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Parasitology/Virology > HIV > Flashcards

HIV Flashcards

1
Q

What is the family and genus of HIV?

A

Family - retroviridae (retrovirus)

Genus - lentivirus

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2
Q

What are the three most important characteristics of retroviruses?

A
  • RNA genome
  • Encode reverse transcriptase RNA –> DNA
  • Integrate into host genome (difficult to eradicate)
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3
Q

What does the term lentivirus mean?

A

Lenti = slow, in reference to long incubation period between primary infection and overt symptom presentation

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4
Q

From what types of SIV did HIV-1 and HIV-2 come from?

A

HIV-1 from SIV chimpanzee

HIV-2 from SIV macaque

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5
Q

What types of SIV have high viremia but do not progress to AIDS?

A

SIV agm (African Green monkey) and SIV sm (Sooty Mangabeys)

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6
Q

Which clade of HIV predominates in the US?

A

Clade B

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7
Q

What two proteins form the envelope spikes on HIV?

A

gp120 and gp41

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8
Q

Of gp41 and gp120, which is the transmembrane subunit and which is the extracellular subunit used for docking?

A

gp41 - transmembrane

gp120 - docking extracellular

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9
Q

What is the matrix protein on the inner face of the HIV envelope?

A

p17

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10
Q

What is the capsid protein that contains the viral core?

A

p24 (24 sounds like core!)

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11
Q

How does the viral core appear in mature viral particles v. immature viral particles?

A

Mature - bullet-like shaped core

Immature - spherical, doughnut-shaped core

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12
Q

What is contained within the viral core?

A
  • 2 copies of viral genome
  • reverse transcriptase
  • integrase
  • nucleocapsid protein (p7)
  • tRNA lysine (primer for transcription)
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13
Q

What are mechanisms by which HIV can get through mucosal barrier to infect CD4 T cells?

A
  • Dendritic cells respond to inflammation triggered by HIV, trap HIV on their surface, and transmit the virus to CD4 T cells that migrate to the site of inflammation
  • Breakages in mucosal epithelium
  • Transcytosis of virus across epithelial cells
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14
Q

What is the general life cycle of HIV?

A
  • Attachment
  • Fusion, release of capsid, uncoating
  • Viral DNA formed by reverse transcription
  • Nuclear entry and integration of viral DNA
  • Synthesis of new viral RNA
  • Synthesis of new viral proteins and viral assembly
  • Virus release and maturation
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15
Q

How does HIV attach and enter a cell?

A
  • gp120 interacts with CD4, inducing a conformational change that allows gp120 to interact with a co-receptor (CCR5 or CXCR4)
  • interaction of gp120 with CD4 and co-receptor induces another conformational change that exposes gp41
  • fusion peptide of gp41 inserts into membrane of target cell and allows fusion to occur
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16
Q

What are the different strains of HIV-1 and which coreceptors do they use and which cells do they prefer?

A

R5 strain - use CCR5 for entry - tropic for CD4 T cells (at mucosal sites) and macrophages

X4 strain - use CXCR4 for entry - tropic for CD4 T cells (in lymph node), INEFFICIENT in macrophages

Also have dual tropic strain - R5X4 tropic - can use both receptors

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17
Q

Which strain is responsible for majority of primary HIV infections?

A

CCR5-tropic (R5)

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18
Q

What mutation makes an individual resistant in vitro to infection with R5 HIV?

A

delta32-CCR5

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19
Q

Are individuals with a delta32-CCR5 homozygous mutation resistant to all HIV?

A

NO, very susceptible to infection with X4-tropic strains

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20
Q

What is essential to be able to reverse transcribe the HIV RNA genome?

A

tRNA-lysine (primer)

and reverse transcriptase duh

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21
Q

What genes are present in the HIV proviral genome (and what proteins do they make)?

A

Long terminal repeat (LTR) regions: 5’ and 3’
Structural genes: gag, pol, env
Transactivator genes: tat, rev
Accessory genes: vif, vpr, vpu, nef

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22
Q

What are the functions of the 3’ and 5’ LTR?

A

5’ LTR = promoter for expression of viral genes

3’ LTR = polyA site

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23
Q

What is the function of the integrase protein?

A

Cleaves some nucleotides off the LTR regions and cuts the cellular genome in one site
Can then ligate provirus into genome

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24
Q

What is the function of Tat?

A

Tat = trans activator of transcription
Allows activation of HIV transcription
(Deletion of Tat inactivates HIV transcription)

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25
Q

What does Tat bind to, allowing RNA pol to transcribe?

A

TAR (Tat-activation region) loop

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26
Q

What is the function of Rev?

A

Rev = regulator of expression of viral proteins
Expressed in the nucleus, binds to Rev-response element (RRE) on viral RNA and transports it from nucleus to cytoplasm where it can be transcribed

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27
Q

What is the function of Nef?

A 
Nef = negative factor
Downregulates molecules of the immune system CD4 and MHC class I
Increases expression of FasL on infected cells (induces apoptosis of healthy, uninfected cells) and counters apoptosis in infected cells
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28
Q

What will be the disease presentation in an individual with nef-deleted HIV?

A

No or delayed disease

29
Q

Is vpu present in HIV-1 or HIV-2?

A

HIV-1 specific

30
Q

What is the function of vpu?

A
  • Induces CD4 downregulation in ER

- Inactivates BST2/tethrin

31
Q

What does BST2/tethrin do normally and how does HIV change that?

A

Prevents release of viral particles

Gets inactivated by vpu, allowing release of the viral particles

32
Q

What is the function of vif?

A

Vif = viral infectivity factor

Targets APOBEC3G and ubiquitinates it for degradation, preventing inactivating mutations in the HIV genome

33
Q

What does APOBEC3G do normally and how does HIV change that?

A

APOBEC3G is an enzyme that induces hypermutation and gets packaged into the virion
Gets inactivated by vif, preventing inactivating mutations

34
Q

What are the mechanisms by which HIV kills cells?

A
  • Direct killing
  • Apoptosis
  • Killing by CTLs
  • Antibody dependent cellular cytotoxicity (ADCC)
  • Infection of precursor cells
35
Q

After initial infection, describe what happens to viral load, number of CD4 T cells, and number of CD8 T cells

A
  • Viral replication will increase exponentially, then drop to a “viral set point” plateau
  • Number of CD4 T cells decreases, accompanied by a compensatory increase in CD8 T cells
  • Inflection point: immune system can no longer maintain T cell homeostasis (CD4 and CD8 numbers decrease, viral load increases, symptoms occur)
36
Q

What factors make HIV vaccine development difficult?

A
  • Highly mutagenic
  • Exists in different groups and clades
  • Can integrate into host genome
  • Heavily glycosylated envelope protein (less prone to elicit neutralizing antibodies)
37
Q

What two populations allow us to study control of HIV infection?

A
  • High risk, seronegative subjects (“exposed uninfected”)
  • Subject who control virus replication or do not progress (“long-term non-progressor” or “elite controller/viral suppressor”)
38
Q

Which bodily fluids have documented transmission of HIV?

A

Blood, breast milk, semen, vaginal secretions

39
Q

What is the key factor in determining infectiousness of someone with HIV?

A

HIV viral load

Higher viral load = more circulating virus = more transmission risk

40
Q

What exposures carry the greatest risk of transmission?

A

Blood transfusion > IDU > Receptive Anal Intercourse > needlestick injury

41
Q

Is risk of transmission greater by percutaneous exposure or by mucous membrane exposure?

A

Percutaneous

42
Q

Who cannot be tested for HIV-1 using serologic testing?

A

Infants s antibodies)

43
Q

When can you get a false negative on an HIV serologic test?

A
  • Window period: HIV antibody takes about 25 days to develop post infection
  • Seroeversion: rarely advanced disease lose antibody response
44
Q

What is the eclipse period?

A

Time it takes to be able to detect viral DNA in blood

45
Q

What is the standard serologic test done for HIV-1?

A

4th generation immunoassay that detects IgM and IgG and p24 (combination of antibody and antigen detection)

Can also do Western Blot for antibodies to the separated HIV antigens (p17, p24, p55, gp41, gp120)

46
Q

What bodily fluids can you do rapid HIV test on?

A

Oral fluid, urine, blood, serum, or plasma

47
Q

When is viral detection test (of plasma viral RNA) called for?

A
  • Diagnosis of acute/primary infection in “window period” before antibody has developed
  • Clinical assessment of known infected person (higher viral load = more rapid progression and higher risk of transmission)
  • Monitoring response to antiretroviral therapy (should suppress viral load)
48
Q

When is viral detection test of pro-viral DNA by PCR called for?

A

Diagnosis of infants <18 months (usually in developing countries)

49
Q

Who should be tested for HIV according to CDC?

A

Routine, voluntary HIV screening for ALL persons 13-64 in health care settings, regardless of risk

50
Q

What happens to viral load and CD4 count during acute HIV infection (acute HIV syndrome)?

A

Viral load rises rapidly and peaks 3-7 weeks after infection

CD4 counts acutely decline

51
Q

What is the clinical presentation of someone with acute HIV infection?

A

Classic “flu-like” illness 5-29 days after exposure

Presents with: fever, lymphadenopathy, pharyngitis, rash, myalgia/arthralgia

52
Q

What is the clinical definition of AIDS?

A

CD4 <200 OR number of AIDS-defining conditions

53
Q

What are major AIDS-defining conditions?

A 
Candidiasis esophageal
Cryptococcus
Cytomegalovirus (CMV) disease
Kaposi's sarcome
Pneumocystis jirovecii pneumonia
Progressive multifocal leukoencephalopathy (PML)
Toxoplasmosis of brain
54
Q

What conditions present in early HIV disease (CD4 > 500)?

A
  • Persistent generalized lymphadenopathy

- Secondary syphilis

55
Q

What conditions present in progressive HIV disease (CD4 200-500)?

A
  • Pulmonary TB
  • Oro-pharyngeal candidiasis (thrush)
  • Zoster
  • Kaposi’s sarcoma
56
Q

What conditions present in AIDS (CD4 <200)?

A

Pneumocystis jirovecii pneumonia (aka PCP)

57
Q

What conditions present in late stage AIDS (CD4 <100)?

A
  • Toxoplasma encephalitis

- Cryptococcal meningitis

58
Q

What conditions present in late stage AIDS (CD4 <50)?

A
  • Cytomegalovirus (CMV) retinitis
  • Mycobacterium avium complex (MAC)
  • Progressive Multifocal Leukoencephalopathy (PML)
59
Q

What is the leading infectious killer of people living with HIV?

A

TB

60
Q

What causes Kaposi’s sarcoma and how does it present?

A

Human Herpes Virus 8 (HHV-8)

Presents as malignant hemangiosarcome anywhere on body, especially skin, GI tract, lungs

61
Q

What causes Toxoplasma encephalitis and how does it present?

A

Toxoplasma gondii - protozal disease associated with cats

Causes massive lesions in brain, due to reactivation of chronic infection

62
Q

How does cryptococcal meningitis present in HIV patient?

A

Severe subacute meningitis without classical meningitis signs (no neck stiffness, have papular rash on face)

63
Q

How does CMV retinitis present?

A

Painless, progressive ‘floaters’, blind spots, visual field defects, can lead to blindness

64
Q

What primary/secondary prophylaxis should be given when CD4 <200?

A

TMP-SMX for Pneumocystis

65
Q

What primary/secondary prophylaxis should be given when CD4 <100 and test positive for toxoplasmosis IgG?

A

TMP-SMX for toxoplasmosis

66
Q

What primary prophylaxis should be given when CD4 <50?

A

Azithromycin for MAC

67
Q

What secondary prophylaxis should be given when presents with cryptococcus infection and CD4 <100?

A

Fluconazole

68
Q

What secondary prophylaxis should be given when presents with CMV infection and CD4 <50?

A

Valganciclovir

Parasitology/Virology (19 decks)

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