Pathologic Diseases Of Immunity Flashcards
(148 cards)
1
Q
Primary lymphoid organs include ……….?
A
thymus and bone marrow
2
Q
Secondary lymphoid organs include?
A
Lymph nodes, spleen, mucosal and cutaneous lymphoid tissue
3
Q
Components of innate immunity include?
A
- Epithelial barriers
- Phagocytes [neutrophils and macrophages]
- dendritic cells,
- natural killer cells
- innate lymphoid cells,
- complement system
- plasma proteins eg., innate immunity are mannose-binding lectin and C-reactive protein
4
Q
Examples of pathogen-associated molecular patterns include?
A
• Pattern recognition receptors
• Toll-like receptors
• NOD-like receptors and the inflammasome.
• C-type lectin receptors (CLRs)
• RIG-like receptors (RLRs)
5
Q
The Reactions of Innate Immunity are?
A
- Inflammation
- Antiviral defense
6
Q
Innate immunity, unlike adaptive immunity, does not have …….. or ……….
A
memory
fine antigen specificity.
7
Q
There are two types of adaptive or specific immunity, they are?
A
- humoral immunity, which protects against extracellular microbes and their toxins
- cell-mediated (or cellular) immunity, which is responsible for defense against intracellular microbes and against cancers.
8
Q
The diseases of immunity can be classified into the following?
A
- Hypersensitivity reactions
- Diseases of Autoimmunity
- Diseases if immunodeficiency
- Amyloidosis
9
Q
Define hypersensitivity reactions?
A
Hypersensitivity reactions refer to an exaggerated response of the immune system to an antigen to
which the individual has been previously exposed.
10
Q
Hypersensitivity reactions can be caused by both exogenous and
endogenous, true or false?
A
True
11
Q
Type 1 hypersensitivity is also known as?
A
Immediate hypersensitivity
12
Q
Immediate, or type I, hypersensitivity is a rapid immunologic reaction occurring in a previously sensitized individual that is triggered by the binding of
an antigen to ……. antibody on the surface of ……..
A
IgE
mast cells.
13
Q
Type 1 hypersensitivity are often called ………., and the antigens that elicit them are ……….?
A
allergy
allergens
14
Q
Type 1 reaction is divided into the ……….. and the ……. reactions
A
Immediate
Late Phase
15
Q
Most immediate hypersensitivity disorders are caused by ……………, and these cells play a central role by stimulating …… production and
promoting inflammation.
A
excessive Th2 responses
IgE
16
Q
Sequence of events in Type 1 Hypersensitivity Reaction, The first step is the presentation of the antigen to ……….. by antigen presenting cells (APC).
A
naïve CD4+ helper T cells
17
Q
Sequence of events in Type 1 Hypersensitivity Reaction, The naïve T cells differentiate into ……….. in
response to …….. present.
A
T helper 2 (Th2) cells
IL4
18
Q
Sequence of events in Type 1 Hypersensitivity Reaction, When this Th2 cells encounter the antigen, they produce ……..
A
IL4, IL5, IL13.
19
Q
Sequence of events in Type 1 Hypersensitivity Reaction, IL-4 acts on ….. and stimulate …………
A
B cells
class switching to IgE.
20
Q
Sequence of events in Type 1 Hypersensitivity Reaction, IL-5 stimulate the activation of ……….?
A
eosinophils
21
Q
Sequence of events in Type 1 Hypersensitivity Reaction, Some environmental antigens may elicit the Th2 cells directly without APC. True or false?
A
True
22
Q
Sequence of events in Type 1 Hypersensitivity Reaction, IL-13 enhances …….. and acts on ……… to
stimulate ……….?
A
IgE production
epithelial cells
mucus secretion.
23
Q
Sequence of events in Type 1 Hypersensitivity Reaction, The IgE Fc portion binds to the ……….. on the ………… The ……….. coated by
the IgE are said to be sensitized.
A
FcεRI receptors
mast cells
mast cells
24
Q
Sequence of events in Type 1 Hypersensitivity Reaction, Subsequent encounter with an
antigen to which the mast cell
has been sensitized lead to
……….?
A
activation
25
Sequence of events in Type 1 Hypersensitivity Reaction, ……….. cross-link adjacent IgE and trigger signal transduction for release of
preformed mediators and synthesis of new ones.
Multivallent antigens
26
Sequence of events in Type 1 Hypersensitivity Reaction, what is degranulation?
Degranulation is the release of the contents of the cytoplasmic granules.
27
Sequence of events in Type 1 Hypersensitivity Reaction, Vasoactive amines include?
histamin, serotonin
28
Sequence of events in Type 1 Hypersensitivity Reaction, Enzymes include?
chymase, tryptase,
hydrolases
29
Sequence of events in Type 1 Hypersensitivity Reaction, Proteoglycans include?
heparin and chondroitin sulphate.
30
Sequence of events in Type 1 Hypersensitivity Reaction, Lipid mediators synthesized are:
Leukotrienes, examples?
Leukotrienes C4 and D4. - spasmogenic, vasoactive
31
Sequence of events in Type 1 Hypersensitivity Reaction, Lipid mediators synthesized are: Prostaglandin D2, what does it do?
This is produced in mast cells by the
cyclooxygenase pathway. It causes intense bronchospasm and increases mucus secretion.
32
Sequence of events in Type 1 Hypersensitivity Reaction, Lipid mediators synthesized are: Platelet-activating factor (PAF), what does it do?
It causes platelet aggregation, histamine release, bronchospasm, increased vascular permeability, and
vasodilation.
33
Sequence of events in Type 1 Hypersensitivity Reaction, Lipid mediators synthesized are: Cytokines, examples include?
TNF, IL-1
34
Sequence of events in Type 1 Hypersensitivity Reaction, The immediate type 1 hypersensitivity response causes ………?
vasodilation
increased vascular permeability
smooth muscle contraction
oedema.
35
Sequence of events in Type 1 Hypersensitivity Reaction, what do the released cytokines do?
The cytokines released set the stage for the next stage of inflammatory cell mobilization.
36
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, ………. are recruited that amplify and sustain the inflammatory response without additional exposure to the triggering
antigen
leukocytes
37
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, ………….. are often an abundant leukocyte population in these reactions.
Eosinophils
38
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, eosinophils are recruited to sites of immediate
hypersensitivity by ……….., such as ………., and others that may be produced by ……………...
chemokines
eotaxin
epithelial cells,
Th2 cells, and mast cells
39
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, The mast cell degranulation promote the release
of chemokines like …., …… and cytokines such as ….., …….. to recruit inflammatory cells to the site of allergen exposure.
CCL-5, CCL-11
IL-4,, IL-13
40
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, the Th2 cells secrete ………..
il-4 and il-5.
41
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, Eosinophils are attracted to the site by …………..?
chemokines, eotaxin (CCL 11) and IL-5.
42
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, Eosinophils then release cytotoxic granules containing …………. leading to cell injury and inflammation.
Major Basic Protein
Eosinophilic cationic protein
eosinophil peroxidase
43
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, …… and ……. contribute to prolonged inflammation.
Th2 cells and regulatory T cells (Tregs)
44
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, Amplification and sustainance is mediated by m cytokines such as ………….?
il4, il5, il13, TNF-alpha.
45
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, The outcomes of late phase reaction include?
sustained inflammation
mucosal oedema and hyper-secretion of mucus
smooth muscle hypertrophy in the airway.
46
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, Other outcomes include ……..
subepithelial fibrosis
epithelial hyperplasia. These are found in bronchial asthma.
47
Sequence of events in Type 1 Hypersensitivity Reaction, in late phase reaction, Chronic inflammation become resolves when …….?
stimulation by further exposure to allergens stop and the inflammatory mediators are cleared.
48
Concerning development of allergies, Susceptibility to immediate hypersensitivity reactions is ……….. determined?
genetically
49
Concerning development of allergies, …….. refers to a genetic predisposition to develop
hypersensitivity in response to common environmental
allergens.
Atopy
50
Concerning development of allergies, Atopy refers to a …………. in response to common environmental
allergens.
genetic predisposition to develop
hypersensitivity
51
Concerning development of allergies, Atopic individuals tend to have higher ……….. and more …….. than does the general population
serum IgE levels
IL-4–producing Th2 cells
52
Concerning development of allergies, …………. refers to hypersensitivity reactions
triggered by non-antigenic stimuli such as temperature extremes and exercise, and do not involve Th2 cells or IgE
Non-atopic allergy
53
Concerning development of allergies, Non-atopic allergy refers to hypersensitivity reactions
triggered by ……… such as …. & ……, and do not involve ….. or ……?
non-antigenic stimuli
temperature extremes and exercise
Th2 cells or IgE
54
Concerning development of allergies, It is estimated that 20% to 30% of immediate hypersensitivity
are due to ………..?
non-atopic allergy.
55
Concerning development of allergies, what is Hygiene hypothesis?
reduced exposure to infections in
early childhood increases the likelihood of allergic diseases later in life.
56
Concerning development of allergies, type II hypersensitivity are also known as?
Antibody-mediated or cytotoxic hypersensitivity.
57
Concerning development of allergies, what is type II hypersensitivity disorder?
In Type II hypersenitivity, antibodies that react with antigens present on cell surfaces or in the extracellular matrix cause disease by destroying these cells, triggering inflammation, or interfering with normal functions.
58
Concerning development of allergies, The following mechanisms are involved in type II hypersensitivity?
1. Opsonization and phagocytosis
2. Complement mediated cytotoxicity
3. Antibody dependent cellular cytotoxicity (ADCC)
59
Concerning development of allergies, examples of type II hypersensitivity are?
Transfusion reactions
hemolytic disease of the fetus and newborn (erythroblastosis fetalis)
autoimmune hemolytic anemia
agranulocytosis
thrombocytopenia
some drug reactions.
60
Opsonisation and Phagocytosis, Target cells or pathogens are firstly coated by …...
IgG
61
Opsonisation and Phagocytosis, The coated cells are recognized by binding to the phagocyte ……..,
fc receptors.
62
Opsonisation and Phagocytosis, Phagocytosis is largely responsible for …….
depletion of cells coated with antibodies.
63
Complement mediated cytotoxicity, When IgM or IgG antibodies are deposited on the surfaces of cells, they may ………
activate the complement system by the classical pathway
64
Complement mediated cytotoxicity, Complement activation generates cleavage products of …., mainly … and …., deposited on the surfaces of the cells and recognized by phagocytes that express receptors for these proteins causing phagocytosis.
C3
C3b and C4b
65
Complement mediated cytotoxicity, Complement activation on cells also leads to the formation of ………., which disrupts membrane integrity by “drilling holes” through the lipid bilayer, thereby causing ………
the membrane attack complex
Osmotic lysis of cells
66
Antibody – mediated cellular cytotoxicity (ADCC), Cells that are coated with IgG antibody are killed by effector cells, mainly …. and ….., which bind to the target by their receptors for the …………., and cell lysis proceeds without ……….
NK cells and macrophages
Fc fragment of IgG
phagocytosis
67
Antibody – mediated cellular cytotoxicity (ADCC), Perforins, granzymes are involved to either ………..?
kill target or induce apoptosis.
68
About Antibody – mediated Inflammation (AMI), This occurs when …….?
antibodies deposit in fixed tissues, such as basement membranes and
extracellular matrix.
69
About Antibody – mediated Inflammation (AMI), The deposited antibodies activate complement,
generating cleavage products, including …………, which direct the
migration of ………….?
chemotactic agents (mainly C5a)
granulocytes and monocytes, and
anaphylatoxins (C3a and C5a).
70
About Antibody – mediated Inflammation (AMI), The leukocytes are activated by engagement of
their ………..?
C3b and Fc receptors.
71
About Antibody – mediated Inflammation (AMI), examples include?
glomerulonephritis
vascular rejection in organ grafts
72
About Antibody – mediated cellular Dysfunction (AMCD), Antibodies directed against cell surface receptors impair or dysregulate function without causing cell injury or inflammation. True or false?
True
73
About Antibody – mediated cellular Dysfunction (AMCD), Myasthenia gravis: antibodies react to …………. in the ……….. and block ……… and cause ………..
acetylcholine receptors
motor end plates of skeletal muscles
neuromuscular transmission
muscle weakness.
74
About Antibody – mediated cellular Dysfunction (AMCD), what is Graves disease?
antibody binding stimulate causing
hyperthyroidism.
75
About Immune Complex–Mediated (Type III) Hypersensitivity, Antigen-antibody complexes produce tissue damage mainly by ……..
eliciting inflammation at the sites of deposition in type 3 hypersensitivity.
76
About Immune Complex–Mediated (Type III) Hypersensitivity, Antigen binds to antibody in the circulation creating immune complexes which deposit in ……...
vessel walls
77
About Immune Complex–Mediated (Type III) Hypersensitivity, In situ immune complexes are formed when antibodies react with antigens fixed in some tissues. True or false?
True
78
Systemic Immune Complex Disease, what is Serum sickness ……….?
It is the prototype of a systemic immune complex disease which follow foreign serum administration for treatment e.g diphtheria.
79
What is arthurs reaction?
Arthus reaction is a localized area of tissue necrosis resulting from acute immune complex vasculitis, usually elicited in the skin.
80
About T Cell–Mediated (Type IV) Hypersensitivity, Cell-mediated hypersensitivity is caused mainly by
……….
inflammation resulting from cytokines produced by CD4+ T cells.
81
Cell killing by ……. cells may also be involved in some autoimmune diseases and viral infections.
CD8+
82
In CD4+ T cell–mediated hypersensitivity reactions, cytokines produced by T cells induce inflammation that may be ….. and …..?
chronic and destructive.
83
About T Cell–Mediated (Type IV) Hypersensitivity, This is also called …………
delayed-type hypersensitivity (DTH).
84
About T Cell–Mediated (Type IV) Hypersensitivity, On subcutaneous injection of antigen, manifestation may show ……… later.
24-48 hours
85
About T Cell–Mediated (Type IV) Hypersensitivity, Naïve CD4+ T cells recognize peptides displayed by ……….. and secrete ……..?
dendritic cells
IL-2.
86
About T Cell–Mediated (Type IV) Hypersensitivity, Naïve T cells differentiate into ……
Th1 or Th17 cells.
87
About T Cell–Mediated (Type IV) Hypersensitivity, IL-12, induces differentiation of CD4+ T cells to the …….?
Th1 subset.
88
About T Cell–Mediated (Type IV) Hypersensitivity, IL-1, IL-6, and IL-23 make the naïve cells to differentiate to the …….?
Th17 subset.
89
About T Cell–Mediated (Type IV) Hypersensitivity, On repeat exposure to the antigen, Th1 cells secrete …….
IFN-γ
90
About T Cell–Mediated (Type IV) Hypersensitivity, IFN-γ activate ……….
macrophages
91
About T Cell–Mediated (Type IV) Hypersensitivity, Activated macrophages express more ……………... If the activation is sustained, ………. follows.
class II MHC molecules, TNF, IL-1, and IL-12
chronic inflammation
92
About T Cell–Mediated (Type IV) Hypersensitivity, Activated Th17 cells secrete …………, and several other cytokines.
IL-17, IL-22, chemokines
93
Examples of diseases in T Cell–Mediated (Type IV) Hypersensitivity include?
Type 1 diabetes, virus infections, graft rejection,
94
About T Cell–Mediated (Type IV) Hypersensitivity, Three pathways have been recognised:
1. CTLs that recognize the target cells secrete a combination of perforin, granzymes, and other proteins which enter target cells by endocytosis. Granzymes are proteases that cleave and activate caspases, which induce apoptosis.
2. Expression of FAS ligand by the CTL causing apoptosis.
3. Secretion of IFN-γ which induce inflammation.
95
Autoimmune disease may be organ-tissue specific or systemic, true or false?
True
96
What is self tolerance?
Self-tolerance refers to lack of responsiveness to an individual’s own antigens, and it underlies our ability to live in harmony with our cells and tissues.
97
The mechanisms of self-tolerance can be broadly classified into ………
central tolerance and peripheral tolerance.
98
What is central tolerance?
immature T cells are cells which recognise self antigens in the central or generative lymphoid organs are
either killed or rendered harmless. This is called negative selection or clonal deletion.
99
In the bone marrow the process of ………. occur. This is antigen receptor gene rearrangement which occur
when …….. come into contact with self antigens.
receptor editing
B cells
100
Peripheral tolerance occur the following mechanisms?
1. Anergy: this is a situation in which T cells that recognize self antigens are rendered functionally unresponsive.
2. Suppression by regulatory T cells
3. Deletion by apoptosis
101
Autoimmunity results from the inheritance of ………., which may contribute to the breakdown of self-
tolerance, and environmental triggers, such as infections and tissue damage, which promote the activation of ………
susceptibility genes
self-reactive lymphocytes.
102
Most autoimmune diseases are complex ……. disorders.
Multigenic
103
Mechanisms of autoimmunity include?
1. Defective tolerance or regulation
2. Abnormal display of self antigens
3. Inflammation or an initial innate immune response.
104
About role of susceptibility genes, Other polymorphisms in genes include those for?
1. PTPN-22: type I diabetes and rheumatoid arthritis
2. NOD-2: inflammatory bowel disease
3. IL-2 and IL-7 receptor polymorphisms: multiple sclerosis
105
About role of infections, Autommunity related to infections may be due to?
1. Up-regulation of co-stimulation which overwhelms peripheral tolerance.
2. Molecular mimicry – a microbe antigen may cross-react with antibodies and damage tissues.
3. Exposure of cryptic antigens from immunologically privileged sites.
4. Epitope spreading
106
Autoimmune disease is characterized by ………..?
chronic inflammation with occasional remissions followed by relapses.
107
What is Systemic Lupus Erythematosus?
Systemic lupus erythematosus (SLE) is the prototypical systemic autoimmune disorder, characterized by numerous autoantibodies, especially antinuclear antibodies (ANAs).
108
Diagnosis of SLE is by?
indirect immunofluorescence.
109
ANAs target?
(1) DNA
(2) histones
(3) nonhistone proteins bound to RNA
(4) nucleolar antigens.
110
Pathogenesis of SLE, The fundamental defect in SLE is a ……….?
failure of the mechanisms that maintain self-tolerance.
111
TLR engagement by nuclear DNA and RNA contained in immune complexes may activate …………?
B lymphocytes.
112
Drugs such as ……., ……. and ……… can induce an SLE-like response in humans.
hydralazine, procainamide, and D-
penicillamine
113
Most of the systemic lesions are caused by ……..?
immune complexes (type III hypersensitivity).
114
What is Antiphospholipid antibody syndrome?
venous and arterial thromboses, recurrent spontaneous miscarriages and focal cerebral or ocular ischemia.
115
In SLE, the skin presentations are?
Characteristic erythema affects the face along the bridge of the nose and cheeks (the “butterfly” rash);
Urticaria, bullae, maculopapular lesions, and ulcerations, worse on exposure to sunlight.
116
Describe spleen morphology in SLE?
Splenomegaly, capsular thickening, and follicular hyperplasia, concentric thickening of arteries (onion-skin
lesions).
117
Clinical features of SLE
SLE is a multisystem chronic illness with relapses and remissions.
118
What is amyloidosis?
Amyloidosis is a condition associated with a number of inherited and inflammatory disorders in which extracellular deposits of fibrillar proteins are responsible for tissue damage and functional compromise.
119
About the physical nature of amyloid, By electron microscopy, all types of amyloid, regardless of clinical setting or chemical composition, consist of……..
continuous, nonbranching fibrils with a diameter of approximately 7.5 to 10 nm.
120
X-ray crystallography and infrared spectroscopy demonstrate a characteristic ………?
cross-β-pleated sheet conformation
121
Approximately 95% of the amyloid consists of …….,, with the remaining 5% being the ……. and other …..
fibril proteins
P component
glycoproteins
122
The three most common forms of amyloid are as follows?
1. Primary Amyloidosis: Amyloid light chain (AL) protein is made up of complete immunoglobulin light chains. It is seen in plasma cell tumours.
2. Secondary Amyloidosis: Amyloid-associated (AA) protein is a form of amyloid derived from a unique non-Ig protein made by the liver.
3. β-amyloid (Aβ) protein constitutes the core of cerebral plaques found in Alzheimer disease.
4. Hereditary Amyloidosis: Transthyretin (TTR) mutation
related amyloidosis. Found in familial amyloid polyneuropathies and heart of aged individuals (senile
systemic amyloidosis).
5. Hemodialysis associated amyloidosis: beta 2-microglobulin:
The smaller nonpolymorphic peptide component of class I HLA molecules and a normal serum protein; it is deposited in a form of amyloidosis that complicates long-term hemodialysis.
123
Histologically, the amyloid deposition is always ……….
and begins between cells, often closely adjacent to basement membranes.
extracellular
124
The histologic diagnosis of amyloid is based almost entirely on its …….?
staining characteristics.
125
Spleen morphology in Amyloidosis?
marked splenomegaly (up to 800 g); tapioca-like granules on gross inspection, designated sago spleen; map- like areas of amyloidosis, called lardaceous spleen.
126
Amyloidosis shows as?
deposits occur first in the space of Disse; liver function is hardly affected.
127
Prognosis of individuals with generalized amyloidosis is …….?
poor
128
Immunodeficiency diseases are categorized into ……… and …….. immune deficiencies
Primary
secondary
129
Primary immunodeficiency diseases are caused by ………… that affect the defense mechanisms of innate immunity and adaptive immunity.
genetic (inherited) defects
130
AIDs Transmission is through three major routes?
• Sexual transmission
• Parenteral inoculation
• mother-to-infant transmission
131
The structure of a virus, The virus core contains?
(1) the major capsid protein p24;
(2) nucleocapsid protein p7/p9;
(3) two copies of viral genomic RNA; and
(4) the three viral enzymes (protease, reverse transcriptase, and integrase).
132
The HIV-1 RNA genome contains the ……., ……. and ………., which are typical of retroviruses. Including ………….., which regulate the synthesis and assembly of infectious
viral particles.
gag, pol, and env genes
tat, rev, vif, nef, vpr, and vpu
133
Although HIV can infect many tissues, the major target of HIV infection is the …….?
immune system.
134
…………, primarily affecting cell mediated immunity, is the hallmark of AIDS.
Profound immune deficiency
135
Other methods of cell death in HIV infection include?
1. activation induced cell death of uninfected cells
2. Pyroptosis
3. Infection and destruction of secondary lymphoid organs eg spleen.
4. Loss of immature precursors of CD4+ T cells.
5. Fusion of infected and uninfected cells with formation of syncytia (giant cells)
136
Loss of infected CD4+ T cells is mainly because of the …….?
direct cytopathic effects of the replicating virus.
137
In HIV, The initial infection starts in ……….., involving mainly ……….. and ………., and spreads to lymph nodes.
mucosal tissues
memory CD4+ T cells & dendritic cells
138
About HIV, In terms of natural history, the infection is divided into
three phases?
1. an acute retroviral syndrome
2. a middle, chronic phase, asymptomatic phase
3. clinical AIDS
139
About HIV, Acute (early) infection is characterized by ………. (which express CCR5) in ………., and death of many infected cells.
infection of memory CD4+ T cells
mucosal lymphoid tissues
140
Dendritic cells in epithelia at virus entry point capture the virus migrate into lymph nodes, pass HIV to CD4+ T cells through ………?
direct cell-to-cell contact.
141
Antiviral humoral and cell-mediated immune responses are mounted as the infection spreads. These responses lead to …….. and the development of …….?
seroconversion (usually within 3 to
7 weeks of presumed exposure)
virus-specific CD8+ cytotoxic T cells.
142
What is acute retroviral syndrome?
is the clinical presentation of the
initial spread of the virus: onset of 3-6 weeks and resolve after 2-4 weeks.
143
Chronic phase in HIV. During the clinical latency period the number of …….. steadily declines.
CD 4+ T cells
144
In chronic phase of HIV, patients are asymptomatic or have minor
opportunistic infections, such as oral candidiasis (thrush),
vaginal candidiasis, herpes zoster or tuberculosis.
True or false?
True
145
About Progression to AIDS?
1. Classical progressors: 7-10 years.
2. Rapid progressors: 2 – 3 years
3. Long – term non-progressors: 10 years or more.
Elite controllers are about 1% have undetectable
levels.
146
The anatomic changes in the tissues are neither specific nor diagnostic. Common pathologic features of AIDS include ……?
opportunistic infections, KS, and B-cell lymphomas.
147
Biopsy specimens from enlarged lymph nodes in the early stages of HIV infection reveal ……,
a marked hyperplasia of B-cell follicles.
148
Lymphnodes burn out at the late stages of HIV/AIDS, true or false?
True
