Y2B3 Micro- Aids And Immune Evasion-1

Front 1

which country is most afflicted with HIV-infected population?

Back 1

sub-saharan african- 22.5 million

Front 2

T/F

Prevalence of AIDS has decreased. Incidence has Increased.

Back 2

FALSE

Prevalence (the number of cases) has increased and incidence (the number of NEW cases) has decreased.

Front 3

which HIV virus is responsible for AIDS in the USA and most other parts of the world? what HIV virus is responsible for AIDS in West Africa and India? Describe them

Back 3

US: HIV-1--> enveloped w/ two copies of its genome--> ssRNA
WA&I: HIV-2--> genome is significantly different from HIV-1 and this virus causes a slow progression to AIDS.

Front 4

what is the only 2x stranded RNA virus?

Back 4

riovirus

Front 5

what is the #1 cause of infantile diarrhea?

Back 5

rotovirus under riovirus family

Front 6

what is the first molecule that attaches to the host cell membrane in HIV? what molecule is the most important molecule for viral entry into the host cell?

Back 6

GP120; GP41

Front 7

what protects the HIVirus from being attacked?

Back 7

heavy glycosidation and mutation

Front 8

which capside antigen in the HIVirus is highly mutagenic? what is the first ab that you will see in a body of a pt w/ HIV? how do you detect that ab?

Back 8

p24; p24- via elisa.

Front 9

what three enzymes are critical for host cell replication in someone who has HIV? what do we use these enzymes for?

Back 9

reverse transcriptase, integrase and protease. We use these three enzymes as targets by anti-viral medications.

Front 10

what matrix protein help maintain the viral structure and transports viral genome to host cell nucleus in a pt w/ HIV?

Back 10

p17

Front 11

what are 6 HIV viral genes that we need to know?

Back 11

GAG- group Antigen
POL- polymerase
ENV- Envelope
TAT-
REV-
NEF-

Front 12

HIV positive pt presents w/ a mutation in p24 gene, which gene is mutated?

Back 12

GAG because gag codes for matrix, capsid and nucleocapside (P24 and P17)

Front 13

HIV positive pt is resistant ot protease inhibitor, which gene is mutated?

Back 13

POL because polymerase codes for protease, reverse transcriptase and integrase.

Front 14

HIV positive pt presents with a mutation in GP120, which gene is mutated?

Back 14

ENV- codes for surface glycoproteins like GP 120 and GP 41 which are responsible for viral entry into the cell.

Front 15

what is the fxn of Tat? Rev?

Back 15

Tat is a transactivator. It is a positive regulator for transcription.
Rev transfers spliced and unspliced molecules from nucleus to cytoplasm.

Front 16

Magin Johnson has been HIV positive for 20 years without progressing to aid, where is the mutation most likely located?

Back 16

nef gene. --> BOARDS --> non white individual that is not progressing to AIDS. most likely is a mutation in the nef gene.

Front 17

what three genes are common to all retroviruses and their protein products?

Back 17

Gag, pol, env genes

Front 18

what does gp120 bind to?

Back 18

CD4 and CCR5

Front 19

what co-receptor is associated with macrophagetrophi HIV cells? what co-receptor is associated with T-cell trophic HIV cells?

Back 19

CCR5

CXCR4

Front 20

what allows the HIV virus to release all of its core materials into the host cell?

Back 20

GP41- via its very strong anchor

Front 21

what enzyme converts HIV RNA into DNA? what is the formula?

Back 21

RNA dependent DNA polymerase

Template dependent product polymerase

Front 22

what happens after the HIV virus enters the cell?

Back 22

1) it uncoats- envelope and rna separate
2) RNA--> DNA
3) Complementary strand is formed- 2x dna and become circular
4) introduced into the host's cell system via integrase
5) host duplicate and so does the viral genome
6) Transcribe RNA and some of the rna will be used as mRNA (structural proteins)
7) reassemble and the HIV will be released via envelop

Front 23

what is the method of release by HIV?

Back 23

budding

Front 24

what is it called when a virus is integrated into a cells genome?

Back 24

provirus

Front 25

T/F

Transcription cannot shut off unless Tat turns it off.

Back 25

true

Front 26

what does the Fab portion do? what does the Fc portion do?

Back 26

Fab-bind to the antigen

Fc-FC receptors on phagocytes

Front 27

in order for a B cell to functional, what does it need help from? what hampers their aid against HIV?

Back 27

CD4+ cells- TH2. Destruction of CD4+ cells leads to B cells not being able to do much. That's why it leads to a lymphoproliferation of B cells.

Front 28

at what CD4 count do we consider the pt to have AIDS?

Back 28

below 200cells/ microliter

Front 29

HIV infected Pt presents w/ rash, enlarged lymph nodes and headaches, dx

Back 29

Acute retroviral syndrome

often confused w/ flu or infectious mononucleosis.

Front 30

IN acute retroviral syndrome, when can you isolate the virus from blood semen and cervix?

Back 30

during the asymptomatic period following the initial sxs (sore throat, fever, muscle and headaches, enlarged LN, rash).

Front 31

what are AIDS associated illnesses?

Back 31

malignant noeplasms (kaposis sarcoma, lymphomas, predominantly B cell lymphomas, cervical or anal carcinoma) or opportunistic infections.

Front 32

what is the definition of AIDS?

Back 32

all patients who are HIV antibody-positive and have CD4+ T cell counts below 200/mm3 have the disease

or, all patients who are HIV antibody-positive and have less than 14% of total T cells have the disease

Front 33

what type of diagnostic method do you use to monitor your AIDS pt over a long time?

Back 33

RPCR: reverse transcriptase PCR

Front 34

how do you diagnose a newborn born of an HIV mother?

Back 34

Regular PCR not a RPCR.

Front 35

how do you confirm an HIV diagnosis? what does a positive sample exhibit?

Back 35

Western-blot analysis- a positive sample should exhibit antibodies to both envelope and GAG proteins or to both envelope proteins (41 and 120/160 kD)

Front 36

CCR5 is a receptor for which chemokines?

Back 36

CCL3 (MIP-1a)
CCL4 (MIP-1b)
CCL5 (RANTES)

Front 37

what population has developed a resistance to HIV? how is that possible?

Back 37

Caucasoid populations d/t a mutation of the CCR5 receptor which induces a certain degree of immunodeficiency which is an advantage. They maintain a high level of CD4 cell count and very low levels of HIV yet never progress to AIDS.

Front 38

how do prevent mother to child transmission when concerned about HIV?

Back 38

antiretroviral agents during pregnancy and labor
use of C-section
formula-feeding

Front 39

what is the biggest challenge against developing anti-HIV vaccine?

Back 39

high rate of mutation

Front 40

what are the four basic mechanisms of immune evasion by HIV?

Back 40

- rapid multiplication of HIV virus
- very high mutation rate giving rise to high antigenic variation: host immune response fails to keep up w/ the rate of change in antigenic epitopes.
- elimination of CD4 T cells by a myriad of immune mechanisms
- misdirected and exhausted B cell response.

Front 41

what is the mechanism of microbial evasion of immune defense of S. pneumoniae? what is the result?

Back 41

capsule- avoids phagocytosis

Front 42

what is the mechanism of microbial evasion of immune defense of M. Tb? what is the result?

Back 42

mechanism: blocks lysosome fusion w/ phagosome
results: avoids antibody and complement opsonization, macrophage killing

Front 43

what is the mechanism of microbial evasion of immune defense of Listeria monocytogenes? what is the result?

Back 43

mech: escapes phagosome into cytoplasm
result: avoid marcophage killing, presentation on class II MHC

Front 44

what is the mechanism of microbial evasion of immune defense of herpes virus? what is the result?

Back 44

mech: persist in host cells w/o dividing (latency)
Result: avoid immune system recognition

Front 45

what is the mechanism of microbial evasion of immune defense of Influenza virus and HIV? what is the result?

Back 45

mech: antigenic variation
result: avoids memory response

Front 46

what is the mechanism of microbial evasion of immune defense of Neisseria M and G and Haemophilus influ? what is the result?

Back 46

mech: expresses IgA protease
result: Avoids IgA neutralization

Front 47

what is the mechanism of microbial evasion of immune defense of EBV? what is the result?

Back 47

mech: inhibits host cell expression of LFA-3, ICAM-1
Result: blocks adhesion of CTL to infected cells

Front 48

what is the mechanism of microbial evasion of immune defense of CMV? what is the result?

Back 48

mech: inhibits host cells class I expression
result: blocks CTL recognition

Front 49

what is the mechanism of microbial evasion of immune defense of mycobacterium leprae? what is the result?

Back 49

mech: stimulates Th2 response (more severe form of the dz)
results: suppresses Th1 response (less from of dz)

Front 50

what type of vaccines should be avoided in HIV-infected pts?

Back 50

live vaccines

Front 51

HIV infected pt presents with a CD4 count of 150 and has never had their MMR vaccine, should you give it to them?

Back 51

nope no siree to both

Front 52

which immunizations are not advised in pts w/ HIV disease?

Back 52

oral poliomyelitis
oral typhoid
BCG
varicella-zoster
yellow fever

Front 53

HIV infected pt presents with a CD4+ cell count of <200, what prophylaxis (es) would you give the individual?

Back 53

PCP--> TMP-SMX

Front 54

HIV infected pt presents with a CD4+ count of less than 50, what new prophylaxis should you start them on?

Back 54

MAC prophylaxis--> azithromycin or clarithromycin + ethambutol

Front 55

HIV infected pt presents with a CD4+ count of less than 100, what new prophylaxis should you start them on?

Back 55

Toxo prophylaxis--> TMP-SMX

Front 56

HIV infected pt presents with a ppd+ induration >5 mm, what new prophylaxis should you start them on?

Back 56

INH

Front 57

what is the goal of HAART? what is HAART composed of?

Back 57

Highly active antiretroviral therapy--> inhibit infection of uninfected CD4+ T cells which will control antiviral replication.
Composed of 2 reverse transcriptase inhibitors and 1 protease

Front 58

what are the current guidelines recommended for starting HAART?

Back 58

in any patient with symptomatic HIV infection or an AIDS-related condition, regardless of the CD4+ T cell count
Or
when the CD4+ T cell count falls below 200/mm3 [

Front 59

what is the current combination drug for HIV pts?

Back 59

ATRIPLA- combo of 3 HIV medicines

Front 60

what are the two categories of reverse transcriptase inhibitors currently in use?

Back 60

nucleoside reverse transcriptase inhibitors (zidovudin, stavudin, lamivudin, didanosine, and zalcitabine)
non-nucleoside reverse transcriptase inhibitors (nevirapine, delavirdine, and efavirenz)

Front 61

what are the four protease inhibitors used in anti-HIV tx?

Back 61

saquinavir, ritonavir, indinavir, nelfinavir.

Front 62

how do NRTI's work?

Back 62

they are structurally similar to the purine and pyrimdine components of viral nucleic acids and during viral replication the viral transcriptase incorporates the NRTIs to the growing DNA chain instead of viral nucleosides which results in blocking the completion of the DNA strand. This stops the extension of the nucleotide and thus stops viral replication.

Front 63

what is the second line of drug for anti-HIV?

Back 63

fusion inhibitor- only given if pt shows resistance to the 1st line of drug.

Front 64

what 2nd line drug interferes w/ the entry of HIV-1 into cells? how does it do that?

Back 64

enfuvirtide- d/t inhibiting fusion of viral and cellular membranes. It prevents the conformational changes of GP41 required for the fusion of viral and cellular membranes.

Front 65

what is the integrase inhibitor that is used to tx HIV pts? what is its mechanism of action?

Back 65

Raltegravir- 2nd line of drug. Its blocks the activity of the integrase enzyme and thus prevents HIV DNA from meshing w/ healthy cell DNA.

Front 66

why do you never use a single protease inhibitor?

Back 66

because all it needs is a single mutation which will develop resistance to the virus to the protease inhibitor.

Front 67

why can you use a single reverse transcriptase inhibitor?

Back 67

this one needs multiple independent mutations to develop resistance, not a single mutation like protease inhibitors.

Front 68

what are the four malignant conditions complicating AIDS?

Back 68

Kaposi's sarcoma
non-hodgkin's lymphoma
lymphoma of the brain
cervical and anal carcinoma

Front 69

what are the three mechanisms involved in retrovirus replication?

Back 69

-oncogenes (interfering w/ regulatory cell signaling)
-insertional mutagenesis (insertion of a provirus into the cellular DNA next to a proto-oncogene
-expression of trans gene that transcriptionally activate other cellular genes that coordinates uncontrolled cellular proliferation.

Front 70

what is the counter part of a viral oncogene?

Back 70

cellular oncogene

Front 71

at the genetic level, what happens to cause a retroviral transformation?

Back 71

there is a mutation that causes a frame shift leading to misaligned ONCO and env genes or gag-pol- env genes.

Front 72

what population that is HIV negative is associated with kaposi's sarcoma?

Back 72

mediterranean and East european

Front 73

what virus is associated with Kaposi's sarcoma (besides HIV)?

Back 73

HHV-8 or herpesvirus

Front 74

what color will the lesion of kaposi's sarcoma be if it affected a vein? what color is it if it involves an artery?

Back 74

deep purple; angry red

Front 75

HIV positive pt living at home with a cat presents with small bumps on the blood vessels, dx

Back 75

Basillary angiomastosis- bartonella hensale

Front 76

what cells are affected w/ kaposi's sarcoma?

Back 76

endothelial cells lining blood vessels and lymphatic vessels.

Front 77

what would you see histologically on a cell that has been infected with HHV-8?

Back 77

1) the cells assume a spindle shape and proliferate
2) extensive formation of new blood vessels occur

Front 78

what significantly increases the incidence of kaposi's sarcoma? why?

Back 78

If a pt infected with HIV-1 is also infected w/ HHV-8. One idea is that HIV-1 induced Tat Protein induces proliferation of endothelial cells and co-infection w/ HHV-8 favor malignant transformation of these cells.

Front 79

what growth factor causes proliferation of endothelial cells?

Back 79

vascular endothelial growth factor (VEGF)

Front 80

what virus is associated with B cell lymphoma in AIDS pts? where is the lymphoma located? why does it happen?

Back 80

EBV- burkitt's lymphoma located in the mandible, maxilla and abdomen.
why?- CD21 is expressed on B cells and that is the EBV receptor. That is why EBV loves to attract B cells.

Front 81

HIV positive pt presents in your office with a large mass growing on their maxilla. They inform you that they just immigrated to the US from W. africa. You do a biopsy and the report shows a proliferation of B-cells. DX

Back 81

Bukitt's lymphoma caused by EBV

Front 82

what is the causative agents of cervical and anal cancer? what strands does the vaccine contain?

Back 82

human papillomavirus 16 and 18 (these 2 are malignant)

vaccine: genital warts 6 and 11, malignancy 16 and 18

Front 83

what would you see on histological evaluation of a cell w/ malignant HPV?

Back 83

koilocytes- enlarge nucleus surrounded by perinuclear halo in the cytoplasm.