human virology......part 3...............

Question 1

Where did AIDS originate?

Answer 1

brazzavile, africa - through monkeys (hunting = blood = travel)
spread really fast to cities along the transAFRICA highways

Question 2

HIV/AIDS is linked to two rare diseases (pretty much diagnoses you)

Answer 2

opportunistic infections (PCP - fungal pneumocytisis carinii pneumonia) 
rare cancer (Kaposi's Sarcoma (KS)

Question 3

Everyone thought it was only in the gay community, but now we know..

Answer 3

it can be IV drug use, blood transfusions (hemophilia A), female sex partners too

Question 4

The process of HIV to AIDS is divided into three stages, which are…

Answer 4

1/ Acute infection (flu like- feels like you have something but you dont know what)
2/ Chronic Subclinical - when the antibodies go super high (hard to diagnosis)
3/ AIDS ( when the helper t cells are completely decreased and you full blown have the disease, the antibodies decrease now)

Question 5

Diagnostic testings for hiv/aids

Answer 5

Serology tests are used to diagnositics by testing antibodies -
this is difficult because in the chronic subclinical phase you have a shit ton of Ab’s so its hard to get a proper diagnosis (not very reliable)

Question 6

when would you get a false negative or a false positive when testing for hiv/aids

Answer 6

false negative: during window period - the infected person can transmit to a bunch of people without being known
False positive: cross reaction -making a bunch of ab’s against other shit that reacts with the proteins in the serological test

Question 7

whats a for sure way to diagnosis hiv/aids

Answer 7

PCP, virus tests, and signs and symptoms

Question 8

Whats an hiv virus test?

Answer 8

a viral antigen test: detects the presence of viral protiens

and PCR test (nucleic acids)- amplify and detects the HIV genome sequence

Question 9

Describe the mother and new-born transmission

Answer 9

its rare -
could occur through, blood, breastmilk and placenta
usally happens because of the birth process
reduce infection: 1 dose of anti hiv before birth, and to baby 72 hours after birth

Question 10

Whats the structure of HIV?

Answer 10

nucleic acid genome, with rna
diploid
has enzymes (reverse transcriptase, integrase, protease), with a protien coat, enveloped, gp120 attachment protiens

Question 11

How does the flow of information work in HIV viruses?

Answer 11

its completely different then normal ‘ it bends all the rules;
the reverse transcriptase takes RNA and transcribes it to DNA ! - thats how it can be read by the hosts - it (tricks it)

Question 12

HAART stands for:

Answer 12

highly active anti-retroviral therapy

Question 13

anti hiv therapy usually involves one and one only drug TRue of FALSE?

Answer 13

false bitches,
- it is a combo therapy usually
involves the use of two reverse transcriptase inhibitors and one protease inhibitors
-comptetive and non competitive drugs

Question 14

is AZT competitive or non competitive

Answer 14

Competitive inhibitor for HIV replication

Question 15

How does AZT work?

Answer 15

targets phosphodiester bonds -
AZT is the same as thymidine but instead of hydroxide has n3 which prevents phosphate from making the phosphodiester bonds

-the viral reverse transcriptase is 100x more susceptible to the inhibition by AZT then the dna polymerase
AZT is best

Question 16

what is a 3tc nucleotide like competitive RT inhibitor

Answer 16

hep b is also a retrovirus so works for that too -
it structured the same as thymide but instead of hydroxide, its sulfur
-competitive inhibitor cause its similar to the nucleotide

Question 17

What is nevirapine?

Answer 17

an aids drug that is non competitive TY inhibitor
- good blocker for mother and child transmission
combo therapy with AZT, resistant mutations not likely to be at multiple sites
-Therapeutic index : >10,000 = used on babies, its safe and works at low concentrations

Question 18

What is protease inhibitor?

Answer 18

protease inhibitors are substrate analogs - stick enzymes with something other then the actual substrate ( binds to it and stops it form cutting itself out of cell and spreading the virus) - aka inhibiting HIV

Question 19

what are we expecting with HAART?

Answer 19

increased level of t helper cells (500/microL)
viral load decreases and u cant infect others
infectivity- full adherence to drug

Question 20

describe efficacy and effectiveness in medical treatment

Answer 20

efficacy: what you get in a lab under close and indeal circumstances
effectiveness: real life mofo

Question 21

what is the major target for HIV to get into cells?

Answer 21

T helper cells - they do this by gp120 binding to the t cells

Question 22

How else besides gp120 does HIV enter the cell?

Answer 22

chemokine receptor CCR5 is necessary

Question 23

Describe why having a mutation in the CCR5 receptor is a good thing

Answer 23

cuz its a way that HIV gets into the cell- so if you have a mutated or fucked up CCR5, it can never get in! - blessing in disguise!

Question 24

What does CMV cause in people with aids?

Answer 24

blindness x(

Question 25

Name some functional abnormalities causes by aids and immuno-suppression

Answer 25

• PCP
  -Candidalsis
  Toxiplasmis
  TB
  HERPES
  EBV, KS (type 8 herpes)

Question 26

Why is it so hard to make a vaccine for hiv?

Answer 26

because it changes so much - by the time you develop antibodies or the vaccine starts to activate your immune system - the virus has already changed so much - so its fucking redundant and dumb to make a vaccine