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30 Cards in this Set
- Front
- Back
What is the structure of HIV?
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Has a lipid envelope that is studded with gp120, attached to gp41 (embedded in the LE). Also incorporates HLA antigens from host.
Contains the matrix protein (MA), which surrounds the capsid protein (CA), kind of like nucleus. CA contains 2 single stranded RNA and viral enzymes: protease, integrase and reverse transcriptase. |
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What are the critical genes in HIV structure formation, and what do they generally do?
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gag/pol --> MA, CA, PR, RT, IN
(everything inside lipid envelope) env --> TM, SU (gp41, gp120) |
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What is the function of protease? reverse transcriptase? integrase?
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PROTEASE
First, gag and pol are transcribed from the whole RNA. Protease splits the transcription into functional segments REVERSE TRANSCRIPTASE Makes dsDNA from RNA template. INTEGRASE Integrates DNA into host chromosome. |
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How does HIV enter the cell?
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Must attach first to a CD4 (Th cells and macrophages/dendritic cells).
Then binds a co-R: Th cells - CXCR-4 macrophage/dendritic cells - CCR5 The membranes fuse and the capsid protein enters the cell. |
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What are the stages of HIV?
What are the implications of each stage? |
INITIAL
Experience "flu" like symptoms (ARS), during short incubation (6d - 6w). Huge drop in CD4, body can't fully recover. Most infectious because high level of circulating HIV. ASYMPTOMATIC Can last months to years. Virus continues to deplete CD4+ lymphocytes. Immune system tries to replenish, but can't keep up with virus. AIDS (Disease stage) CD4 count drops below 200/microL. AIDS defining disease come on. |
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What are AIDS defining diseases?
Common examples? |
These are those that only appear in immunocompromised individuals. Die from complications due to these, not HIV.
Ex: diarrhea (Wasting syndrome); meningoencephalitis, pneumonia, malignant tumors, etc. |
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Why is HIV so hard to fight?
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Rapid mutator: reverse transcriptase makes a lot of mistakes. Mutates surface antigens constantly.
Also, HLA antigens on surface keep it from initial detection. |
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How is HIV transmitted?
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breast milk/transplacental infection
semen/vaginal fluid (predominantly heterosexual) blood contact Note: once out of the body, practically dead. It's a fragile virus. |
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How is HIV diagnosed?
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ELISA used to screen for antibodies (serocoversion in patient). Because there are many false positives, a Western blot is done for antibodies to confirm.
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How do we treat HIV?
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HAART (highly active antiretroviral therapy)
Cocktail of drugs that attacks multiple facets (i.e. multiple viral enzymes) to keep the viral load low, and to avoid it mutating and evading a single attack. Must stay on the drugs, otherwise virus has a chance to mutate resistance. |
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Acute Infection
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characterized by symptoms that have rapid onset, but don't last very long
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chronic infection
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develops slowly
lasts for months/years |
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colonization
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establishment/growth of microorg on body surface
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disease
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condition that results in noticeable impairment of body function
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endotoxin
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part of GN bac outer membrane
lipid A responsible for toxicity Response: fever, DIC, low BP Note: heat stable, so confuses immune system. |
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exotoxin
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toxic protein produced by microorg
simply: toxin |
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infection
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colonization by pathogen on or within body
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latent infection
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infectious agent is present but not causing symptoms
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opportunistic pathogen
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microorg or virus that causes disease only when introduced into an unusual location or into an immunocompromised host
ex: S. aureus |
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primary infection
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infection by microorg/virus that is able to cause disease in otherwise healthy individual; org is called primary pathogen
ex: adenovirus |
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virulence factors
(determinants) |
attributes of a microorg or virus that promote pathogenicity
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Describe the standard pattern (stages) of infection...
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Incubation period: usually no symptoms.
Prodromal period: starting to feel bad Acute period: signs/symptoms (i.e. fever, rash, etc.) Convalescent period: recuperation/recovery |
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secondary infection
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occurs during/immediately after the primary infection
ex: bacterial pneumonia due to the flu |
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Koch's postulates
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1) all cases must present microorganism
2) organism must be grown in a pure culture from diseased host 3) cultured organism must infect healthy host with disease 4) organism must be recovered from infected host |
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What are the 2 types of exotoxins and what do they do?
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Note: both are secreted and heat labile
AB toxin B binds A is activated when cleaved Superantigen Nonspecifically activate Th cells by binding to TCR and MHC II. This induces cytokine storm. Body cannot handle inflammatory response. |
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plague
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sporadic outbreaks of epidemic
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outbreak
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epidemic limited to a region/population
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What is the difference between LD50 and ID50?
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LD50 = lethal to 50% of inoculated subjects
*ID50 = infectious to 50% inoculated subjects |
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What factors affect epidemiology?
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dose
incubation period population characteristics (i.e. herd immunity) |
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What is the difference between hypersensitivity and autoimmune response?
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Hypersensitivity
immune system overreacts to a potential threat Autoimmune response immune system mistakenly destroys itself |