Mcro 251 Hiv And Epidemiology

Front 1

What is the structure of HIV?

Back 1

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.

Front 2

What are the critical genes in HIV structure formation, and what do they generally do?

Back 2

gag/pol --> MA, CA, PR, RT, IN
(everything inside lipid envelope)

env --> TM, SU
(gp41, gp120)

Front 3

What is the function of protease? reverse transcriptase? integrase?

Back 3

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.

Front 4

How does HIV enter the cell?

Back 4

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.

Front 5

What are the stages of HIV?

What are the implications of each stage?

Back 5

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.

Front 6

What are AIDS defining diseases?

Common examples?

Back 6

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.

Front 7

Why is HIV so hard to fight?

Back 7

Rapid mutator: reverse transcriptase makes a lot of mistakes. Mutates surface antigens constantly.

Also, HLA antigens on surface keep it from initial detection.

Front 8

How is HIV transmitted?

Back 8

breast milk/transplacental infection
semen/vaginal fluid (predominantly heterosexual)
blood contact

Note: once out of the body, practically dead. It's a fragile virus.

Front 9

How is HIV diagnosed?

Back 9

ELISA used to screen for antibodies (serocoversion in patient). Because there are many false positives, a Western blot is done for antibodies to confirm.

Front 10

How do we treat HIV?

Back 10

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.

Front 11

Acute Infection

Back 11

characterized by symptoms that have rapid onset, but don't last very long

Front 12

chronic infection

Back 12

develops slowly
lasts for months/years

Front 13

colonization

Back 13

establishment/growth of microorg on body surface

Front 14

disease

Back 14

condition that results in noticeable impairment of body function

Front 15

endotoxin

Back 15

part of GN bac outer membrane
lipid A responsible for toxicity
Response: fever, DIC, low BP


Note: heat stable, so confuses immune system.

Front 16

exotoxin

Back 16

toxic protein produced by microorg
simply: toxin

Front 17

infection

Back 17

colonization by pathogen on or within body

Front 18

latent infection

Back 18

infectious agent is present but not causing symptoms

Front 19

opportunistic pathogen

Back 19

microorg or virus that causes disease only when introduced into an unusual location or into an immunocompromised host

ex: S. aureus

Front 20

primary infection

Back 20

infection by microorg/virus that is able to cause disease in otherwise healthy individual; org is called primary pathogen

ex: adenovirus

Front 21

virulence factors
(determinants)

Back 21

attributes of a microorg or virus that promote pathogenicity

Front 22

Describe the standard pattern (stages) of infection...

Back 22

Incubation period: usually no symptoms.

Prodromal period: starting to feel bad

Acute period: signs/symptoms (i.e. fever, rash, etc.)

Convalescent period: recuperation/recovery

Front 23

secondary infection

Back 23

occurs during/immediately after the primary infection

ex: bacterial pneumonia due to the flu

Front 24

Koch's postulates

Back 24

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

Front 25

What are the 2 types of exotoxins and what do they do?

Back 25

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.

Front 26

plague

Back 26

sporadic outbreaks of epidemic

Front 27

outbreak

Back 27

epidemic limited to a region/population

Front 28

What is the difference between LD50 and ID50?

Back 28

LD50 = lethal to 50% of inoculated subjects

*ID50 = infectious to 50% inoculated subjects

Front 29

What factors affect epidemiology?

Back 29

dose
incubation period
population characteristics (i.e. herd immunity)

Front 30

What is the difference between hypersensitivity and autoimmune response?

Back 30

Hypersensitivity
immune system overreacts to a potential threat

Autoimmune response
immune system mistakenly destroys itself