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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
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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
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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
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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
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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
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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
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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
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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
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