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SMP - MIM Part 2 > Lecture 14 - Human Retroviruses > Flashcards

Lecture 14 - Human Retroviruses Flashcards

1
Q

HIV origin? 5 theories.

A
  1. Hunter theory: SIVcpz (almost identical) transferred to humans by killing and eating animals that contained the virus in their blood (Avert)
  2. “Oral Polio Vaccine Theory”: polio vaccines prepared in chimpanzee tissue cultures were administered to up to one million Africans in experimental mass vaccination campaigns
  3. “Contaminated Needle Theory”: huge potential for the virus to mutate and replicate in each new individual it entered, even if the SIV within the original person infected had not yet converted to HIV
  4. “Colonization Theory”: many Africans were forced into labor camps where sanitation was poor, food was scarce and physical demands were extreme => poor health so SIV could easily have infiltrated the labor force and taken advantage of their weakened immune systems to become HIV
  5. “Conspiracy Theory”
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2
Q

Highest HIV prevalence in the US?

A

DC (2.4%)

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3
Q

First HIV specimen?

A

Leopoldville (now Kinshasa) in central Africa in 1959

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4
Q

3 HIV groups?

A

M, N, and O

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5
Q

Origin of HIV 1?

A

Chimpanzees

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6
Q

Origin of HIV 2?

A

Sooty Mangabeys

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7
Q

What triggered the HIV pandemic?

A

Thought to be triggered by European colonization of the African continent because before that HIV repeatedly crossed from monkeys to people, but did not spread because infected humans lived in isolated communities

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8
Q

When did HIV enter the population?

A

1908

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9
Q

How many subtypes of HIV? What are these called? What to note?

A

10 subtypes or clades

NOTE: all appear to have emerged from a single event or closely related group of events

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10
Q

Where do the largest number of cases of HIV occur?

A

Where the epidemic began in sub-Saharan Africa

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11
Q

What HIV clade is found in US/Europe?

A

B

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12
Q

What HIV clades are found in Asia?

A

A and E

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13
Q

What is Kaposi’s sarcoma?

A

Endothelial skin cancer

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14
Q

What are the 4 subfamilies of retroviruses?

A
  1. Oncovirinae (B, C, and D
  2. Lentivirinae
  3. Spumavirinae
  4. Endogenous viruses
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15
Q

What are oncovirnae associated with? 2

A
  1. Cancer

2. Neurological disorders

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16
Q

Describe subfamily oncovirnae B retroviruses.

A

They have an eccentric nucleocapsid core in mature virion

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17
Q

Example of subfamily oncovirnae B retroviruses?

A

Mouse mammary tumor virus

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18
Q

Describe subfamily oncovirnae C retroviruses.

A

They have an centrally located nucleocapsid core in mature virion

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19
Q

2 examples of subfamily oncovirnae C retroviruses?

A
  1. Human T-lymphotropic virus (1, 2, and 5)

2. Rous sarcoma virus (chickens)

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20
Q

Describe subfamily oncovirnae D retroviruses.

A

They have a cylindrical nucleocapsid core

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21
Q

Example of subfamily oncovirnae D retroviruses?

A

Mason-Pfizer monkey virus

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22
Q

Describe lentivirinae retroviruses.

A

Slow onset and cause neurological disorders and immunosuppression and have a cynlindrical nucleocapsid core

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23
Q

3 examples of lentivirinae retroviruses?

A
  1. HIV (1 and 2)
  2. Visna virus (sheep)
  3. Caprine arthritis/encephalitis virus (goats)
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24
Q

Describe spumavirinae retroviruses.

A

Cause no clinical disease but characteristic vacuolated foamy cytopathology

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25
Q

Example of spumavirinae retroviruses?

A

Human foamy virus

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26
Q

Describe endogenous retroviruses.

A

Have retrovirus sequences that are integrated into the human genome

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27
Q

Example of endogenous retroviruses?

A

Human placental virus

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28
Q

How was HIV misclassified when first discovered?

A

First thought to be an HTLV (first named HTLV-3)

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29
Q

7 features of retroviruses?

A
  1. Have a capsid containing two copies of the positive-strand RNA genome, aka diploid
  2. RNA-dependent DNA polymerase (reverse transcriptase) and integrase enzymes are carried in the virion
  3. Replication proceeds through a DNA intermediate, termed the provirus
  4. The provirus randomly integrates into the host chromosome and becomes a cellular gene
  5. Transcription of the genome is regulated by the interaction of host transcription factors with promoter and enhancer elements in the long-terminal repeat (ltr) portion of the genome
  6. Virus assembles and buds from the plasma membrane
  7. Final morphogenesis of HIV requires protease cleavage of gag and gag-pol polypeptides after envelopment
30
Q

2 types of retroviruses and the genes they encode?

A
  1. Simple retroviruses encode gag, pol, and env genes

2. Complex retroviruses also encode accessory genes (e.g., tat, rev, nef, vif, vpu for HIV)

31
Q

Describe the structure of the HIV.

A
  1. Knobs: each includes three sets of protein molecules with gp120, which is anchored to another protein called gp41
  2. Core: includes a protein called p25 or p24, RNA that carries the virus’s genetic information, and reverse transcriptase, which enables the virus to make DNA corresponding to the viral RNA
32
Q

What does gag gene stand for?

A

Group specific antigen

33
Q

What is found at both the 3’ and 5’ ends of HIV?

A

LTR

34
Q

What does pol gene stand for? What does it code for?

A

Polymerase - codes for:

  1. Polymerase
  2. Reverse transcriptase
  3. RNAse H
  4. Integrase
35
Q

Describe the life cycle of HIV. 3

A
  1. HIV (via gp120) binds to CD4 and chemokine co-receptors (CCR5) and enters by fusion
  2. The genome is reverse transcribed into linear cDNA in the cytoplasm => circular cDNA
  3. cDNA is integrated into the nuclear DNA
  4. The virus assembles at the plasma membrane and matures after budding from the cell
36
Q

What is the transcription and translation of the HIV genome similar to?

A

Fashion similar to that of HTLV-1

37
Q

What chemokine receptor is used by HIV after mutation of the env gene? What is the virus called at this point?

A

CXCR4

T-tropic virus

38
Q

Which cells does HIV infect? What does this cause?

A
  1. CD4 T cells => AIDS dementia, severe systemic opportunistic infections, Kaposi’s sarcoma, lymphoma
  2. Cells of the MO lineage (monocytes, macrophages, alveolar macrophages of the lung, dendritic cells of the skin, and microglial cells of the brain) => dysfunction, virus release, monokine release and dysregulation of immune functions

=> causes lytic and subsequently latent infection of CD4 T cells and persistent low-level productive infection of macrophage lineage cells

=> causes syncytia formation with cells expressing large amounts of CD4 antigen (T cells) with subsequent lysis of the cells

=> Alters T cell and macrophage cell function

39
Q

What are the initial stages of HIV infection mediated by?

A

Mediated by M-tropic viruses which bind to CD4 and CCR5 chemokine receptors on dendritic and other monocyte-macrophage lineage cells

40
Q

What individuals are resistant to HIV infection?

A

Individuals who are deficient in the CCR5 receptor

41
Q

What is a target for an antiviral drug against HIV?

A

CCR5 receptor

42
Q

What shifts the tropism of the HIV virus? Explain. What does this shift correlate with?

A

Mutation in the env gene for the gp120 shifts the tropism of the virus from M-tropic (R5) to T-tropic (X4 virus)

=> shift correlates with disease progression

43
Q

Can some viruses use both CCR5 and CXCR4 chemokine receptors to enter cells?

A

YUP (R5X4 viruses)

44
Q

What are 4 ways HIV escapes the immune system? Explain each.

A
  1. Inactivates key elements of immune defense by infection of lymphocytes and MOs
  2. Loss of activator of the immune system and delayed type hypersensitivity response by inactivating CD4 helper T cells
  3. Evades antibody detection by antigenic drift and glycosylation of the gp120
  4. Evades immune resolution by having a latent infection
45
Q

Role of CD4 T cells in the normal immune system?

A

Play a critical role in the regulation of the human immune response by mediating the release of soluble factors and the DTH response toward intracellular pathogens

46
Q

3 routes of transmission of HIV?

A
  1. Sexual (anal, vaginal, and oral)
  2. Exposure to blood
  3. Perinatal (pregnancy, intrapartum, and postpartum)
47
Q

Can HIV be transmitted by close personal contact?

A

NOPE

48
Q

What are the HIV disease stages defined by?

A

CD4 T cell levels and opportunistic infections

49
Q

Normal CD4 T cell count?

A

800-1,200 cells per cubic mm

50
Q

2 peaks of HIV virus (measured with p24)?

A

Upon initial infection and during stage 3

51
Q

Describe the levels of anti-HIV antibodies during the 3 stages of HIV infection.

A
  1. Stage 1: rising
  2. Stage 2: steady high
  3. Stage 3: decrease to close to 0
52
Q

At what HIV infection stage do you have AIDS?

A

Stage 3

53
Q

Describe the in vivo effects of antiretroviral treatment on HIV-1 and CD4 T cells. 3

A
  1. Upon initiation of antiretroviral therapy, the relative amount of free wild-type virus in the blood drops dramatically
  2. Simultaneously, the number of CD4 T cells in the blood rises
  3. After a relatively short time, free mutant virus, which is insensitive to the antiviral agent in use, appears at levels that eventually approach the initial titer of wild-type virus and CD4 T cells decline to nearly pre-treatment levels
54
Q

4 types of lab tests for HIV infection?

A
  1. Serology
  2. p24 antigen
  3. Isolation of virus
  4. CD4/CD8 T-cell ratio
55
Q

4 types of serological tests to detect HIV? Purpose for each?

A
  1. ELISA: Initial screening
  2. Latex agglutination: initial screening
  3. Western blot analysis of HIV antibodies: confirmation test
  4. Immunofluorescence: confirmation test
56
Q

What is the presence of p24 antigen used for?

A

Early marker of infection

57
Q

Issue with isolating HIV virus?

A

Not readily available

58
Q

What is the CD4/CD8 T-cell ratio used for?

A

Correlate of HIV disease

59
Q

Do all infected persons produce antibody against all HIV proteins?

A

NOPE

60
Q

What are the 6 major types of drugs used to treat HIV/AIDS? How are they grouped?

A
  1. Entry inhibitors
  2. Fusion inhibitors
  3. Reverse transcriptase inhibitors
  4. Integrase inhibitors
  5. Protease inhibitors
  6. Multi-class combination products

Grouped by how they interfere with steps inHIV replication

61
Q

Describe entry inhibitors.

A

They interfere with the virus’ ability to bind to receptors on the outer surface of the cell it tries to enter => when receptor binding fails, HIV cannot infect the cell

62
Q

Describe fusion inhibitors.

A

Theyinterfere with the virus’s ability to fuse with a cellular membrane, preventing HIV from entering a cell

63
Q

What are reverse transcriptase inhibitors? 2 types? Describe each.

A

They prevent the HIV enzyme reverse transcriptase from converting single-stranded HIV RNA into double-stranded HIV DNA (reverse transcription)

  1. Nucleoside/nucleotide RT inhibitors (NRTIs): faulty DNA building blocks => when one of these faulty building blocks is added to a growing HIV DNA chain, no further correct DNA building blocks can be added on, halting HIV DNA synthesis
  2. Non-nucleoside RT inhibitors (NNRTIs): bind to RT, interfering with its ability to convert HIV RNA into HIV DNA
64
Q

Describe integrase inhibitors.

A

They block the HIV enzyme integrase, which the virus uses to integrate its genetic material into the DNA of the cell it has infected

65
Q

Describe protease inhibitors.

A

They interfere with the HIV enzyme called protease, which normally cuts long chains of HIV proteins into smaller individual proteins => when protease does not work properly, new virus particles cannot be assembled

66
Q

Describe multi-class combination products.

A

They combine HIV drugs from two or more classes, or types, into a single product

67
Q

How to prevent strains of HIV from becoming resistant to a type of antiretroviral drug?

A

Recommend that people infected with HIV take a combination of at least 2 different antiretroviral drugs in an approach called highly active antiretroviral therapy (HAART)

68
Q

Is HIV enveloped?

A

YUP

69
Q

Is there aymptomatic HIV shedding?

A

YUP

70
Q

Who is at risk for HIV infections? 5

A
  1. IV drug abusers
  2. Multi-partner sexually active individuals (homosexual and heterosexual)
  3. Sex workers
  4. Newborns of HIV-positive mothers
  5. Before 1985: blood and organ transplant recipients, hemophiliacs were at risk
71
Q

Describe the drug Truvada. Purpose?

A

Composed of 2 reverse transcriptase antivirals:

  1. Tenofovir disoproxil (245 mg)
  2. Emtricitabine (200 mg)

Purpose: help reduce the risk of getting an HIV infection when used together with safe-sex practices (taken pre-exposure as prophylaxis)

SMP - MIM Part 2 (13 decks)

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