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BIO 435: Virology > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

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Biology 101 flashcards
1
Q

Go over the structure of HIV?

A

Enveloped virus
- Obtains envelope when budding from host cell

Cone-shaped capsid w/ key glycoproteins

  • gp 120
  • gp 41 “transmembrane protein”
       - linear RNA genome 
         (2 identical + ss RNAs)
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2
Q

What are the key virion proteins that have to come in w/ the 2 ssRNA segments?

A

RT (reverse transcriptase)
IN (integrase)
PR (protease)

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3
Q

What do the various structural DNA segments code for?

A

Gag - structure
Pol - polymerase
Env - envelope
Extra gene segments to code for accessory proteins

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4
Q

HIV is a Member of what subfamily?

A

lentivirus subfamily of retroviruses

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5
Q

How does HIV infect and kill the very cells that the body needs to fight the infection?

A

Macrophages + Dendritic Cells infected first (APC) then interact w/ T helper cells and infect them

Depletion of CD4+ Thelper cells over time

RNA RT virus replication creates alot of mutations = immune cells can’t keep up w/ viral mutation
Immune system can keep viral load at low levels but can’t clear virus

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6
Q

Go over attachment/entry of HIV.

A

CD4 is primary receptor => gp120 binds CD4 receptor on cell surface

Co-receptor Engagement by gp120
- gp120 changes structure => can now bind coreceptor

CCR5 (chemokine receptor 5) or CXCR4
- CCR5 most common coreceptor that is bound

As virus remains, more CXCR4 coreceptors are bound
More aggressive form of HIV
gp41 binds for fusion to occur and entry into cell

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7
Q

What happens after HIV enters host cell?

A

(+) ssRNA => DNA via reverse transcriptase

Binds ssRNA and synthesizes complementary (-) ssDNA strand

RT binds (-) ssDNA strand and synthesizes (+) dsDNA strand

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8
Q

What does HIV DNA do once in host?

A

Integrase takes newly synthesized viral (+) dsDNA and integrates into host genome

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9
Q

How does HIV produce viral proteins?

A

Transcription/Translation of Viral Proteins

  • Cellular DNA Dep RNA Polymerase transcribes viral mRNA
  • Viral mRNA exits nucleus
  • Cellular ribosomes translate the viral mRNA into viral polyproteins
  • Polyproteins have to be cleaved into functional units by viral protease
  • Polyprotein collect at cell surface and join newly replicated viral ssRNA
  • Protease cleaves polyprotein into individual proteins

Now an infectious virion and can exit via budding and gain envelope
- Protease inhibitors (antiviral) stop polyprotein cleavage

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10
Q

How are GP 120 and GP 141 made?

A

Gp41 + gp120 are made via RNA translation in the RER and processed in golgi then sent to cell surface so when virion buds the proteins are on the envelope surface

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11
Q

What happens to virus after the surface proteins are made?

A

Assembly and release via budding

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12
Q

What are phases of HIV?

A

ACUTE (1-2 months)
- flu or mono-like symptoms

ASYMPTOMATIC (8-10 yrs)

  • “clinical latency”
  • immune system in constant battle with HIV

AIDS

  • immunodeficiency (<200 CD4+)
  • diseases of nervous, respiratory, and gastrointestinal systems
  • opportunistic infections (KS, PCP, thrush)
  • death
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13
Q

What are the Opportunistic Infections Arising During Clinical AIDS?

A

conditions most commonly associated with immune-suppressed persons

Kaposi’s sarcoma (KS)

Candidiasis (thrush)

Pneumocystis carinii pneumonia (PCP)

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14
Q

What are the different outcomes for HIV patients?

A

1) Rapid progressors ≈ 10% progression to AIDS within 2 years
- co-infection with other pathogens (activated T cells) correlate w/ rapid progression
- Activated T cells b/c of other STDs spread virus faster
- higher viral load during asymptomatic phase

2) Intermediate progressors ≈ 80% develop end stage disease within 10 years

3) Slow progressors ≈ 10% are AIDS free for over 20 years
- strong cytotoxic T cell (CTL) response
- high number of CD4+ T cells

4) Non-progressors (rare)
≈ 0.1-1% asymptomatic no progression to AIDS
- co-receptor mutations (CCR-5)

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15
Q

What are the Factors influencing the rate of disease progression?

A

1) Treatment
- intervention with drug therapies
- access to health care
- compliance with treatment regimen

2) HIV strain
- viral load

3) Co-infection with other pathogens

4) Host factors
- genetics co receptor mutation = slower progression
- CD4+ T cell numbers

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16
Q

WHere did HIV come from?

A
  • HIV-1 evolved from the closely-related

simian immunodeficiency virus (SIVcpz)

17
Q

What are the types of HIV?

A

M = Major: most HIV strains
> 90% of HIV isolates
Responsible for most epidemics

N = New: rare
- discovered in 1998

O =Outlier: rare
- restricted to West-Central Africa

18
Q

How is HIV transmitted?

A

1) Humans are the sole reservoir

2) Spread by direct contact with
     HIV-infected cells, blood, semen

3) Modes of transmission
        - intimate contact (STD)

          - i.v. drug use

          - mother to child
                in utero
                breast-feeding
19
Q

What factors influence HIV transmission?

A

Presence of other STDs

 - herpes, gonorrhea, syphilis (activated CD4+ T Cells)
 - genital ulcerations, abrasions

Risk behaviors

  - iv drug use (needle sharing)
  - number of partners

Education (decrease transmission)

   - preventive measures against infection
   - safer sex practices

Geopolitical

  - poverty
  - wars
  - breakdown of national borders
  - migration of large populations
20
Q

What are the types of HIV drugs?

A

RT inhibitors

Protease inhibitors

HAART

21
Q

What are RT inhibitors?

A
  • blocks HIV replication
  • early in virus lifecycleWh
    Drawbacks:
    • toxic side effects
    • emergence of resistant HIV strains
22
Q

What are protease inhibitors?

A
  • blocks the ability of the viral protease to
    cleave virus proteins into functional units
  • end of virus lifecycleDrawbacks:
    - toxicity
- emergence of drug-resistant HIV
23
Q

What are Highly active antiretroviral therapy (HAART)?

A
  • “Drug cocktail”
    2 RT inhibitors + 1 protease inhibitor
    • decrease in HIV resistant strains
    Drawbacks:
    • toxicity
    • does not eliminate HIV
24
Q

What are the new HIV drugs?

A

Fusion Inhibitors
- blocks fusion of viral envelope with
plasma membrane

Entry Inhibitors
- binds HIV co-receptor CCR5
and blocks entry

Integrase Inhibitors
- Blocks HIV integration into the
host genome

25
Q

What are the limitations of HIV drug therapy?

A

1) Daily, life-long therapy
- cost
- strict compliance to medication regimen required

2) Acute and chronic toxicities
- hyperlipidemia
- neuropathy
- muscle wasting

3) Drug resistance

26
Q

What are the Major hurdles to the development

of an HIV vaccine?

A

high mutation rate

  • large number of different HIV strains

failure to stimulate the appropriate immune response

lack of small animal models

political/ethical issues involved with testing live
attenuated vaccines

BIO 435: Virology (18 decks)

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