETES (TYPE 1)

A
  • the IMMUNOLOGICAL DESTRUCTION of INSULIN SECRETING CELLS within the PANCREAS
  • T CELLS are implicated
  • has GENETIC COMPONENTS
43
Q

describe PSORIASIS

A
  • have ITCHY RED PATCHES OF THICK SKIN
  • have DENDRITIC CELLS (IL-17) + Th1 CELLS = creates ABUNDANT PSORIATIC CYTOKINES (IFN-y / TNF)
  • TREATMENT; IMMUNOSUPPRESSANT FOR T CELLS + TNF
  • around over 25% of cases lead to PSORIATIC ARTHRITIS
44
Q

what is the HUMAN LEUKOCYTE ANTIGEN (HLA) COMPLEX?

A
  • codes within HUMAN GENES that code for the MAJOR HISTOCOMPATIBILITY COMPLEXES
  • the MHCs interact with ANTIGENS and PRESENTS THEM TO OUR IMMUNE SYSTEM
  • found in MOLECULES OF OUR CELL SURFACES – part of our INHERITED GENETIC CHARACTERISITC
45
Q

define HLA TYPING

A
  • used to COMPARE + IDENTIFY HLAs
  • can look for CERTAIN HLAS – that can INDICATE INCREASED SUSCEPTIBILITY to a SPECIFIC DISEASE
46
Q

why is HLA TYPING SO IMPORTANT?

A
  • important for IDENTIFYING COMPATIBLE DONOR ORGANS
  • must be MATCHED WITH TISSUE TYPING
  • cont. of PCR to AMPLIFY + COMPARE HLA GENES of RECIPIENT + DONOR
  • ABO BLOOD TYPE MATCH + DNA MATCH = GREATER TRANSPLANT SUCCESS RATE :) !
47
Q

what are SOME REACTIONS TO TRANSPLANTATION?

A
  • the TRANSPLANTED TISSUE can be NOT RECOGNIZED AS SELF – attacking by IMMUNE SYSTEM
  • attacked by T CELLS + MACROPHAGES + ANTIBODIES = TRANSPLANT REJECTION
48
Q

definition of PRIVILEDGED SITE

A
  • able to TOLERATE INTRODUCTION OF FOREIGN ANTIGENS – does not INDUCE IMMUNE RESPONSE
  • there is NO CIRCULATING ANTIBODIES in these areas
  • ex. EYES, PLACENTA/FETUS, and TESTICLES
49
Q

describe PRIVILEGED TISSUE

A
  • tissue that DOES NOT ELICIT IMMUNE RESPONSE
  • ex. PIG HEARTS
50
Q

describe PREGNANCY and reactions

A
  • have TISSUE OF TWO COMPLETLY GENETICALLY DIFFERENT PEOPLE in DIRECT CONTACT = but still NO DIRE REACTION TO FETUS
  • IMPORTANT FACTOR; MHCI + MHCII COMPLEXES of PLACENTA – does not STIMULATE CELLULAR IMMUNE RESPONSE
  • the FETUS IS PROTECTED by PROTEINS that has IMMUNOSUPPRESSANT PROPERTIES
51
Q

describe STEM CELLS

A
  • can DEVELOP INTO OVER 200 DIFFERENT CELL TYPES
  • has transformed TRANSPLANTATION MEDICINE
  • has NO MORE REJECTION as these EXPRESSES OWN SELF ANTIGENS
  • have EMBRYONIC STEM CELLS + ADULT STEM CELLS
52
Q

describe EMBRYONIC STEM CELLS

A
  • harvested from BLASTOCYSTS
  • PLURIPOTENT; can be used to GENERATE any KIND OF CELL
53
Q

describe ADULT STEM CELLS

A
  • type of SPECIALIZED STEM CELLS
  • gives rise to SPECIFIC FAMILIES of CALL TYPES (ex. BLOOD CELLS)
  • called MULTIPOTENT
  • replenishes ORGANS and TISSUES as NEEDED
  • ex. SKIN CELLS + CARDIAC CELLS + BRAIN CELLS
54
Q

describe GRAFTS and what are OUR FOUR TYPES?

A
  • transplanted LIVING TISSUE
  1. AUTOGRAFT
  2. ISOGRAFT
  3. ALLOGRAFT
  4. XENOGRAFT
55
Q

definition of AUTOGRAFT

A
  • one’s OWN TISSUE is USED in TRANSPLANT
  • NO REJECTION – can be used for BURN PATIENTS – used to GROW NEW SKIN to COVER DAMAGED AREA
56
Q

describe ISOGRAFT

A
  • a GENETICALLY IDENTICAL GRAFT
  • used typically in TWINS
57
Q

describe ALLOGRAFTS

A
  • graft between PEOPLE WHO ARE NOT GENETICALLY IDENTICAL
  • usage of TISSUE TYPING to MATCH HLAs – to REDUCE CHANCE OF REJECTION
  • often seen in CLOSE RELATIVES – SIBLINGS
58
Q

describe XENOGRAFT

A
  • usage of ANIMAL TISSUE being TRANSPLANTED
  • causes SEVERE IMMUNE REACTION
  • greater research to make HUMANIZED PIGS (less reactive) – creation of BETTER DONORS
  • main concern is ANIMAL VIRUSES
59
Q

describe BONE MARROW TRANSPLANTS

A
  • type of HEMATOPOIETIC STEM CELL TRANSPLANT
  • given when PATIENTS CANNOT PRODUCE B CELLS + T CELLS / or have LEUKEMIA
  • allows to TRANSPLANT produces HEALTHY RBC IMMUNE SYSTEM CELLS
  • can cause GRAFT vs. HOST DISEASE
60
Q

describe GRAFT vs HOST DISEASE

A
  • where TRANSPLANTED BONE MARROW has IMMUNOCOMPETENT CELLS – CREATION OF CELL MEDIATED IMMUNE RESPONSE in TISSUE
  • can be FATAL
  • seen as EPITHELIAL CELL DEATH in the SKIN, GI TRACT, and LIVER
61
Q

describe UMBILICAL CORD BLOOD

A
  • full of MULTIPOTENT STEM CELLS - develops into a NUMBER OF BLOOD CELLS
  • harvested from PLACENTA + UMBILICAL CORD of NEWBORNS
  • allows for LESS IMMUNE REACTION - cells are LESS MATURE
  • LESS RISK FOR GRAFT v. HOST DISEASE
62
Q

describe IMMUNOSUPPRESSION in TRANSPLANT PATIENTS

A
  • have a more SUPPRESSED CELL-MEDIATED IMMUNITY
  • leaves the HUMORAL IMMUNITY intact to deal with INFECTIONS
63
Q

describe CYCLOSPORINE

A
  • the FIRST DRUG USED FOR IMMUNOSUPPRESSION
  • isolated from a FUNGUS
  • suppresses Il-2 DISRUPTING CYTOTOXIC T CELLS
  • does NOT AFFECT Ab PRODUCTION
64
Q

describe SIROLIMUS

A
  • inhibits BOTH HUMORAL + CELL MEDIATED IMMUNITY
  • HYPERACUTE REJECTION
  • is TAKEN FOR LIFE
65
Q

Can we AVOID IMMUNOSUPPRESSANT DRUGS ?

A
  • sometimes! – ex. KIDNEY TRANSPLANT PATIENT
  • usage of BONE MARROW from PATIENT and TRANSPLANTS BOTH KIDNEY AND BONE MARROW TOGETHER–creation of a REBUILT IMMUNE SYSTEM
  • creation of CHIMERA; the MIX OF IMMUNE MARKERS of the DONATED KIDNEY + PATIENT’S OWN CELLS
  • acceptance of ORGAN + stops drugs less than a year after surgery
  • CHIMERA STATE NOT PERMANENT HOWEVER
66
Q

what happens to our IMMUNE SYSTEM AS WE GET OLDER?

A
  • thymus cannot EFFICIENTLY MATURE and DIFF. T-LYMPHOCYTES
  • LOWER ABILITY to FIGHT DISEASE
  • more SUSCEPTIBILITY to DISEASE
67
Q

describe CANCER

A
  • the FAILURE within the BODY’S NORMAL FUNCTION
  • cells transform and GROW WITHOUT CONTROL – cancerous growth
  • NORMAL CELLS KNOW WHEN TO STOP GROWING – has CONTACT INHIBITION (creates only a MONOLAYER OF CELLS)
68
Q

are cancer cells always popping up in the body?

A

YES!

  • eliminated by the immune system through IMMUNE SURVEILLANCE; a type of CELL MEDIATED IMMUNE RESPONSE
  • looks for TUMOR ASSOCIATED ANTIGENS – marks cancer cells as NON-SELF
  • then is ATTACKED BY THE CELL MEDIATED IMMUNE SYSTEM - CYTOTOXIC T CELLS
69
Q

describe Dr. William Coley’s cancer research

A
  • noted that CANCER PATIENTS that get TYPHOID FEVER – cancer is DIMINISHED
  • injection of TYPHOID FEVER (Streptococci + Serratia) into CANCER PATIENTS
  • had mixed results
  • NOW USE ENDOTOXINS from BACTERIA – to create TUMOR NECROSIS FACTOR (TNFalpha)
70
Q

definition of SPONTANEOUS REMISSION

A
  • the ACTIVATION OF THE IMMUNE SYSTEM
  • apoptosis/tumor microenvironment
71
Q

describe VACCINES

A
  • THERAPEUTIC
  • treats EXISTING CANCER
  • 2010; first approved vaccines for METASTATIC PROSTATE CANCER
72
Q

describe PROPHYLACTIC IMMUNOTHERAPY

A
  • prevents the DEVELOPMENT OF CANCER
  • have TWO;
  1. HUMAN PAPILLOMAVIRUS VACCINE HPV (GARDASIL)
    - cervical, rectal, head, and neck cancer
  2. HEPATITIS B VIRUS VACCINES
    - liver cancer
73
Q

describe MONOCLONAL ANTIBODIES

A
  • new promising tool to FIGHT CANCER
  • interferes with CANCER CELL FUNCTION
  • ex. HERCEPTIN – neutralizes GF HER2 (seen in around 25 - 30% of cancer)
  • also is COMBINED WITH TOXIC AGENTS - IMMUNOTOXINS
  • able to TARGET CANCER CELLS where the TOXIN WORKS
  • ex. ADCETRIS - for HODGKIN’S LYMPHOMA
74
Q

describe IMMUNODEFICIENCY

A
  • the ABSENCE OF A ROBUST IMMUNE SYSTEM
  • can have ACQUIRED or CONGENITAL IMMUNODEFICIENCY
75
Q

describe CONGENITAL IMMUNODEFICIENCY and DIGEORGES SYNDROME

A
  • is BORN with DEFECTS to IMMUNE SYSTEM
  • syndrome where we have a SMALL DELETION in CHROMOSOME 22
  • causes ABNORMAL THYMUS DEVELOPMENT
  • have POOR T CELL PRODUCTION = INCREASES SUSCEPTIBILITY for INFECTIONS
76
Q

describe ACQUIRED IMMUNODEFICIENCY

A
  • CANCER
  • DRUGS
  • INFECTION
77
Q

describe ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)

A
  • was originated of symptoms of Pneumocystis pneumonia
  • development of rare skin cancer - Kaposi’s sarcoma (seen in several homosex. men)
  • thought to be correlated to SEXUALITY – named GRID (gay-related immune deficiency)
  • 1983; discovered correlation of NOVEL RETROVIRUS HIV + AIDS
78
Q

describe HIV - ORIGin

A
  • mutation from VIRUS ENDEMIC in PRIMATES in AFRICA
  • from the SIMIAN IMMUNODEFICIENCY VIRUS SIV – consumed BUSHMEAT by humans (got SIV)
  • began to MUTATE into HIV
  • starts to SPREAD after URBANIZATION OF AFRICA
79
Q

what type of VIRUS is HIV?

A
  • RETROVIRUS (Lentivirus)
  • has TWO IDENTICAL STRANDS of RNA
  • has REVERSE TRANSCRIPTASE
  • has ENVELOPE with GLYCOPROTEIN SPIKES (gp120)
80
Q

how does HIV infect people?

A

infects our T HELPER CELLS

  • usage of path; ATTACHMENT, FUSION and then ENTRY
  • usage of REVERSE TRANSCRIPTION of its VIRAL RNA into cDNA
  • is able to INTEGRATE INTO THE HOST CHROMOSOMAL DNA
  • and stays HIDDEN (LATENT) !!
81
Q

what are the FACTORS that AFFECT HIV SURIVIVAL with the ABSENCE of TREATMENT?

A
  • OLD AGE
    (harder to replace T helper cells)
  • IMMATURE IMMUNE SYSTEM
  • SUBSET – you are exposed but not INFECTED
    (T cells don’t have co-receptor for HIV binding)
  • NO PROGRESSION into FULL AIDS
    (very active CTLs)
82
Q

what are the MEANS of HIV TRANSMISSION?

A
  • UNPROTECTED SEX
  • SHARING NEEDLES
  • TRANSMISSION FROM MOTHER TO FETUS
  • INFECTION FROM BLOOD PRODUCTS
83
Q

how does HIV hide from our IMMUNE SYSTEM?

A
  • a POOL of LATENT INFECTED T CELLS – very hard to remove
  • REVERSE TRANSCRIPTASE – very HIGH MUTATION RATE
  • very hard to MAKE VACCINE
  • only good model is PRIMATES–ethically questionable

MICROBIO BIOL-160 LEC (21 decks)

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