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x virology term 2 post-quiz > AIDS > Flashcards

AIDS Flashcards

1
Q

what kind of virus is HIV (class)?

A

retrovirus

also a human T-cell lymphotropic retrovirus

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2
Q

is HIV enveloped?

A

yes

contains glycoproteins including gp120 and gp41

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3
Q

does HIV virion contain reverse transcriptase?

A

yes

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4
Q

what is the genome structure of HIV?

A

two identical molecules of single-stranded positive RNA (diploid)

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5
Q

what type of cells does HIV infect? what happens to these cells once they’re infected?

A

infects helper (CD4) T lymphocytes
kills these cells
can also infect other cells that have CD4 proteins on their surfaces, such as macrophages and monocytes

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6
Q

what is the consequence of HIV on the immune system?

A

since it kills helper T cells, infected individuals lose cell-mediated immunity, resulting in a high probability of developing opportunistic infections and certain cancers including Kaposi’s sarcoma and lymphoma

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7
Q

what is the incubation period of HIV?

A

very long - it’s a slow virus

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8
Q

which genes does the HIV genome encode for?

A

the three typical retrovirus genes: gag, pol, env
six regulatory genes:
- tat and rev required for replication
- nef, vif, vpr, and vpu = accessory genes - not required for replication

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9
Q

what does the gag gene encode? what is its importance medically?

A

encodes internal core proteins - including p24

antigen in initial serological test that determines whether patient has antibody to HIV

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10
Q

what does the pol gene encode?

A

virion reverse transcriptase
integrase
protease

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11
Q

what does the virion reverse transcriptase in HIV do?

A

synthesizes DNA by using the genome RNA as a template
also has ribonuclease H activity - degrades RNA when it’s in the form of an RNA-DNA hybrid molecule = essential step in synthesis of double-stranded proviral DNA

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12
Q

what does HIV integrase protein do?

A

integrates viral DNA into the cellular DNA

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13
Q

what does the viral protease in HIV do?

A

cleaves various viral precursors

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14
Q

what does the env gene in HIV encode? what does this protein do?

A

gp160 protein

precursor glycoprotein that is cleaved to form the two surface glycoproteins = gp120 and gp41

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15
Q

what are clades and how are they determined? what factors vary between clades?

A

subclasses of HIV
classified based on differences in the base sequence of the gp120 gene
seem to vary geographically and also by transmission

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16
Q

what HIV clade is most common in north america? what type of cells does it preferentially infect? how is it most easily spread?

A
  • b most common in north america
  • preferentially infects mononuclear cells
  • readily passed during anal sex
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17
Q

where do HIV clade E virions preferentially infect? how are they most easily transmitted?

A

infect female genital tract cells

transmitted readily during vaginal sex

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18
Q

what enzymes are located in the HIV virion nucleocapsid? (3)

A

reverse transcriptase
integrase
protease

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19
Q

how does HIV affect cell-mediated immunity? what viral proteins are involved?

A

tat and nef proteins repress synthesis of MHC class I proteins - reduces ability of cytotoxic T cells to kill HIV infected cells

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20
Q

what does the protein encoded by the HIV rev gene do?

A

controls passage of late mRNA from nucleus into cytoplasm

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21
Q

what does the HIV protein vif do?

A

enhances infectivity by inhibiting action of APOBEC3G = enzymet hat causes hypermutaton in retroviral DNA

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22
Q

what is APOBEC3G and what viral gene affects it?

A

enzyme that causes hypermutation in retroviral DNA
deaminates cytosines in both mRNA and retroviral DNA - inactivates these molecules
vif inhibitis

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23
Q

what are the important antigens of HIV? (list)

A

gp120 and gp41

p24

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24
Q

what are gp120 and gp41?

A

type-specific envelope glycoproteins in HIV

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25
Q

what does gp120 do?

A

protrudes from surface of HIV

interacts with CD4 receptor and a chemokine receptor

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26
Q

what does gp41 do?

A

mediates fusion of viral envelope with the cell membrane at the time of infection

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27
Q

how many antigenic variants are there? what regions of the protein display the most antigenic variation?

A

gene encoding it mutates rapidly => many antigenic variants

most immunogenic region is V3 loop - varies antigenically to significant degree

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28
Q

why is production of an HIV vaccine difficult?

A

antibody against gp120 can neutralize the virus, but the gene for gp120 mutates so rapidly that antigenic variants are generated too quickly

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29
Q

where is p24 protein located? how many antigenic variations are there? how is it used clinically?

A

located in core
doesn’t seem to vary, so no variations
antibodies to it don’t neutralize DNA, but it’s used as a serological marker for HIV infection

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30
Q

what is the range of species HIV can infect?

A

mostly humans but can infect certain primates in the laboratory

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31
Q

what is the difference between HIV-1 and HIV-2? where is HIV-2 found?

A

most common is HIV-1, and that’s what we mean usually when talking about HIV
HIV-2 found in AIDS patients in west africa
proteins only 40% identical to those in HIV-1
still localized primarily to west africa
much less transmissible than HIV-1

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32
Q

what is simian immunodeficiency virus (SIV)? what species is it in? how does it compare with HIV?

A

isolated from monkeys with aids-like illness but antibodies in some african women cross-react with it
proteins compare with HIV-2 more than those of original HIV isolates

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33
Q

describe the steps of the HIV entry into cells

A

1: virion gp120 envelope protein binds CD4 protein on host cell
2: gp120 protein interacts with chemokine receptor on host cell
3: virion gp41 mediates fusion of viral envelope with cell membrane
4: viral core with nucleocapsid, RNA genome, and reverse transcriptase enters cytoplasm

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34
Q

how are chemokine receptors involved in HIV infection? which receptors are important for which strains of HIV?

A

receptors required for entry into CD4 positive cells - gp 120 protein interacts with them
CXCR4 and CCR5 proteins are examples
T-cell tropic strains bind CXCR4
macrophage-tropic strains bind to CCR5

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35
Q

how can genetic mutation in CCR5 affect development of AIDS? (what is CCR5?) what is a common mutation?

A

chemokine receptor that macrophage-tropic strains preferentially bind to

mutations in CCR5 protect from infection - homozygotes completely protected, heterozygotes have slow disease progression

most common mutation is delta-32 mutation - 32 base pairs deleted from gene

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36
Q

describe the steps in HIV replication.

A
  1. in cytoplasm, virion reverse transcriptase transcribes genome RNA into double-stranded DNA
    2: DNA migrates to nucleus
    3: DNA integrated into host cell DNA
    4: viral mRNA transcribed from proviral DNA by host cell RNA polymerase
    5: mRNA translated into several large polyproteins
    6: immature virion with precursory polyproteins forms in cytoplasm
    7: cleavage by viral protease occurs as immature virion buds from cell membrane
    8: cleavage process results in mature, infectious virion
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37
Q

where in the host cell genome does HIV DNA integrate? what mediates this integration?

A

can integrate at multiple sites and multiple copies can integrate
mediated by integrase (virus-encoded endonuclease)

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38
Q

what proteins does the gag polyprotein make when cleaved?

A

main core protein - p24
matrix protein - p17
several smaller proteins

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39
Q

what proteins does the pol polyprotein make when cleaved?

A

reverse transcriptase
integrase
protease

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40
Q

which proteins cleave the HIV polyproteins?

A

gag and pol polyproteins cleaved by viral protease, env polyprotein cleaved by cellular protease

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41
Q

on which cellular proteins is HIV replication dependent?

A

CD4 and the chemokine receptors
actin and tubulin to move viral DNA to nucleus
cyclin T1 involved in complex that transcribes viral mRNA
some proteins also involved in budding process

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42
Q

how is HIV transmitted?

A

primarily by sexual contact and by transfer of infected blood
perinatal transmission can also occur - both across placenta and at birth and through breast milk
50% neonatal infections at time of delivery and rest split equally between transplacental and breast milk transmission

small amount of virus have been found in other fluids, inc. saliva and tears, but no evidence that this plays role in infection

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43
Q

what is transmitted when HIV is transmitted?

A

transfer of either HIV-infected cells or free HIV

generally follows pattern of transmission of hep B but HIV much less effectively transmitted

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44
Q

what factors increase risk of acquiring HIV?

A

having an STD, especially those with ulcerative lesions (syphilis, chancroid, herpes genitalis)
uncircumcised males have higher risk

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45
Q

how is HIV transmission through blood transfusion prevented?

A

blood banks test for p24 antigen

there is still a window period between when infection occurs and when can be detected in blood

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46
Q

what are HIV infection rates in the US?

A

at end of 2008, 1.1 million people infected
aprox. 50,000 people infected each year
600,000 have died of AIDS since 1981

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47
Q

how has the HIV transmission rate in the US changed since the epidemic began and why?

A

has gone down due to increased prevention efforts and improved treatments, which reduce the number of people with high titers of HIV virions

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48
Q

what are HIV infection rates worldwide? where are the rates highest?

A

33 million people infected
2/3 of these are in sub-saharan africa
africa, asia and latin america have highest rates of new infections
AIDS is 4th leading cause of death worldwide

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49
Q

what is the predominant mode of HIV infection in Africa?

A

heterosexual transmission

50
Q

how high must the dose of HIV be to be infectious?

A

thought that it must be very high because there have been very few cases of infection due to needle-stick injuries and continuing exposure in health care personnel

51
Q

where does HIV initially infect? how does it spread?

A

in the genital tract in the dendritic cells that line mucosa (Langerhans cells)
CD4 positive helper T cells then become infected
HIV first found in blood 4-11 days after infection

52
Q

what subsets of cells does HIV target? what are these cells important in? what is the consequence of the infection of these cells?

A

targets subset of CD4-positive cells = Th17 cells
important mediator in mucosal immunity, esp in GI tract
produce IL-17, which attracts neutrophils to site of bacterial infection
killing them predisposes infected individuals to infections by bacteria in normal flora of colon

also infects brain monocytes and macrophages => multinucleated giant cells and significant central nervous system symptoms

53
Q

how does HIV cause giant multi-nucleated cells? what is the consequence?

A

mediated by gp41

cells in syncytia that’s formed ultimately die

54
Q

what kills HIV infected cells?

A 
those that join a syncytia die
can also be attacked by cytotoxic CD8 lymphocytes - depending on the ability of the viral tat and nef proteins to reduce MHC class I proteins
HIV could also act as superantigen = indiscriminately activates many helper T cells
55
Q

where is the main site of ongoing HIV infection?

A

lymphoid tissue - infection doesn’t have to have cytopathic effect and so virus can actively reproduce

56
Q

how long is a person infected with HIV infected for? why?

A

infected for life

likely because of integration of viral DNA into host genome

57
Q

what are elite controllers? what factors affect whether someone is one?

A

rare group of HIV-infected people who have no detectable HIV in their blood
CD4 counts are normal
mechanism unclear but doesn’t depend on gender, race or mode of transmission
evidence that certain HLA alleles are protective adn that inhibitor of cyclin-dependent kinase (p21) plays important role

58
Q

why might some HIV infected individuals be long-term “nonprogressors”?

A

some viruses have mutation in Nef gene - allows cytotoxic T cells to retain their activity

some may produce large amounts of alpha-defensins = family of positively charged peptides with antibacterial and antiviral activity - interfere with HIV binding to CXCR4 receptor

59
Q

what does HIV do to B cells?

A

polyclonal activation of B cells
results in high Ig levels
autoimmune diseases occur such as thrombocytopenia

60
Q

what is the main immune response to HIV infection?

A

cytotoxic CD8-positive lymphocytes
respond to initial infection, can control it for many years even if mutants in HIV occur (since they can proliferate and control the new mutuant strain)

61
Q

why does HIV develop into AIDS?

A

failure of cytotoxic T cells
lose their effectiveness because so many CD4 helper T cells have died => supply of lymphokines such as IL-2 required to activate cytotoxic T cells is no longer sufficient

62
Q

mutations in what human genes can accelerate progression of AIDS?

A

mutations in any of the genes encoding class I MHC because these proteins can’t present HIV epitopes => cytotoxic T cells can’t kill infected cells

63
Q

are there antibodies to HIV produced? are these effective?

A

yes, to various HIV proteins, such as p24, gp120, and gp41

neutralize virus poorly and so have little effect

64
Q

what are the mechanisms HIV uses to evade the immune system?

A

1: integration of viral DNA into host cell DNA => persistent infection
2: high rate of mutation on the env gene
3: production of tat and nef proteins that downregulate class I MHC proteins
4: can infect and kill CD4 helper T cells

65
Q

what are the stages of the clinical picture of HIV infection? (summary card)

A

1: early, acute stage: usually begins 2-4 weeks after infection - get mono-like picture including fever, lethargy, sore throat, generalized lymphadenopathy, maculopapular rash on trunk, arms, legs, leukopenia, but CD4 cell count usually normal
high-level viremia typically occurs - infection readily transmissible
resolves spontaneously in about 2 weeks, usually accompanied by lower level of viremia and rise in CD8+ T cells directed against HIV

2: middle, latent stage: long latent period, can be years - typically 7-11 years - patient asymptomatic during this period but lots of HIV still being produced in lymph node but is sequestered in the nodes (virus not in a latent state)
AIDS-related complex can occur during this period - persistent fevers, fatigue, weight loss, lymphadenopathy - often progresses to AIDS

3: late stage, AIDS: decline in number of CD4 cells to below 400/uL and increase in frequency and severity of opportunistic infections, patient immunocomprimised, severe neurological problems

66
Q

when do antibodies to HIV typically appear?

A

10 to 14 days after infection

67
Q

how long after infection will most patients have seroconverted?

A

3-4 weeks (seroconverted means development of specific detectable antibodies in blood) - can get false negative before that time

68
Q

how should you test for HIV?

A

look for antibodies
if test is negative but infection is still suspected, use PCR-based assay for viral RNA cause can get false negatives with serological tests

69
Q

what percentage of HIV infected patients are symptomatic following initial infection?

A

87% who become seropositive during the acute phase are symptomatic

70
Q

what is the viral set point? when is it established? how does this affect progression of the disease?

A 
after initial viremia
represents amount of virus produced 
remains constant for years
varies from person to person
higher the set point, more likely the person is to progress to AIDS
71
Q

how would you determine a patient’s set point?

A

assay for viral RNA in patient’s plasma - detects RNA in free virions in plasma

72
Q

how is set point used clinically?

A

amount of RNA in patient’s blood used to determine whether drug regimine is effective, as an effective one would reduce viral load
predicts prognosis

73
Q

how can the number of CD4 positive T cells that a patient has be used clinically?

A

used to determine whether person needs chemoprophylaxis against opportunistic organisms and determine whether patient needs anti-HIV therapy and response to this therapy

74
Q

what’s the lower limit of CD4 count considered normal?

A

500 cells/mm3

people with this level or higher are usually assymptomatic

75
Q

what are the common opportunistic infections associated with AIDS?

A

pneumocystis pneumonia and kaposi’s sarcoma but also viral infections such as herpes simplex, herpes zoster, and CMV and progressive multifocal leukoencephalopathy, funcal infections, cryptococcal meningitis, desseminated hestoplasmosis, protozoal infections, disseminated bacterial infections

76
Q

what is the clinical presentation of a patient during the early/acute stage of HIV infection?

A

get mono-like picture including fever, lethargy, sore throat, generalized lymphadenopathy, maculopapular rash on trunk, arms, legs, leukopenia
but CD4 cell count usually normal

77
Q

when does the early/acute stage of HIV infection usually occur?

A

usually begins 2-4 weeks after infection

78
Q

is the HIV infection transmissible during the early stages of infection?

A

yes, high-level viremia typically occurs - infection readily transmissible

79
Q

how long does the early/acute stage of HIV infection usually last? what are the signs that it’s ended?

A

resolves spontaneously in about 2 weeks, usually accompanied by lower level of viremia and rise in CD8+ T cells directed against HIV

80
Q

how long does the latent/middle stage of HIV infection usually last?

A

long latent period, can be years - typically 7-11 years

81
Q

what are the clinical symptoms of HIV during the middle/latent phase of HIV infection? is the virus still being produced?

A

patient asymptomatic during this period but lots of HIV still being produced in lymph node but is sequestered in the nodes (virus not actually in a latent state even though this is called the latent phase)

82
Q

when does AIDS-related complex (ARC) occur and what is the clinical presentation?

A 
can occur during latent/middle stage of infection
- persistent fevers
- fatigue
- weight loss
- lymphadenopathy
often progresses to AIDS
83
Q

what is the clinical presentation of a patient in the late stage of HIV infection?

A

AIDS: decline in number of CD4 cells to below 400/uL and increase in frequency and severity of opportunistic infections, patient immunocomprimised, severe neurological problems

84
Q

how would you diagnose HIV? (laboratory diagnosis)

A

detection of antibodies to p24 protein of HIV in patient’s serum - using ELISA test
because this can create false positives, definitive test made by western blot - viral proteins would be detected
OraQuick = rapid screening for antibody - uses blood sample from finger prick - results in 20 minutes but positive results require western blot confirmation

85
Q

can HIV be grown in culture?

A

yes, but it’s not readily available

86
Q

when can false-negative tests for HIV occur? why do they occur?

A

occur during first month after infection - antibody tests may be negative

due to insufficient antibody being made early in infection to be detected by ELISA

87
Q

can the diagnose of HIV be made by serological tests?

A

yes, but not in everyone and not for a while. most infected patients seroconvert in 10-14 days, and almost all have converted by 4 weeks, but not all, so you don’t know if the test is negative because the patient doesn’t have HIV or if it’s because he/she hasn’t seroconverted yet

88
Q

what is the best test for HIV during the acute phase?

A

plasma HIV RNA assay (used to determine viral load)
useful because viremia is typically high at this stage
can also use p24 antigen test or viral culture

89
Q

what are the goals of HIV treatment?

A

restore immunologic function => reduction of incidence of both opportunistic infections and certain malignancies and viral load => reduction of risk of transmission to others

90
Q

why does treatment of HIV require multiple drugs?

A

high rate of mutation of HIV => drug resistance

91
Q

what factors must be considered when deciding on drugs for HIV treatment?

A

whether its an initial infection or an established infection
number of CD4 cells
viral load
resistance pattern of the virus
whether patient is pregnant
whether patient is coinfected with HBV or HCV

92
Q

what are the two drug regimens initially used to treat HIV?

A

1: two nucleoside reverse transcriptase inhibitors (NRTI) and a protease inhibitor
2: two NRTIs plus a nonnucleoside reverse transcriptase inhibitor (NNRTI)

both combinations known as HAART

93
Q

what is HAART? what does it stand for?

A

combinations of drugs used to treat HIV

stands for “highly active antiretroviral therapy”

94
Q

how effective is HAART?

A

effective in improving quality of life, reducing viral load, prolonging life
but does not cure chronic HIV infection
discontinuation almost always results in viremia and fall in CD4 count so must continue use

95
Q

what are some nucleoside/nucleotide reverse transcriptase inhibitors (NRTI)? (list of drug names)

A 
abacavir
didanosine
emtricitabine
lamivudine
stavudine
zidovudine
tenofovir (nucleotide - all others nucleoside)
96
Q

how do NRTIs work? what is a limitation of these drugs?

A

don’t have 3’ hydroxyl group on ribose ring - chain terminating
inhibit HIV replication by interfering with proviral DNA synthesis by reverse transcriptase
cannot cure infected cell of already integrated copy of DNA

97
Q

what are the main problems with NRTI?

A

1: emergence of resistance
2: adverse effects - eg suppression of bone marrow leading to anemia and neutropenia

98
Q

what are some NNRTIs? (list of drug names)

A 
delavirdine
efavirenz
etravirine
nevirapine
rilpivirine

efavirenz (sustiva) and nevirapine (viramune) most commonly used

99
Q

how do NNRTIs work?

A

not base analogues (nothing else said…)

100
Q

how are vertical transmissions of HIV prevented?

A

the NNRTI nevirapine and the NRTI zidovudine (ZDV)

101
Q

what are some side effects of NNRTIs?

A

skin rashes and stevens-johnson syndrome

102
Q

what are some protease inhibitors (list of drugs)?

A 
amprenavir
atazanavir
darunavir
fosamprenavir
indinavir
nelfinavir
ritonavir
saquinavir
tipranavir
combination of lopinavir and ritonavir
103
Q

how do protease inhibitors work in the treatment of HIV?

A

in combination with nucleoside analogs, inhibit viral replication and increase CD4 cell counts

104
Q

how would you treat a patient with HIV that is resistant to protease inhibitors?

A

resistance to one usually conveys resistance to all
but combining two (ritonavir and lopinavir) effective against both mutant and nonmutant strains
darunavir effective against many strains that are resistant to others

105
Q

what is a side effect of protease inhibitors?

A

abnormal fat deposition in specific areas including back of neck = buffalo hump
abnormal fat deposits = type of lipodystrophy

106
Q

what should be done for a neonate born to a mother infected with HIV?

A 
give zidovudine
(mother should have been treated during pregnancy too)
107
Q

what are some entry inhibitors used in HIV treatment? (list of drugs)

A

enfuvirtide and maraviroc

108
Q

what are fusion inhibitors? what is an example?

A

prevent fusion of viral envelope with the cell membrane

first was enfuvirtide (fuzeon)

109
Q

how does enfuvirtide work?

A

binds to gp41 on HIV viral envelope

blocks entry of HIV into cell

110
Q

what are the disadvantages of enfuvirtide treatment?

A

must be administered by injection

expensive

111
Q

how does maraviroc (selzentry) work?

A

blocks binding of gp120 envelope protein to CCR-5 - prevents virion entry into cell

112
Q

what type of drug is raltegravir (isentress) and how does it work? which patients is it used in?

A

integrase inhibitor
inhibits HIV encoded integrase
used in patients for whom other antiretroviral drugs haven’t worked in reducing the levels of HIV

113
Q

what is immune reconstitution syndrome? in what patient population does it occur? what would be the clinical presentation?

A

in patients with HIV who are coinfected with other microbes (such as Hep B, C, and some bacterias) and are also treated with HAART
exacerbation of clinical symptoms occurs because antiretroviral drugs enhance inflammatory response

114
Q

how can acquisition of HIV be prevented?

A

no vaccine
avoid exposure - condoms, don’t share needles, discard donated blood contaminated with HIV
give anti-retroviral therapy to infected mothers and neonates, hiv infected mothers shouldn’t breastfeed, use c-section
circucision

115
Q

what types of post and pre-exposure prophylaxis can be used?

A

in post exposure (for example, after a needle stick) - give two drugs
can also give truvada for pre-exposure to men who have sex with men

116
Q

does HIV contain a viral oncogene?

A

no

117
Q

list of HIV virus life cycle steps:

A 
attachment
co-receptor binding
fusion
reverse transcription
integration
transcription
translation
cleavage of precursor proteins
nucleocapsid assembly
budding
virion maturation
118
Q

what determines HIV tropism?

A

the viral gp120 protein in the virion envelope

119
Q

describe the steps in the genome replication process of HIV (be very specific, sort of summary card)

A

1: HIV-associated reverse transcriptase engages a host tRNA molecule as a primer and the HIV RNA genome as the template - uses these to make single-stranded DNA copy of the RNA genome
RNaseH activity of reverse transcriptase removes the RNA strand and reverse transcriptase uses ssDNA template to make linear double-stranded DNA copy of HIV genome
this DNA copy then goes to the host cell nucleus and is integrated into the host cell chromosome - mediated by HIV integrase enzyme
HIV genome transcribed by host cell RNA polymerase to make HIV mRNA
this is translated into proteins

120
Q

how does activation of the immune system affect transcription of HIV genetic material?

A

activated CD4+ cells will activate the expression of HIV mRNA from the proviral integrated HIV genome => production of new HIV virions

x virology term 2 post-quiz (5 decks)

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