Exam 3: Chapter 13 Flashcards
(155 cards)
1
Q
A history of repeated infections suggests a diagnosis of…..
A
immunodeficiency
2
Q
What type of immunodeficiency diseases are caused by inherited gene defects (congenital)?
A
primary immunodeficiency
3
Q
What type of immunodeficiency diseases are acquired as a consequence of other diseases, or result from other issues such as starvation or medical intervention?
A
secondary immunodeficiency
4
Q
Most gene defects resulting in immunodeficiency are ______________ and many caused by mutations on the ____ chromosome
A
recessive, x
5
Q
SCID is caused by mutations in gene __________ on X chromosome. It encodes IL2 receptor
A
IL2RG
6
Q
What does SCID stand for?
A
severe combined immunodeficiency
7
Q
SCID will have problems with what cells? What immune system does this effect?
A
B and T cells
will affect the adaptive immune system
8
Q
If there is a mutation in the IL2RG gene on the X chromosome and causes SCID, what cytokines are affected?
A
problem w/ signaling of all the IL2 family cytokines (specifically IL7 and IL15)
This can affect the production of cytokines (more common) or the receptor is defective
9
Q
What interleukins don’t work and will cause T cells and NK cells to not develop properly in SCID patients?
A
IL7 and IL15
These two are a part of signaling of the IL2 family cytokines
10
Q
Immunodeficiency diseases can have a genetic defect in B or T cell development. What other issues can arise?
A
how the cells are called and activated
11
Q
What happens in immunodeficiency diseases if there is defects in T cell development?
A
no T cell dependent Ab response nor cell mediated responses
and can result in SCID
12
Q
Defects in T cell development can result in….
A
SCID
13
Q
Defects in signaling from T cell antigen receptors can cause….
A
SCID
14
Q
Defects in B cell development result in deficiencies in _________ production that causes an inability to clear extracellular bacteria and some viruses
A
antibody
15
Q
If the genetic defect is not a cytokine defect, then it can be a ____ or _____ cell defect
A
B, T
16
Q
What do TAP1/2 proteins do?
A
help to load antigen onto MHC
17
Q
What does a CD4 T cell help with?
A
B cell activation
18
Q
What does a common lymphoid progenitor differentiate into?
A
B, T, or NK cell
19
Q
What are the basic steps of B cell differentiation
A
1) common lymphoid progenitor
2) pro B cell
3) pre B cell
4) immature B cell
5) plasma or memory B cell
20
Q
What happens if theres a B cell deficiency between the pro B cell and pre-B cell stages?
A
the appropriate BCR will not show up and will not develop into an appropriate B cell (this can also happen between the pre-B cell and the immature B cell stage)
In this case, the individual is making the B cell, but not enough B cells are capable of actually generating antibodies (incomplete)
21
Q
B cell development can impact Ab production. How?
A
may not be able to make multiple types of Abs
B cell decides on class switching when there is a specific antigen here
22
Q
How does B cell development change from birth to infancy?
hint: 4 bullet points
A
-born with high level maternal IgG (move across placenta)
-after birth, IgM starts immediately
-IgG starts at 6 months, total IgG falls because maternal IgG is catabolized
-IgG levels are low from 3 months to 1 year of infant
23
Q
What antibody are we born with high levels?
A
maternal IgG (moves across placenta)
24
Q
What antibody starts developing immediately after birth?
A
IgM
25
baby IgG starts at ___ months, total IgG falls because maternal IgG is catabolized
6
26
When are IgG levels low in childhood?
from 3 months to one year
27
What gene is important for B cell development?
BTK (Bruton's tyrosine kinase) gene
28
Stimulation of the pre-B cell receptor recruits cytoplasmic proteins including _______ to transduce a signal that triggers B cell development
BTK (Bruton's tyrosine kinase)
29
In X-linked agammaglobulinemia (XLA) the ______ protein gene on the X chromosome is defective.
BTK
in normal situations, BTK allows tyrosine kinase to phosphorylate and produce IgM
BTK is involved in the signaling of receptor
30
What happens in males with X-linked agammaglobulinemia (XLA)?
no signal is transduced even though the receptor is there
31
In females w/ X-linked agammaglobulinemia (XLA), half of the pre-B cells will be expressing the defective BTK gene and will not develop further. Why only half?
because this is only 1/2 of the X chromosomes
so 1/2 x chromosomes in each cell is permanently inactivated early in development
32
Immune deficiencies can be caused by defects in B-cell or T-cell activation and function that lead to abnormal ___________ responses
antibody
33
Defects in activation and differentiation will have an impact on ______ ____________ and Ab response
cell mediated
34
Defects specific to activation and differentiation of B cells can impair their ability to do class switching to ___________ and leave cell mediated response intact
IgG, IgA or IgE
35
Common feature of patients with defects in B-cell class switching is ___________ syndrome. They have normal B & T cell development and normal or high serum IgM, but make limited Ab response that require ____ cell help
hyper-IgM, T
36
In X-linked hyper-IgM syndrome, the mutation is in the ________. This is on activated T cells allowing them to engage with CD 40 on APCs
CD 40 L
so the defect here would be in B cell development
37
In X-linked hyper-IgM syndrome, in males w/ this deficiency in CD 40 L the ____ cells are normal but don't engage w/ ___ cells. B cells do not undergo isotope switching or initiate the formation of germinal centers
B , T
38
In X-linked hyper-IgM syndrome, patients have severely reduced circulating Ab levels of all except ______ and are highly susceptible to bacterial infections
IgM
39
Normal pathways for host defense against different infectious agents are pinpointed by genetic deficiencies of cytokine pathways central to type _________ and type __________ responses
1/TH1, 3/TH17
40
Genetic defects in CD4 T cells are not in antibody production, but in the __________ ___________. Such defects make them susceptible to some bacterial infections.
signaling pathways
41
Inherited defects in the cytolytic pathway of lymphocytes can cause uncontrolled ______________________ and inflammatory responses to viral infections
lymphoproliferation
42
While there is impaired release of cytotoxic granules, there is uncontrolled activation and expansion of CD 8 T-cells and macrophages that infiltrate multiple organs, this causes tissue necrosis and organ failure. IFN-gamma is released from CTLs and NK cells and this leads to greater activity of macrophages, and pro-inflammatory cytokines such as....
TNF, IL-6 and CSF
43
What is the function of CD 8 T cells?
kill infected cell by apoptosis
44
What defects can happen after cytotoxic T cell activation?
45
Defects in complement components and complement-regulatory proteins cause defective ________ immune function and tissue damage.
humoral
46
T/F: bacteria has evolved overtime to mess up our complement system
True!!!!
47
Extracellular pathogens can subvent all 3 branches of the ____________ cascade (lectin, classical, and alternative pathways) to evade immune destruction
complement
48
What are the 6 proteins we talked about that S. aureus makes to inhibit complement pathway?
1) SAK (staphylokinase)
2) SSL10
3) Sbi and Spa
4) SCIN
5) Ecb and Efb
6) CHIPS
49
S.aureus makes several proteins to inhibit the complement system. SAK is one of them. What does SAK (staphylokinase) do?
SAK cleaves IgG and removes it from the bacterial surface
50
S.aureus makes several proteins to inhibit the complement system. SSL10 is one of them. What does SSL10 (staphylococcal superantigen-like protein 10) do?
SSL10 binds to IgG and blocks initiation of the classical pathway
51
S.aureus makes several proteins to inhibit the complement system. Sbi and Spa are one of them. What does Sbi (2nd immunoglobulin binding protein) and Spa (staphylococcal protein A) do?
Sbi and Spa block C1q binding to the Fc receptor portion of immunoglobulin, and also blocks the initiation of the classical pathway
52
S.aureus makes several proteins to inhibit the complement system. SCIN is one of them. What does SCIN (staphylococcal complement inhibitor) do?
SCIN stabilizes C3 convertase in an inactive state (bind to whole entity, so next complement step doesn't happen, and gets arrested)
53
S.aureus makes several proteins to inhibit the complement system. Ecb and Efb are one of them. What does Ecb (extracellular complement-binding protein) and Efb (extracellular fibrinogen-binding protein) do?
Ecb and Efb bind to C3d and inactivate both C3 and C5, which prevents C5 convertase activity
54
S.aureus makes several proteins to inhibit the complement system. CHIPS is one of them. What does CHIPS (chemotaxis inhibitory protein of staphylococcus) do?
CHIPS blocks the C5a receptor on phagocytes (so vasodilation and immune cells will never arrive)
55
If theres a defect in C1, C2, or C4 protein of the classical pathway, what can happen as a result?
deficiency leads to immune complex disease (immune complex is made, but nothing happens next)
56
If theres a defect in MBL, MASP1/2, C2, or C4 protein of the MBL pathway, what can happen as a result?
Deficiency of MBL leads to bacterial infections (most commonly in childhood years)
57
Factor D and Factor P regulate which pathway?
complement, specifically alternative pathway
58
If theres a defect in Factor D or Factor P of the alternative pathway, then what happens as a result?
deficiency leads to infection w/ pyogenic bacteria and Neisseria spp. but no immune complex disease
In this case, bacteria makes proteins to destroy Factor D and Factor P which means the body will not be able to regulate how much C3 is in the system
If theres low levels of C3, then alternative pathway will not work
59
What happens if theres a deficiency in the C3b deposition and affects C3 protein?
deficiency leads to infections w/ pyogenic bacteria and Neisseria spp. and sometimes immune complex disease
60
What happens if there is a deficiency in the membrane attack components, like the C5, C6, C7, C8, or C9 proteins?
deficiency leads to infection w/ Neisseria ssp. only
61
What are the 2 main treatments to correct genetic defects?
1) hematopoietic stem cell transplantation
2) gene therapy
62
Extracellular bacterial pathogens have evolved different strategies to avoid detection by ____________ and destruction by antibody, complement, and antimicrobial peptides
pattern recognition receptors
63
Intracellular bacterial pathogens can evade the immune system by seeking shelter within.....
phagocytes
64
RNA viruses use different mechanisms of __________ ___________ to keep a step ahead of the adaptive immune system
antigenic variation
65
DNA viruses use multiple mechanisms to subvert ______ cell and CTL responses
NK
66
Extracellular bacterial pathogens have evolved different strategies to avoid detection by pattern recognition receptors and destruction by antibody, complement, and antimicrobial peptides. What are the 5 main bacterial strategies?
1) shielding on MAMPs (seen w/ TLRs in normal situations)
2) antigenic variation (changing antigen)
3) inhibition of opsonization (coating to engulf pathogen in normal immunity, but bacteria can make it slippery to prevent this coating)
4) inhibition of ROS (our cells should be producing ROS to kill bacteria)
5) resistance to antimicrobial peptides (such as defensins)
67
What is an example of an extracellular bacteria that shields MAMPs?
Streptococcus pneumoniae
68
What are the 6 main bacterial strategies for intracellular bacteria to inhibit immune system?
1) antigenic variation
2) inhibition of MAMP recognition/signaling
3) resistance to antibacterial peptides
4) inhibition of fusion of phagosome w/ lysosome
5) survival within phagolysosome
6) escape from phagosome
69
What is an example of an intracellular bacterial pathogen that can evade the immune system by seeking shelter inside of macrophages?
mycobacterium (TB)
70
Which intracellular bacteria escapes from the phagosome into the cytoplasm of the macrophage where they multiple?
Listeria monocytogenes
71
Which intracellular bacteria uses type 3 secretion system to secrete SifA into host cytosol and membranes to alter composition of this bacteria containing vacuole to avoid destruction?
salmonella
It has an injector protein on its surface that bores hole into your cell to release proteins which will destroy your cell by destroying the cytoskeleton so salmonella can make its way in
72
Do gram negative or gram positive bacteria have type 3 or type 4 secretion systems/injectisomes?
gram negative bacteria has injection system to release proteins into your cell
73
Gram negative bacteria has type 3 or type 4 secretion systems/injectisomes. How does this work?
-assembly of proteins on membrane
-bacterial proteins injected into host cell
-virulence factors aid in escaping immune response and block signaling cascade (NFkB and MAP kinases)
74
Besides Salmonella, what is another example of a gram negative bacteria that has type 3 or type 4 secretion systems/injectisomes? How does it work?
yersinia pestis (black plague)
TOP proteins are injected into phagosomes and destroys the actin cytoskeleton which is needed for phagocytosis
75
The induction of and response to type I interferons are major targets for immune subversion by viruses. In normal situations, the body should release IFNs in response to viral infections, but in this case, the body will not release IFNs because the virus interferes. Several pattern-recognition receptors that recognize microbial forms of DNA and RNA produced in the course of viral infection and replication activates the production of interferons by the infected cell. Heterodimeric receptors for these cytokines are expressed on nearly all cells of the body and activate _______ and ________ to amplify production of the interferons and induce expression of restriction factors that block replication of viruses. Key sites in the interferon signaling cascades are blocked by many viruses.
STAT1, STAT2
76
Antigenic changes from reassortment of segments of ______ genome leads to antigenic shift = global pandemics every 10-50 years
RNA
77
What is antigenic drift?
RNA viruses do this, like HIV or influenza
78
What is antigenic shift (also known as genetic reassortment)?
RNA viruses do this, like influenza
there are 3 types of influenza: human, pig, and bird
in this case, influenza is switching viral particles from different variants
pig influenza is the only one that can get infected by all three types
humans can only get infected by human influenza
so pig influenza can get infected with bird and human influenza
in the case of influenza, each viral particle must always have 8 pieces
antigenic shift only happens w/ viruses that have numerous segments and can infect numerous species
79
Point mutations can cause antigenic _______
drift
80
DNA viruses have a low mutation rate but employ __________ __________. They have larger genomes than RNA viruses, and more proteins that help them fight off immune cells
antigenic variation
81
What is an example of a DNA virus that has a low mutation rate? How does it work?
Herpesviruses
have a latent phase (remains dormant, hides in immune cells)
no viral proteins will be loaded onto MHC class 1
82
DNA viruses repress cytolytic activity of _____ cells. Viral homologs of MHC class 1 will end up binding to these cells and block the action
NK
83
DNA viruses have viral homologs of cytokines and their receptors. They decoy receptors that interfere w/ natural ligand signaling, or make proteins that inhibit __________ signaling
JAK/STAT
84
What are immunoevasins?
This is a part of DNA viruses
many proteins which prevent the appearance of viral peptide:MHC class 1 on the infected cells (this viral peptide complex ensures that MHC class 1 will never arrive on the surface)
85
What are dislocation proteins?
This is a part of DNA viruses
some viral proteins degrade the newly made MHC class 1 molecule using a pathway that usually degrades misfolded proteins
86
Some DNA viruses can inhibit the loading of MHC class 1. For example, viral evasins US6 and ICP47 block antigen presentation by preventing peptide movement through the TAP peptide transporter. Then, the adenovirus protein E19 competes w/ tapasin and inhibits peptide loading onto nascent MHC class 1 proteins. Lastly, the mK3 protein of murine gamma herpes viruses is an E3-ubiquitin ligase that targets MHC class 1 for degradation by the...
proteasome
87
In DNA viruses, some latent viruses persist in vivo by ceasing to replicate until immunity wanes. These viruses enter latency by expression of a small region of their genome called __________. This suppresses the transcription of viral genome and produces factors that interfere w/ apoptotic host cell death and immune mechanisms that could clear the virus
LATs (Latency Associated Transcript)
88
What are 3 examples of DNA viruses that go into a latency phase?
1) herpes simplex/herpes zoster
-sensory neurons are good targets since they have very few MHC class 1 expression and have limited capacity for regeneration
-herpes causes cold sores that will eventually go away, but stress can trigger it to come back from its latency period
-it hides in the trigeminal ganglion until it gets opportunity to come back out
-the virus produces proteins that keep our immune cells from reaching the ganglion and the virus is protected
2) EBV (infectious mononucleosis)
-latency in B cells
3) chicken pox that can develop into shingles later on
-also sits in trigeminal ganglion like herpes
89
What does AIDs stand for?
Acquired Immune Deficiency Syndrome
90
AIDs develops after what?
HIV (HIV1 or HIV2)
91
Which HIV is predominantly found in humans and is more rapid?
HIV1
92
Which HIV replicates in higher viral loads in blood and has a higher rate of transmission from mother to child?
HIV1
93
Where did HIV originate from?
SIV (simian immunodeficiency virus) , came from monkey population
SIV has 4 separate transmissions to humans from chimps or lowland gorillas
HIV2 originated in the sooty mangabey monkeys
94
How many transmissions are there of HIV?
4
95
What are the 4 major groups of HIV1?
1) main (M)
2) outlier (O)
3) N (non-M, non-O)
4) P (non-M, N, or O)
96
Which HIV1 group is the biggest one and the most prevalent?
main (M)
97
How many lineages are there for HIV2?
9
98
Which HIV1 group has clades and what are the clades?
M group
clades A-K
99
HIV is a ___________ that establishes a chronic infection that slowly progresses to AIDS
retrovirus
100
HIV is in what group of retroviruses?
lentivirus
101
Is HIV an RNA or DNA virus?
RNA virus
102
HIV infects and replicates within cells of the immune cells. What cells are the major source of HIV replication?
activated CD4 T cells (specifically, macrophages and CD4 T cells with a CCR5 receptor)
103
There are ___________ routes by which HIV is transmitted and establishes infection
several
104
HIV enters ___________ first, which then travel and get the virus everywhere
macrophages
105
HIV has virus particles that binds to CD4 and co-receptor (CCR5) on T cell. The viral envelope fuses w/ cell membrane allowing viral genome to enter the cell. ____________ ____________ copies viral RNA genomes into double stranded cDNA. The viral cDNA then enters the nucleus and is integrated into host DNA into chromosomes
reverse transcriptase
106
Once HIV enters the nucleus and is integrated into host DNA, T cell activation induces low-level transcription of _______. RNA transcripts are multiplying and spliced, which allow translation of early genes _____ and _____. Tat amplifies transcription of viral RNA. Rev increases transport of spliced or unspliced viral RNA to the cytoplasm. The late proteins Gag, Pol, and Env are translated and assembled into virus particles which bud from the cell
provirus, tat, rev
107
What are the 2 gene proteins specific to HIV?
tat and rev
HIV makes these proteins to kick up its own transcription/translation but they need T cell to be activated to go along with this
108
Which HIV gene protein amplifies transcription of viral RNA?
tat
109
Which HIV gene protein increases transport of spliced and unspliced viral RNA to the cytoplasm?
rev
110
Activation of CD4 T cells induces expression of transcription factor ________ which binds to proviral LTR (long terminal repeat) and transcribe HIV genome
NFkB
111
Activation of CD4 T cells induces expression of transcription factor NFkB which binds to proviral LTR (long terminal repeat) and transcribe HIV genome. First viral transcripts are processed and produce spliced mRNAs encoding the regulatory proteins ______ and ______.
TAT, REV
112
________ enhances transcription from provirus and binds to RNA transcripts and stabilizes them for translation
Tat
113
________ binds to RNA transcripts and transports them out to cytosol
Rev
114
HIV infects CD4 T cells that have a CD4 molecule and _______ co-receptor
CCR5
115
HIV R5 variants target __________ memory and __________ memory CD4 T cells, dendritic cells and macrophages (this is partially the reason why this is known as "M-tropic"). R5 variants of HIV are thought to represent the major population of virus that establishes initial infection
effector (TEM), resident (TRM)
116
HIV X4 variant (T-tropic) has HIV virions that bind the ________ chemokine receptor and target naive and central memory (TCM) CD4 T cells. X4 variants of HIV emerge after initial infection
CXCR4
117
HIV adheres to the surface of intraepithelial dendritic cells by the binding of viral _______ to DC-SIGN. It gains access to dendritic cells at sites of mucosal injury or possibly to dendritic cells that have protruded between
epithelial cells to sample the external world; HIV can also bind directly to some epithelial cells and is transported across them to subepithelial dendritic cells. Dendritic cells internalize HIV virions into mildly acidic
early ___________ and migrate to lymphoid tissue. HIV virions are translocated back to the cell surface,
and when the dendritic cell encounters CD4 T cells in a secondary lymphoid tissue, the HIV is transferred to the ____ cell
gp120, endosomes, T
118
What are the 4 proteins that HIV makes to inhibit our immune system?
1) Nef
2) Vif
3) Vpu
4) Vpr
119
HIV makes several proteins that inhibit our immune system. Nef is one of them. Nef sustains T cell activation (this to activate T cell so HIV can replicate inside), downregulates expression of inhibitory co-stimulatory ________, promoting viral replication. Nef also downregulates MHC class 1/2 expression (cannot present any antigens!). Nef also promotes clearance of CD4 surface molecules so that new progeny don't get stuck on the surface
CTLA4
(so Nef downregulates CTLA4, MHC 1/2, and CD4)
120
HIV makes several proteins that inhibit our immune system. Vif is one of them. Vif overcomes acytidine deaminase (_________) which could change cDNA of virus by converting deoxycytidine to deoxyuridine
APOBEC
121
What is acytidine deaminase (APOBEC)?
an enzyme produced by our immune cells that ensures that theres enough nucleotides around
so in the case of HIV, it wants to over-express this enzyme so that it can transcribe/translate more DNA
122
What 2 HIV proteins are similar? Why?
Vif and Vpr
both do nucleotide modulation
123
HIV makes several proteins that inhibit our immune system. Vpu is one of them. What does Vpu do?
Vpu takes down tetherin
124
What is tetherin?
protein in our immune cells that tethers to a virus and holds onto it so our immune cells can get rid of it
but in the case of HIV, it inhibits this so that the virus can escape from our immune cells
125
HIV makes several proteins that inhibit our immune system. Vpr is one of them. Vpr overcomes/takes down restriction factor ____________
SAMHD1
126
What is SAMHD1?
a human host factor found in myeloid cells which restricts HIV1 replication. It depletes the dNTPs pool for viral cDNA synthesis, thus preventing the viral replication in our cells
127
In the acute phase of HIV, there is a rapid rise in blood, rapid drop on _________ expressing CD4. T cell death in GELT from viral replication and exit
CCR5
128
What is the next phase of infection after acute in HIV?
asymptomatic phase (latency)
129
During the asymptomatic phase of HIV, there is a seroconversion. What does this mean? Additionally, CTL kill infected cells and drop in viral RNA load to combat the virus
seroconversion= Abs arrive in serum (all of them) and this takes 2-6 weeks
130
What phase is after the asymptomatic phase of HIV infection?
symptomatic
131
During the symptomatic phase of HIV, there is a drop in viremia and drop in CD4 T cells. The virus is held in check by CTL and Abs. There are escape mutants approx. 50% of cases and the dominant viral type switched from _____ to ______ variant.
R5 to X4
132
What happens after the symptomatic phase of HIV?
progresses to AIDS
133
What happens for CD4 T cells once HIV progresses to AIDs?
CD4 T cells drop below 200 cells/microL
(a normal healthy individual should have approx. 1000)
134
There are Abs being made against which 2 HIV proteins?
Env and core p24
135
The immune system wants to make neutralizing antibodies against which HIV proteins?
gp120 and gp41
136
Non-neutralizing Abs target infected cells for....
antibody-dependent cytotoxicity (ADCC)
(talking about HIV here)
non-neutralizing Abs do not neutralize the virus and gives the virus a home within macrophages
137
AIDS is the destruction of immune function as a result of HIV infection leads to increased susceptibility to ____________ infection and eventually to death.
opportunistic
138
What are the major reservoirs for HIV infection?
lymphoid tissue
139
What is the half life of CD4 T memory cells?
44 months
140
Long term non-progressors, also known as elite controllers, are individuals infected w/ HIV who maintain a CD4 T cell count greater than 500 without any antiviral therapy. In these cases, will their viral load increase or decrease? This happens in 1/300 people
DECREASE
141
What are the 3 genetic variations that can inhibit HIV?
1) CCR5 delta 32 (homozygous alleles blocks HIV infection, heterozygous alleles slow infection down)
2) HLA polymorphisms
3) mutations that affect cytokine production
142
What is used to determine genetic variations and can distinguish highly susceptible or resistant individuals for HIV?
genome wide association studies (GWAS), its a high throughput sequencing technique
143
Drugs that block HIV replication lead to a rapid decrease in titer of infectious virus and an increase in _______ cells
CD4 T
144
Mortality of patients w/ HIV in US falls in parallel w/ rise in.....
combo treatment availability
145
What does HAART stand for?
highly active anti-retroviral therapy
its a multi-drug therapy to combat HIV antigen
146
With HAART treatment, there is reduction in HIV particles. The life of virus decay happens in ___ phases
3
147
With HAART treatment, there is reduction in HIV particles. The life of virus decay happens in 3 phases. Phase 1 is 2 days and has infected T cells. Phase 2 virus half life is 2 weeks and viral production declines, infected T cells die, and released viruses are cleared from system (takes approx 6 hours to be cleared from system). This phase lasts ____ months. Phase 3 is much longer and has latently infected cells that are present. The virus can be reactivated from ________ cells
6, memory T
148
What are the 3 main drug options for HIV therapy?
1) entry inhibitors (not always given with other 2)
2) integrase inhibitors
3) enhance activity of HIV restriction factors including APOBEC and TRIM 5 alpha. APOBEC causes mutations in cDNA of virus. TRIM 5 alpha targets the nucleocapsid and prevents uncoating and release of RNA as it enters the cell
149
How can we activate latent reservoirs of HIV?
kick up T cells to get virus to come back and get rid of virus then
150
The Berlin/London patients was where 1 patient underwent hematopoietic stem cell transplantation (HSCT) to treat _____________. The stem cell donor cells were altered to be homozygous for CCR5 delta 32 gene. The patient has a rebound of __________. They were free of HIV infection and leukemia following stopping antiretroviral post-transplantion. Latency reservoir was eradicated in this case because of inductive chemoradiation for leukemia and blocking viral replication
leukemia, CD4 T cells
151
In the course of infection, HIV accumulates many mutations which can result in the outgrowth of drug-resistant variants. This results in....
quasispecies
152
Is there a vaccine for HIV/AIDS?
no
153
What is a therapeutic vaccine?
vaccine that boosts immunity of those infected
154
What are some HIV/AIDS vax challenges?
-HIV highly variable genetically due to high error rate
-lack of good animal model
-HIV can avoid humoral and cell-mediated immune responses by becoming latent (persisting as provirus), also by forming syncytia (virus particles pass from cell to cell)
-infected individuals do indeed mount immune response
155
Can an mRNA vax be used for HIV/AIDS?
maybe
Canarypox viral vector delivering HIV gap, pol, and env followed by gp120 boost
