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MHD > Retroviruses II > Flashcards

Retroviruses II Flashcards

1
Q

HIV Transmission

  1. How infectious is it?
  2. How is it not spread?
  3. What body fluids is it found in?
  4. What cells are infected?
A
  1. not particularly infectious/contagious
  2. not by respiratory, alimentary, or vector routes
  3. plasma, semen, vaginal fluids
  4. Peripheral blood mononuclear cells, semens, vaginal/cervical fluid
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2
Q

HIV Transmission

  1. What increases HIV transmission?
  2. How stable is HIV in the enviroment?
  3. What are some ways to reduce HIV infectivity in the environment?
A
  1. Genital ulcer disease
  2. not stable
  3. air drying, heating, 10% bleach, 70% alcohol, pH extremes (10), detergents
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3
Q

HIV strain variation

  1. What clade predominates in US and Europe?
  2. What clade predominates in Thailand?
  3. What clade is spreading in Africa?
  4. What is the trouble with developing vaccines?
A
  1. B
  2. E
  3. C
  4. HIV is genetically plastic, hard to make vaccines against it
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4
Q

HIV Structure

  1. Surface proteins
  2. Proteins in the core
  3. Genome
A
  1. gp120 and gp41
  2. ribonuclease H, protease, integrase
  3. diploid ssRNA
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5
Q

HIV Infection

  1. What 2 cell types can it infect?
  2. How does it infect each one?
  3. What can give immunity to HIV?
A
  1. T cells and macrophages
  2. gp 120 variant can bind CXCr4 on CD4+ T cells
    gp 120 variant can bind CCr5 on Macrophages
  3. increased Beta-chemokines that bind CCr5 can block the receptor and lead to protection from infection
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6
Q

HIV infection

  1. What does HIV require to infect cells?
  2. What if a pt doesn’t have this?
A
  1. CCr5 to infect macrophages

2. pt does not get HIV/AIDS

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7
Q

HIV pathogenesis

  1. What kind of replication does HIV go through?
  2. What extra stuff does HIV have?
A
  1. classic retroviral replication program w/ notable complexities
  2. accessory genes controlling pathogenicity: tat and rev
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8
Q

HIV genes

  1. What does tat do?
  2. What does rev do?
A
  1. transcription activator

2. allows newly synthesized mRNA to move quickly into the cytoplasm

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9
Q

HIV pathology

  1. What does it do to CD 4+ cells?
  2. What is seen in lymph node? Why?
  3. What 2 words cahracterize HIV infection?
  4. Why is HIV infection of CD4 T cells dangerous?
A
  1. forms highly vacuolated blasts that don’t last long
  2. multi-nucleated giant cells; HIV induces CD4+ cells to express gp120 –> fusion
  3. robust and cytolytic
  4. CD4 cells regulate the immune system; allows virus to evade/modify immune responses
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10
Q

Three Stages to HIV induced disease

A
  1. Infection
  2. Seroconversion
  3. AIDS
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11
Q

Serology of HIV

  1. What occurs early to CD4 cells?
  2. What happens then?
  3. What happens to precipitate AIDS?
A
  1. transient decline in CD4 cells
  2. rebounds, but CD4 cells don’t ever recover to pre-infection levels
  3. Drop in CD4 cells
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12
Q

Serology of HIV

  1. What happens to viral load early? middle? late?
  2. What happens to Ab to HIV Env and p24?
  3. What happens to HIV-specific CTL?
A
  1. large increase early; falls middle; rises as AIDS sets in
  2. increase in Ab early that stays high, then drops as AIDS sets in
  3. rises early and stays high, then drops as AIDS sets in
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13
Q
  1. What are the three ways HIV can progress?

2. What are the 3 main parts of the HIV progression?

A
  1. Typical (normal, 12+ years); Rapid Progressor (–> AIDS w/in months); Nonprogressor (stays clinically latent for years)
  2. Acute Infection, Clinical Latency, Clinical Disease (AIDS)
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14
Q

Acute Infection

  1. What disease does it look like?
  2. When is it observed?
  3. Symptoms
  4. What happens to T cells?
A
  1. mono-nucleosis
  2. 3 weeks after initial infection
  3. fever, fatigue, swollen lymph nodes; symptoms can vary considerably; most don’t seek medical care for these symptoms
  4. T cell levels drop, may rebound slightly, but rarely reach pre-infection levels
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15
Q

Clinical Latency

  1. How long does it last?
  2. Clinical Manifestations
  3. What is the virus doing?
  4. What can be detected in blood?
A
  1. 8-12 years
  2. few, if any
  3. not latent, high levels of viral replication;
  4. live, infectious virus
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16
Q

Treatment of HIV disease

  1. What is HAART?
  2. What does it target?
  3. What is the danger in using 1 drug?
A
  1. Highly-Active Anti-Retroviral Therapy
  2. Reverse transcriptase and protease
  3. virus is plastic; it can proliferate and generate resistance to a single drug easily
17
Q

HIV treatment

  1. How do RT inhibitors work?
  2. How doe protease inhibitors work?
  3. When are mutations in viral DNA created? (2)
  4. What does #3 mean?
A
  1. block reverse transcription
  2. prevent virion capside morphogenesis
  3. reverse transcription and forward transcription
  4. 1000s of viruses can be released from 1 cell which can differ from each other in >1 nucleotide position
18
Q
  1. What is the goal of HAART?

2. Why must HAART be prolonged?

A
  1. lower the virologic set point: lower viremia correlates with slower disease progression
  2. There are latently-infected cells that are long-lived; pt must be compliant
19
Q

Clinical Disease of HIV (AIDS)

  1. What occurs when CD4 T cell counts fall below 500/ul?
  2. What occurs when CD4 T cell counts fall below 200/ul?
  3. What occurs in lymph nodes in prolonged infection?
A
  1. AIDS related symptoms appear: oral lesions, basal cell carcinomas, latent activation of herpes, mycobacteria infections
  2. protozoal, bacterial, and fungal infections; viral infections and malignancies (Kaposi’ Sarcoma); Neurological disorders (AIDS dimentia- macs bring virus to CNS)
  3. degeneration of follicular-dendritic cell network; hard to repair
20
Q

What occurs in the degeneration of lymph node follicular dendritic cell network?

A

Vigorous immune response to HIV is elimnated and virus spills over into circulation and there is a loss of HIV-specific immune responses;
Pt has lost the ability to respond to other pathogens as well –> compounding of immunosuppression

21
Q
  1. How is HIV similar to HTLV? (2)

2. How are they different? (3)

A
  1. similar transmission patterns and both are common
  2. HTLV has lower disease penetrance than HIV (only 1% of infected individuals get the disease)
  3. HTLV has a longer clinical latency period (over 20 years from infection to clinical disease)
  4. HTLV causes T cell leukemias by immortalizing T cells; it doesn’t encode a classic viral oncogene
22
Q
  1. What protein does HTLV have that increases transcription?

2. What protein does HTLV cause T cells to make in order to make them proliferate more?

A
  1. tax protein

2. IL-2

MHD (17 decks)

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