ch 17

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ch 17
2011-03-27 02:20:50


ch 17
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  1. What molecules are needed for attachment, from both the HIV and host perspective?
    • glycoprotein- gp120 & gp41
    • They bind to helper T cells (CD4), dendritric cells, and macrophages
    • for infection to be successful co-receptors are required

    • Two receptors have been identified
    • Chemokine receptor known as CXCR4

    • binds to chemokin CXCL12 and causes formation of synctia (giant cells)
    • Co-receptor CCR5

    • This doesn’t result in the formation of synctia
    • Mutations in these 2 receptors, among others, block infection
  2. Describe the acute phase of HIV infection
    • Occurs in the first few days after infection
    • virus is produced in large quantities by infected lymphocytes
    • this results in lymphadenopathy & flu-like symptoms
    • viremia is greatly reduced by ten weeks after initial infection
    • This is probably the result of cytotoxic T cells killing HIV infected cells
  3. Describe the asymptomatic phase of HIV infection
    • Begins 3-4 months after initial infection:
    • - viremia is very low
    • - occasional small bursts of virus are released
    • 3 ways in which helper T cell #’s can decline are:
    • - direct killing by the virus
    • - increased induction of apoptosis
    • - increased killing of infected helper T cells by cytotoxic T cells
    • This is a protracted phase that can last for years- clinical latency
    • during clinical latency:
    • - virus population within the host becomes more heterogeneous
    • - mutations occur w/ greater frequency
    • HIV easily mutates
  4. Describe the symptomatic phase of HIV infection
    • - Infected individuals develop clinical symptoms
    • - Helper T cell count drops below 200 per cubic milliliter of blood
    • - Cytotoxic T cell #’s are greatly decreased
    • - Viral replication increases in the lymph nodes
    • -Architecture of the lymph node deteriorates
  5. Clinical symptoms of HIV include?
    • Increased susceptibility to opportunistic infection
    • generalized lymphadenopathy
    • appearance of lesions
    • the most common lesions are thrush (normal yeast infection in the mouth) and hairy leukoplakia
  6. How does HIV progress to AIDS?
    • - approximately 10% of HIV infections progress to AIDs in the 1st 3 years
    • - to be diagnosed w/ AID CD4 count has to be low, be diagnosed w/ a specific parasitic, intracellular bacteria, fungi, or viral infection
    • - More than 80% show signs of clinical disease w/in 10 years
    • - The remaining 20% are free of disease for long periods- more than 20 years in some cases
    • - Small percentage never move past the asymptomatic phase
  7. Why does HIV replicaton work so well in T cells?
    • The greater # of opportunistic infections, the greater the # of T cells activated
    • The more T cells activated, the larger the quantity of virus particles produced
    • The more virus particles, the more infected cells and so on
  8. Dynamis of HIV replications in ppl with AIDS
    • The rate of HIV replication is astonishingly high
    • 10^10 virions are released in a single cycle of infection per infected cell per day
    • The estimated genetic diversity of HIV produced in a single infected person is greater than all the diversity seen in a worldwide epidemic of influenza