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
2
Q
what happens if we have DEFECTIVE IMMUNE RESPONSE?
A
- due to OLD AGE
- can be CONGENITAL
- can be INFECTION – ex. HIV
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
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)
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
6
Q
what are our TWO TYPES OF ANAPHYLACTIC REACTIONS?
A
- SYSTEMIC – anaphylactic shock
- LOCALIZED – hay fever, asthma, hives
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
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
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)
10
Q
describe PENICILLIN ALLERGY
A
- PENICILLIN combines with CARRIER PROTEIN in SERUM – becomes IMMUNOGENIC
- around 2% have allergy + tested with SKIN TEST
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
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)
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)
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
15
Q
what are the TWO WAYS TO PREVENT ANAPHYLATIC SHOCK?
A
- SKIN TEST
- DESENSITIZATION
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
17
Q
describe DESENSITIZATION
A
- series of using GRADUAL INCREASING DOSES injected under the skin
- around 65 - 75% effective VS. INHALED ANTIGENS
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
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
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
21
Q
what happens if we get the WRONG BLOOD TYPE?
A
- a TRANSFUSION REACTION
- opposing antibodies of blood begin AGGLUTINATION (clumping) + HEMOLYSIS
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)
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)
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
25
what happens if we have an RH- MOTHER that is pregnant with an RH+ fetus?
- 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
26
how do we TREAT HEMOYLTIC DISEASE OF NEWBORNS?
- 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
27
describe TYPE III - IMMUNE COMPLEX REACTION
- 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
28
describe GLOMERULONEPHRITIS
- a type of IMMUNE COMPLEX CONDITION
- due to an INFECTION
- see DAMAGE to the KIDNEY GLOMERULI + SITE OF BLOOD FILTRATION
29
describe TYPE IV - DELAYED CELL MEDIATED REACTION
- does NOT INVOLVE ANTIBODIES
- takes around 2 - 3 days to KICK IN
- caused by our T CELLS
- mediated by CYTOTOXIC T CELLS + NK CELLS
30
what is an EXAMPLE of DELAYED CELL-MEDIATED HYPERSENSITIVITY OF SKIN?
- 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
31
describe AUTOIMMUNE DISEASES
- where our IMMUNE SYSTEM begins to INTERACT with SELF-ANTIGENS causing DAMAGE to OWN TISSUES + ORGANS
- around 75% of autoimmune cases -- affects WOMEN
32
what CAUSES AUTOIMMUNE DISEASES?
- 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
33
what are the THREE TYPES OF AUTOIMMUNE DISEASES?
1. CYTOTOXIC
2. IMMUNE COMPLEX
3. CELL MEDIATED IN NATURE
34
what are our CYTOTOXIC AUTOIMMUNE REACTIONS?
1. GRAVES DISEASE
2. MYASTHENIA GRAVIS
35
describe GRAVES DISEASE
- 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
describe MYASTHENIA AGRAVIS
- 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
what are our IMMUNE COMPLEX AUTOIMMUNE REACTIONS?
1. SYSTEMIC LUPUS ERYTHEMATOSUS
2. RHEUMATOID ARTHRITIS
38
describe SYSTEMIC LUPUS ERYTHEMATOSUS
- 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
describe RHEUMATOID ARTHRITIS
- 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
what are OUR CELL-MEDIATED AUTOIMMUNE REACTIONS?
1. MULTIPLE SCLEROSIS
2. INSULIN DEPENDENT DIABETES (TYPE 1)
3. PSORIASIS
41
describe MULTIPLE SCLEROSIS
- 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
describe INSULIN DEPENDENT DIABETES (TYPE 1)
- the IMMUNOLOGICAL DESTRUCTION of INSULIN SECRETING CELLS within the PANCREAS
- T CELLS are implicated
- has GENETIC COMPONENTS
43
describe PSORIASIS
- 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
what is the HUMAN LEUKOCYTE ANTIGEN (HLA) COMPLEX?
- 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
define HLA TYPING
- used to COMPARE + IDENTIFY HLAs
- can look for CERTAIN HLAS -- that can INDICATE INCREASED SUSCEPTIBILITY to a SPECIFIC DISEASE
46
why is HLA TYPING SO IMPORTANT?
- 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
what are SOME REACTIONS TO TRANSPLANTATION?
- the TRANSPLANTED TISSUE can be NOT RECOGNIZED AS SELF -- attacking by IMMUNE SYSTEM
- attacked by T CELLS + MACROPHAGES + ANTIBODIES = TRANSPLANT REJECTION
48
definition of PRIVILEDGED SITE
- 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
describe PRIVILEGED TISSUE
- tissue that DOES NOT ELICIT IMMUNE RESPONSE
- ex. PIG HEARTS
50
describe PREGNANCY and reactions
- 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
describe STEM CELLS
- 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
describe EMBRYONIC STEM CELLS
- harvested from BLASTOCYSTS
- PLURIPOTENT; can be used to GENERATE any KIND OF CELL
53
describe ADULT STEM CELLS
- 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
describe GRAFTS and what are OUR FOUR TYPES?
- transplanted LIVING TISSUE
1. AUTOGRAFT
2. ISOGRAFT
3. ALLOGRAFT
4. XENOGRAFT
55
definition of AUTOGRAFT
- 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
describe ISOGRAFT
- a GENETICALLY IDENTICAL GRAFT
- used typically in TWINS
57
describe ALLOGRAFTS
- 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
describe XENOGRAFT
- 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
describe BONE MARROW TRANSPLANTS
- 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
describe GRAFT vs HOST DISEASE
- 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
describe UMBILICAL CORD BLOOD
- 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
describe IMMUNOSUPPRESSION in TRANSPLANT PATIENTS
- have a more SUPPRESSED CELL-MEDIATED IMMUNITY
- leaves the HUMORAL IMMUNITY intact to deal with INFECTIONS
63
describe CYCLOSPORINE
- the FIRST DRUG USED FOR IMMUNOSUPPRESSION
- isolated from a FUNGUS
- suppresses Il-2 DISRUPTING CYTOTOXIC T CELLS
- does NOT AFFECT Ab PRODUCTION
64
describe SIROLIMUS
- inhibits BOTH HUMORAL + CELL MEDIATED IMMUNITY
- HYPERACUTE REJECTION
- is TAKEN FOR LIFE
65
Can we AVOID IMMUNOSUPPRESSANT DRUGS ?
- 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
what happens to our IMMUNE SYSTEM AS WE GET OLDER?
- thymus cannot EFFICIENTLY MATURE and DIFF. T-LYMPHOCYTES
- LOWER ABILITY to FIGHT DISEASE
- more SUSCEPTIBILITY to DISEASE
67
describe CANCER
- 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
are cancer cells always popping up in the body?
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
describe Dr. William Coley's cancer research
- 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
definition of SPONTANEOUS REMISSION
- the ACTIVATION OF THE IMMUNE SYSTEM
- apoptosis/tumor microenvironment
71
describe VACCINES
- THERAPEUTIC
- treats EXISTING CANCER
- 2010; first approved vaccines for METASTATIC PROSTATE CANCER
72
describe PROPHYLACTIC IMMUNOTHERAPY
- 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
describe MONOCLONAL ANTIBODIES
- 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
describe IMMUNODEFICIENCY
- the ABSENCE OF A ROBUST IMMUNE SYSTEM
- can have ACQUIRED or CONGENITAL IMMUNODEFICIENCY
75
describe CONGENITAL IMMUNODEFICIENCY and DIGEORGES SYNDROME
- 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
describe ACQUIRED IMMUNODEFICIENCY
- CANCER
- DRUGS
- INFECTION
77
describe ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
- 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
describe HIV - ORIGin
- 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
what type of VIRUS is HIV?
- RETROVIRUS (*Lentivirus*)
- has TWO IDENTICAL STRANDS of RNA
- has REVERSE TRANSCRIPTASE
- has ENVELOPE with GLYCOPROTEIN SPIKES (gp120)
80
how does HIV infect people?
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
what are the FACTORS that AFFECT HIV SURIVIVAL with the ABSENCE of TREATMENT?
- 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
what are the MEANS of HIV TRANSMISSION?
- UNPROTECTED SEX
- SHARING NEEDLES
- TRANSMISSION FROM MOTHER TO FETUS
- INFECTION FROM BLOOD PRODUCTS
83
how does HIV hide from our IMMUNE SYSTEM?
- 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
