Microbiology - Hiv And Prions

Front 1

What is gag?

Back 1

Gene that encodes for p24 capsid, the nucleocapsid in HIV

Front 2

What is env?

Back 2

Gene that encodes for gp41 and gp120 proteins, the envelope proteins in HIV.

Front 3

What is p17?

Back 3

Interior envelope protein in HIV

Front 4

What is p24?

Back 4

Nucleocapsid protein in HIV, coded for by gag gene.

Front 5

What is gp41?

Back 5

Envelope protein which traverses bilayer. If it is a mushroom stalk, then gp120 is the head. Both coded for by env.

Front 6

What is gp120?

Back 6

Envelope protein that serves as mushroom cap to gp41 stalk. Both coded for by env.

Front 7

What is pol?

Back 7

Gene which codes for HIV reverse transcriptase

Front 8

HIV diagnostic tests

Back 8

Presumptive diagnosis: ELISA (sensitive, high false-positive rate, and low threshhold) - Confirmation: Western blot assay (specific, high false-negative rate, and high threshold) - PCR viral load used to monitor drug therapy on viral load

Front 9

Timeframe for HIV diagnosis

Back 9

ELISA/Western blot often: Falsely negative in first 1-2 months of HIV infection - Falsely positive initially in babies born to infected mothers (anti-gp120 crosses placenta)

Front 10

AIDS diagnosis

Back 10

One of the following: 1. less than 200 CD4 cells 2. HIV positive with AIDS indicator condition (eg pneumocystis infection) 3. CD4/CD8 ratio less than 1.5

Front 11

CCR5 mutation: What does it mean in terms of susceptibility?

Back 11

HIV susceptibility.
Homozygous = immunity
Heterozygous = slower course (long-term non production)

Front 12

CXCR1 mutation: What does this mean in terms of susceptibility?

Back 12

HIV susceptibility.
Rapid progression to AIDS.

Front 13

What is the likelihood of CCR5 mutation among Caucasians for homo and heterozygous?

Back 13

% of US caucasians: Homozygous: 1 Heterozygous: 20

Front 14

Relative HIV-related levels aproximately 1.5 months after infection

Back 14

In descending order:
1. CD4 lymphocytes (initial through)
2. Virus p24 antigen (initial peak)
3. Anti-p24 Ab
4. Anti-gp120 Abs - Highest period of acute symptoms

Front 15

Relative HIV-related levels aproximately 2 months after infection

Back 15

In descending order:
1. CD4 lymphocytes (rise from initial trough back to near pre-infection levels before leveling out [the mark of end of acute symptoms])
2. Anti-p24 Ab (Reaching peak [not reached until approximately 3 years])
3. Anti-gp120 Abs (Reaching peak [not reached until approximately 3 years])
4. Virus p24 antigen (very low levels)

Front 16

Relative HIV-related levels more than 3 years after infection: Early phase

Back 16

In descending order:
1. CD4 lymphocytes (begins linear descent)
2. Anti-p24 Ab (descent begins at faster rate than CD4)
3. Anti-gp120 Abs (slow descent begins)
4. Virus p24 antigen (slow rise)

Front 17

Relative HIV-related levels more than 3 years after infection: First middle phase

Back 17

In descending order:
1. CD4 lymphocytes (continues linear descent)
2. Anti-gp120 Abs (slow descent continues)
3. Anti-p24 Ab (having dropped below Anti-gp120, descent continues at slower rate)
4. Virus p24 antigen (fast rise begins)

Front 18

Relative HIV-related levels more than 3 years after infection: Second middle phase

Back 18

In descending order:
1. CD4 lymphocytes (continues linear descent) AND
2. Virus p24 antigen (already passed gp-120 Abs and about to pass CD4 lymphocytes)
3. Anti-gp120 Abs (slow descent continues)
4. Anti-p24 Ab (approximately 1/3 amount of p24 antigen, slow descent continues)

Front 19

Relative HIV-related levels more than 3 years after infection: Third middle phase

Back 19

In descending order:
1. Virus p24 antigen (already passed gp-120 Abs and about to pass CD4 lymphocytes)
2. CD4 lymphocytes (continues linear descent, about to drop below anti-g120 Abs)
3. Anti-gp120 Abs (slow descent continues)
4. Anti-p24 Ab (approximately 1/3 to 1/4 amount of p24 antigen, slow descent continues)

Front 20

Relative HIV-related levels more than 3 years after infection: Late phase

Back 20

In descending order:
1. Virus p24 antigen (leveled out at nearly 20x anti-p24 antibody)
2. Anti-gp120 Abs (little less than half p24 antigen)
3. Anti-p24 Ab (1/20 amount of p24 antigen) AND
4. CD4 lymphocytes

Front 21

Opportunistic infections and disease in AIDS attacking the brain

Back 21

1. Cryptococcal meningitis 2. Toxoplasmosis 3. CMV encephalopathy 4. AIDS dementia 5. PML (JC virus)

Front 22

Opportunistic infections and disease in AIDS attacking the eyes

Back 22

CMV retinitis

Front 23

Opportunistic infections and disease in AIDS attacking the mouth and throat

Back 23

1. Thrush (Candida albicans) 2. HSV 3. CMV 4. Oral hairy leukoplakia (EBV)

Front 24

Opportunistic infections and disease in AIDS attacking the lungs

Back 24

1. Pneumocystis pneumonia (PCP) 2. TB 3. Histoplasmosis

Front 25

Opportunistic infections and disease in AIDS attacking the GI tract

Back 25

1. Cryptosporidiosis 2. Mycobacterium avium-intracellulare complex 3. CMV colitis 4. non-Hodgkin's lymphoma (EBV)

Front 26

Opportunistic infections and disease in AIDS attacking the skin

Back 26

1. Shingles (VZV) 2. Kaposi's sarcoma (HHV-8)

Front 27

Opportunistic infections and disease in AIDS attacking the genitals

Back 27

1. Genital herpes 2. Genital warts 3. Cervical cancer (HPV)

Front 28

When does HIV encephalitis occur?

Back 28

Late in the course of HIV infection

Front 29

Mechanism of HIV encephalitis

Back 29

Virus gains CNS access via infected macrophages

Front 30

Pathologic presentation of HIV encephalitis

Back 30

Microglial nodules with multinucleated giant cells

Front 31

What are prions?

Back 31

Infectious agents that do not contain RNA or DNA, only proteins, that are encoded by cellular genes.

Front 32

Diseases caused by prions

Back 32

1. Creutzfeldt-Jakob disease 2. Kuru 3. Scrapie (in sheep) 4. Mad cow disease (association with human spongiform encephalopathy) 5. Fatal familial insomnia

Front 33

What is Creutzfeldt-Jakob disease

Back 33

Prion caused disease with rapid progressive dementia

Front 34

Mechanism of prion pathology

Back 34

Normal proteins (alpha-helices) become pathologic (beta-pleated sheets)