Path Fall Final Hiv

Front 1

what are the routes of transmission for HIV

Back 1

1. Sex- body fluid. most common world wide
2. needles
3. verticle, mom to infant

Front 2

what factors increase the likihood in sexually contracting HIV

Back 2

infection FROM a male who is NOT cicumscised
increased transmission if you have other STD- esp those that cause ulcers (HSV, syphalis, chancroid) chlamydia, gonorrhea


**virus is in mononuclear cells in semen and just floating around. virus gets to host via
1. Abrasion (rectal, oral, vaginal) puts inoculum directly into blood
2. Direct Contact with mucosal dendritic cells.

*the virus is just hanging out in the seman and the recipient of the seman can get HIV through abraisions or bu uptake of the virus by their own dendritic cells or CD4 cells

**decreased transmission with circumscision

Front 3

what are the 2 ways HIV is taken up in the recipient of sex

Back 3

sexual recipient gets the infection

HIV in semen (in mononuclear cells and free floating)

HIV enters recipient
1. through abraisions, direct entry into blood
2. taken up by dendritic cells or CD4 cells

Front 4

what is paraenteral HIV transmission

Back 4

needles, transfusions,

effectient for transmission

Front 5

how is HIV spread from mom to babe

Back 5

from the birth itself, not placental
Really depeneds on MATERNAL viral load

Breast milk- well this is the thing breast milk is REALLY good at fighting infection so in places with high infection rates you breast feed anyway in US you DO NOT breast feed

Front 6

how can health care workers prevent HIV nocosomial

Back 6

be safe, if you do get stuck ask permission to test pt.

start on ANTIRETROVIRAL therapy IMMEDIATLY

Front 7

will kissing transmit HIV

Back 7

nope, no salivary transmission

Front 8

what are some of the basics of HIV

Back 8

causes AIDS
retrovirus
HIV1- common in US, out focus
HIV2- common in W africa

Front 9

describe the structure of HIV virus.

there WILL be a q on this

Back 9

Caspid protein, p24. AG that is detected

2 copies of ssRNA genome

3 enzymes: protease, reverse transcriptase, integrase

Envelope: gp120, gp41

Front 10

what is...

p24
gp120
gp41

Back 10

p24- caspid protein, uused as AG to test for HIV infection

gp120, gp41: envelope glycoprotein

Front 11

what enzymes does HIV bring to the party

what is the HIV genome

Back 11

1. reverse transcriptase, protease, integrase

2. 2 copies of ssRNA

Front 12

what are hte genes and gene products of HIV

Back 12

1. ENV- gp120, gp41
2. gag, pol: protein precursors. gag- p24 (AG for testing) pol- enzymes (protease, reverse transcriptase, integrase)
3. regulators of synthesis nad assembly of viral particles: rev, vif, nef, vpr, vpu, tat
4. tat- transactivator. increases viral replication 1000x!!!

Front 13

what does this HIV gene make?

ENV
GAG
POL
REV, VIF, NEF, VPR, VPU,
TAT

Back 13

ENV- gp120, gp41. viral envelope

GAG- p24. AG used in HIV test

POL- enxymes (integrase, protease, reversetranscriptase)

REV, VIF, NEF, VPR, VPU- regulators of viral synthesis and viral assembly

TAT- increases viral replication 1000x

Front 14

what is the mech of HIV infection in the mucosa

Back 14

1. Abrasion- direct entry of HIV into blood

2. Dendrites in recipient take it up or CD4 take it up

**the HIV wants to get into immune cells (macro,T, dendritic) or the CNS

Front 15

what immune cells are infected by HIV

Back 15

T cells
Macrophages
dendritis cells

**these cells then migrate to lymphoid tissue and remain in the resevoire for HIV infection. --> long latency

Front 16

describe the mech of infection of immune cells by HIV, include receptor and viral interaction

Back 16

1. HIV gp120 binds to CD4 T cells, macro, and microglia in CNS

2. CCR5 or CXCR4 are chemokine co receptors on our cells that HIV gp120 binds to

3. binding causes conformational change in gp41, insertion of fusion peptide into cell membrane

4. Viral ssRNA genome enters our cytoplasm

Front 17

loss of what cell is that cause of the severe immunosuppression in clinical AIDS

Back 17

CD4 T cells


**CD4 is actually the R that HIV binds to initially in infection (CD4 found in T, macro, microglia)

Front 18

how are gp120, gp41, CD4, CCR5 all related

Back 18

gp120, gp41- on HIV
CD4, CCR5- on us

1. gp120 on HIV binds to our CD4
2. We get a conformaitonal change and gp120 binds to our CCR5
3. Another conformational change and gp41 on HIV which allows it to insert fusion peptide into our cell membrane and the HIV viral core enters our cytoplasm

Front 19

what is the significance of a CCR5 mutation

Back 19

well... lets recap HIV mech of infection
1. gp120 on HIV binds to our CD4
2. then gp120 binds to CCR5
3. we get a conformational change that allows gp41 on HIV to do membrane fuision and HIV RNA enters our cytoplasm

SO... if you cant get that second signal you wont get AIDS hard and fast

Homozygous- dont get AIDS
hetero- delayed development of AIDS

CCR5 antagonist for HIV tx

Front 20

whats M trophic and T trophic HIV

Back 20

** describes ability of virus to bind co receptors on us like CCR5

M trophic; bind to CCR5 on macro and T cells

T trophic: bind only CXCR4 on T cells. more virulent, emerges in final disease stage,

M to T evolution caused by mutations in gp120

Front 21

what are the main points in the lifecycle of HIV

Back 21

1. gp120 binds CD4 and chemokine CCR5 (CD4, T macro or microglia)
2. gp41 fuses membrane and RNA enters our cell
3. HIV RNA genome is reverse transcribed into proviral DNA
4. Integrase puts viral DNA into our genome
5. Cytokine R stim causes our cells to replicate DNA (including HIV that is now incorporated)
6. HIV RNA transcript is packaged into a new virion and exported.

**are are HIV making machines!!!!

Front 22

after HIV RNA enters the cytoplasm bc of gp41 fusion what happens

Back 22

RNA --> DNA by viral reverse transcriptase

it can...
1. remain episomal and be a latent quiescent cell
2. Integrate into host DNA with integrase

**stim to replicate DNA when cytokines stim CD4 to replicate....Everytime we have an infection (EBV, CMV, Hep B) and want to ilicit an IR we are actually making MORE HIV. HIV also can stim these cytokines

Front 23

how is HIV DNA that is integrated into host CD4 DNA stim to replicate

Back 23

by cytokines (IL2) that stim CD4 cells

**so everytime we need CD4 cells we are making more virus, can be other AG (EBV, CMV, hep B) or the HIV itself that causes this

Front 24

what are the infections that commonly help HIV progress by stim CD4 to replicate via cytokine release

Back 24

1. EBV
2. CMV
3. Hep B
4. HIV itself

**diminished T cell fx predisposes to thse infections. but really anything can provoke CD4 replication

Front 25

what are the mechs for CD4 t cell loss in HIV infection

Back 25

we have HIV causing chronic T cell activation

1. Viral replication in infected Cd4 leads to death of infected cells, cytopathic effect of virus

2. activation of UNINFECTED t cells, activation induced apoptosis

3. Expression of HIV peptides on infected CD4 T cells--> killing by CTL

Front 26

what is latent infection of T cells

Back 26

provirus is integrated into genome, T cells not dividing in LN can hang out for years/months and/or serve as a resevoir of virus and escape antiviral therapy

Front 27

ok so we saw that HIV just wipes out our T cells (3 mechs, not asked to know specifically), whats the consequence of this (think of the 5 cells that CD4 interacts with)

Back 27

CD4: decreased response to soluble AG, decreased lymphokine secretion

CD8: decerased specific cytotoxicity

Macro: diminished cytotoxic ability, decreased chemotaxin, decreases IL1 secretion, poor AG presentation, cant form granulomas

NK cells: decreased killing of tumor cells

B cells: depressed Ig production in response to NEW AG. will have increased Ig but its no good

Front 28

can HIV pts make granulomas

Back 28

nope,

NO good macro to present AG to CD4 Th1 cells

Front 29

so if we have no CD4 T cells...

Back 29

these are PIVITOL in regulating the immune response

1. Lymphopenia: decreased CD4 ratio. we should have 2x more CD4 than CD8

2. susceptible to opprotunistic infections

3. Susceptible to neoplasms

4. Decreased type IV hypersensitivity reaction, NO granuloma formation (no skin tests)

Front 30

what is the Cd4:CD8 normally, what is it in HIV

Back 30

usually we have way more CD4 than CD8

in HIV we have decreased CD4, so we have an inverted ratio

Front 31

why do we have hypergammaglobunemia with AIDS infection

Back 31

B cell activation

EBV infection will activate B cells

we get SO much AB we can actually get autoimmune disease bc we can deposit complexes.

but we also have a decreased ability to make AB agaisnt NEW AG --> risk for s pneumonia, H influenza

Front 32

ok so in AIDS we have...

1 Lymphoopenia
2. Decreased/Altered T cell Fx
3. Polyclonal B cell Activation and
4. Altered Mono/Macrophage fx.

list an example from each category, what is the overarching reasion we have all of this

Back 32

all of this is bc of DECREASED CD4 fx

1. Lymphopenia: decreased CD4, incerted CD4:CD8 ratio

2. Decreased T cell Fx: loose memory T cells, susceptible to opprotunistic infections nad neoplasm, decreased skin tests (HS 4 rxn)

3. Altered T cell Fx: decreased specific sytotoxicity

4. Polyclonal B cell activation: hyperagammaglobuniema, no response to NEW AG, risk for immune complex deposition

5. Altered Macro: poor presentation, decreased MHC II, decreased chemotaxis and phago

Front 33

how do macro contribute to HIV infection

Back 33

HIV resevoire, its the trojan horse of HIV. it holds HIV and carries it around, will disseminate to the CNS


**HIV likes CNS, micro glia take it up and also macro takes it to CNS

Front 34

how do mucosal dendritic cells contribute to HIV

what about follicular dendirtic cells

Back 34

1. mucosal dendritic- take up HIV in the mucosa (the seman has HIV and then the HIV enters the host through abraision or mucosal dendritic cells- send to LN)

2. in germinal centers of LN, resevoire for HIV. trap virus particles on cell surface that is AB doated. virions are released to maintain the infection

Front 35

what cell does HIV hang out in and be carried all through the body by this cell

Back 35

macrophage

Front 36

describe the pathogenesis of the CNS infection by HIV, what is the morphology

Back 36

CNS is a major target of HIV

1. HIV carried to CNS by macro/mono and infect microglia --> form giant cells

*neuron samage by soluble ivral products, gp41 and gp120 ad soluble factors from microglia

Front 37

where might we see giant cell formation as a result of HIV infection

Back 37

CNS

Front 38

what are the 3 phases of untreated HIV infection

Back 38

1. Acute retroviral Syndrome: early acute HIV infection. T cells drop and virus is on the rise

2. Middle chronic phase (latent)

3. clinical aids

Front 39

what are the clinical and lab findings of acute retroviral syndrome

Back 39

T cells decline, Virus increases

Front 40

whats the deal with HIV AB

Back 40

ehh, good fro dx but dont help fight infection

**show up like 3 weeks after infection, can get diarrhea, large LN, mono like illness. if you test for mono, test for HIV

**hmm bc thhe serology is + by 12 weeks. this is the set point adn indicated disease progression

Front 41

what happens in the primary HIV infection

Back 41

mucosal CD4 are infected and depleted

virus is low level in blood

dendritic cells disseminate HIV to LN

in the LN more cells are infected

Front 42

how are mono and HIV related

Back 42

all pts with mono are also tested for HIV.

**the acute retroviral syndrome can mimic mono like illness. also diarrhea and rash- seroconversion rash

Front 43

what is the set point of viral load, how does it impact the natural history of the HIV infection

Back 43

sert point is when the virus load drops really low

*this is a strong predictor of disease progression. it its a low viral load is a better outcome

Front 44

what goes on with the T cells throughout the progression of an HIV infection

what goes on with the virus load during HIV infection

Back 44

initialy sharp decrease and then we get a bit of a rebound. then there is just a steady decline

sharp increase then during latency its down to like non, then as we progress into the late phase it starts to incline more and more til you die

Front 45

when are HIV infected T cells killed and then rebound and then we get to a viral set point

Back 45

early acute HIV infection


**viral load drops off to low set point at 12 weeks

Front 46

what are hte ABC categories of HIV

Back 46

A- asymptomatic acute HIV, persistent generalized lymphadenopathy

B- symptomatic, not A or C

C- AIDS indicator conditions (>500, if CD4 is more than 500, you DONT have AIDS)

Front 47

whats persistent generalized lymphadenopathy

Back 47

enlarged LN at multiple sites- follicular hyperplasia. can be seen in the "A" category infection. occurs in some pts in whom it persists throughout latency

Front 48

what happens in the latent/middle chronic phase of HIV infection

Back 48

continuous replication of HIV in LN/spleen

CD4 gradually decreases as viral load slowly increases

lasts 7-10 years

HIV +, low levels of detectable virus in blood.

can be asymptomatic, thrombocytopenic or some minor opprotunisitc infections

Front 49

in what phase of HIV infection are you HIV AB + and you have low levels of detectable virus

Back 49

latent (chronic middle)

**may be asymptomatic, minor opprotunistic infection, or thrombocytopenia

Front 50

in clinical AIDS what is going on

Back 50

1. DRAMATC increase in virus load in blood.
2. DROP in CD4
3. Fever for more than 1 month
4. HIV + and any AIDS indicator, opprotunistic infections or AIDS related neoplasm

Front 51

when CD4 lymphs are... whats the A/B

>500
200-499
<200

Back 51

>500 A1/B1

200-499 A2/B2

<200 A3/B3

Front 52

what things will increase the rate of progression of HIV

Back 52

large innoculum as seen with blood transfusion
OLD at seroconversion
when acute is symptomatic
infants
smoking
HIGH viral load set point

**low set point will be the best indicator of slow progression, CCR5 mutation

Front 53

what things decrease the rate of progression of HIV

Back 53

if you are asymptomatic for more than 10 years
low viral set point, stable Cd4
CCR5 mutation
* infection by nef mutated virus
Th1 dominant response to infection (Th1 will kill, Th2 will lead to AIDS faster)

Front 54

is infection with a nef mutated virus good or bad for us

Back 54

good!!! slower progression of disease

Front 55

who gets tested for HIV

Back 55

1. anyone who asks
2. high risk behavior
3. other STD
4. ppl with TB, Hep B/C, mono
5. recurrent shingles (or a young person with shingels)/candidia
6. ppl in prisions

Front 56

what labs are used to dx HIV
what is used to follow the course of disease

Back 56

1. Initial- serology to detect for AB, p24 detection. confirm with Western Blot

2. Monitor course of disease with virual load. and CD4 cells

Front 57

what are the significant levels of CD4 T cells and correlations

Back 57

>500: no opprotunistic infections

<200: less than 200 IS AIDS, will have opprotunistic infections

Front 58

when will we start seeing opprotunistic infections in HIV + pts

Back 58

when CD4 cells are LESS THAN 200!!!!

Front 59

This 38 y/o male presented to the ER with a history of HIV and fever of 104o, dysuria with pain in the prostate on urination, and watery diarrhea. He was seen 1 month earlier for burning dysphagia that was diagnosed as esophageal candidiasis. He previously had Pneumocystis jiroveci pneumonia, and CMV retinitis for which he took gancyclovir. It was discontinued due to elevated serum creatinine. He had multiple Kaposi’s sarcoma lesions of
the face, arms and chest. His central line though
which he received some medications had to be
removed due to gram negative sepsis. He had
severe wasting. Six weeks earlier, he stopped
his antiviral drugs in discouragement.
His CD4+ lymphs were 8 (>goal 500)
His viral load was 53, 000/mL
What is his stage of HIV?

Back 59

Kaposi indicated sexual transmission

Late stage, AIDS

when CD4 >200 its AIDS, and viral load is REALLY HIGH

Front 60

what kills the AIDS pt
when will HIV/AIDS get neurologic conditions
what are some signs

Back 60

opprotunistic infections

neurologic: will always get it, even if you are on meds. HIV LOVES the CNS

fever, weight loss, diarrhea, generalized lymphadenopathy

Front 61

why do AIDS pts age prematurely

Back 61

testosterone deficiceny

Front 62

HIV wasting is...

Back 62

difining AIDS sx

you better have CD <200

Front 63

what are some things we see with pediatric HIV

Back 63

pneumocystic jiroveci pneumonia
lymphocystic interstitial pneumonia
Molluscum contagiosum

**will see clubbing of the fingers bc of chronic pulm distress

Front 64

what are the characteristics of pediatric HIV infections

Back 64

they get puffy little cheecks bc of parotid gland enlargement (spleen, liver, nad LN too!)

URI can be the only sign (non of the diarrhea stuff like adults get)

if untreated its fatal is less than 10 years- FAST progression. remember we talked about this being a factor for fast progression

Front 65

infections and neoplasms are really common with HIV infections, what else is common with HIV

Back 65

CNS, Aids nephropathy, diarrhea, GI bleed, skin, pneumonis, mucosa

Front 66

what is teh common respiratory infection seen in AIDS, whats teh morphology

Back 66

PCP- pneumocystis jiroveci, RESTRICTIVE lung disease. makes foamy exudate. dx with silver stain

will have CD4 <200!!! prophylax with trimethiprim sulfa

Front 67

Pneumocystis jiroveci, what the deal with this and AIDS

Back 67

its common in AIDS
**restrictive lung disease
**dx with silver stain
**alveolar foamy exudate
**CD4 <200, its opprotunistic,
**prophylax with trimethiprim silfa

Front 68

describe candida infection in HIV

Back 68

its common in early HIV infections, its part of normal flora but is opprotunistic. can also occur in latency

**get it oral (thrush) and vaginal,

**when its in the esophagous, trachea or pneumonia, its AIDS defining

**budding yeast with germ tubes

**

Front 69

what is the white mucous pseudomembrane that is seenin HIV pts, when do you see it

Back 69

in the mouth and vagina in early infections

esophagous, trachea and pneumonitis is AIDS defining

Front 70

what are hte locations nad morphology of CMV in HIV pts

Back 70

in AIDS it causes infections outside of the normal places like LN, liver, and spleen! Commonly with aids its in the GI --> ulcers and diarrhea
*can also be ling and brian, can cause blindness

**ID this micro on test

Front 71

what is the thing that gives AIDS pts ulcers, where else can it be

Back 71

CMV- normally causes infections in LN, spleen and liver. with AIDS its in other places like GI, brain, nad ling. can also cause blindness

**ID this on the test!

Front 72

if you see a viral inclusion with halo whats the problem

Back 72

CMV, its the one that AIDS gets and they get ulcers

CMV in the lings, little inflammation. KNOW THIS PIC

Front 73

whats the relation btwn HIV and Herpes zoster and herpes simplex

Back 73

Herpes Zooster is HIV associated with HIV when it is in a young person, recurrent, involves 2+ dermatomes, leision lasts for months

Herpes Simplex: normally its self limited and short duration and causes cold sores. in HIV leisions involve mucosa in the esophagous, lungs, or temporal bones

Front 74

in HIV what causes temporal lobe encephalitis

Back 74

HSV

*temporal lobes are infected

Front 75

how are EBV and HIV related

what diseases are associated with this virus

Back 75

common, polyclonal B cell activation- polyclonal gammapathy

**causes HIV related B cell lymphoma and hairy leukoplakia- tongue leisions

Front 76

what causes hairy leukoplaquia, what else

Back 76

EBV, EBV also causes poly clonal B cell activation for b cell lymphomas

Front 77

what are the manifestations and significance of Mycobacterial disease in HIV

Back 77

seen when CD4 <50 (recall <200 is AIDS), uncommon if you are immunocompetent.

colonizes GI, respiratory tract--> disseminates to LN, spleen, liver

Sx: fever, chills, night sweats, anemia

**its significant bc it means our T cells are super low- bad prognosis, can disseminate easily

Front 78

what causes diarrhea in HIV

Back 78

**caused by things that dont normally cause diarrhea in normal ppl

**protozoa- cryptosporidiosis, massive fluid loss (ring enhanceing leision is abcessd)
**shigella and salmonella

Front 79

why test ppl with TB for HIV

Back 79

Mycobacterium tuberculosis (MAC) is more common when Cd4 are super low. if our pt has TB they prbly have a depleted immmune system

Front 80

This 34 y/o male was admitted to the hospital
c/o shortness of breath, fever and abdominal
pain for 1 week.
He had a history of HIV for 7 years duration.
He was bisexual, the father of 4 children.
Previous illnesses in the past year included
CMV retinitis for which he took gancyclovir,
microsporidiosis (cause of diarrhea), anemia
and pancytopenia. On physical exam, his temperature was 101o.
He evidenced wasting and dyspnea. He had
extensive molluscum contagiosum.
A nodule in the lung was new since his previous
chest x‐ray 5 months earlier. He underwent
bronchoscopy and washings yielded Candida
and Mycobacteria that was identified as MAI
Lab:
WBC 2480 (5,000‐10,000/mm3)
68% segs, 2 bands, 22 lymphs and 8 monos.
Hb 11.8 (14‐16 gm), Hct 36.8%
CD4+ lymphs were 4 ( > 500 goal)
Stool cultures were positive for MAI

He developed headaches and a CT
demonstrated a large ring enhancing mass
with edema and midline shift.
Presumptive diagnosis of toxoplasmosis was
made.
Neurologic disease progressed with left leg
 paralysis, confusion, incontinence and
 convulsions.
He died during his second week of
hospitalization.

Back 80

CD4 was 4, AIDS

so with MAI you get TB but NO GRANULOMA

toxoplasmosis is CNS lymphoma/abcess

Front 81

whats molluscum contagiosum

Back 81

bumps on HIV pts

Front 82

what brain leision is associated with toxoplasma

Back 82

cerebral abcess, ring enhancing defect

prophylax against this when CD4 <100

Front 83

what 2 vascular leisions are associated with HIV and what is that direct cause of each

Back 83

1. Bacillary Angiomatosis: caused by bartonella. not common in immunocompetent ppl. red papules, subcu nodules, liver, spleen, LN involved. can be related to AIDS dementia, responds to AB

2. Kaposies: HHV8, slit like vascular channels and spindle cells

Front 84

what is bacillary angiomatosis

Back 84

its a vascular leision caused by bartonella in HIV pts

causes red plaues and subcut nocules on the liver, spleen, LN. can contribute to AIDS dementia. Responds to AB

Front 85

what are the AIDS related neoplasms

Back 85

1 Lymphoma- usually a B cell caused by EBV.

2. CNS lymphoma

3. Carcinoma- caused by HPV.

**Dysplasia progresses rapidly to carcinoma in situ
to invasive squamous cell carcinoma

4. Kaposi: HHV8, more common with sexual HIV transmission. AIDS defining

Front 86

what causes B cell lymphoma in aids pts

what causes carcinoma in aids spts

Back 86

EBV

HPV

Front 87

is kaposi AIDS defining

Back 87

yes

can be skin, liver, stomach

SLIT LIKE VASCULAR channels nad spindle cells

Front 88

what are the types of CNS involvemnt in HIV

Back 88

90% have neurologic involvemnet

**CNS can be the only sx or early sx

Front 89

whats the deal with HIV tx

Back 89

antoretroviral, decrease viral load,

switch drugs as necessary

**side effects of drugs are a major problem

Front 90

what are the complications of antoretroviral therapy

Back 90

SIDE EFFECTS

Lipodystrophy Syndrome
-2 to protease inhibitors
-redistributes fat: peripheral wasting, central obesity, buffalo hump
- Metabolic Problems: glucose intolerance, frank Diabetes

Front 91

why might a person with HIV have a buffalo hump and central obesity

Back 91

side effect of therapy- LIPODYSTROPHY

*residtribution of fat
*metabolic problems --> glucose intolerance, and frank diabetes

Front 92

ok so a kid with HIV might have chipmunk cheecks bc...

an adult with HIV might have chipmunk cheecks bc

Back 92

1. parotid gland enlargement

2. lipodystrophy, redistribution of fat and metabolic havoc as a side efect of entiretroviral tx

Front 93

This 53 y/o man had HIV‐related lymphoma,
in remission. CD4+ lymphs were 510/uL,
 HIV RNA 5000 copies/mL.
Indinavir was added to zidovudine and lamivudine
with nondetectable HIV RNA load and CD4+
count increasing to 918.
Cholesterol increased to 298, triglyceride to 239
(<180), glucose intolerance was noted.
There was fat redistribution as illustrated: facial,
 buffalo hump and abdomen.

Back 93

super high fats, redistrubution of fat as a result of treatment. lipodystrophy

510 Cd4 is good!

central adiposity and peripheral wasting, buffalo hump

Front 94

what is immune reconstruction inflammatory disease

Back 94

complication of antiretroviral tx

appearance of symptoms nad infections as CD4 t count increases (infection present b4 therapy is started becomes symptomatic- masked)

**happens in 25% of treated AIDS pts, can take 30 weeks to develop after initiation of therapy

Front 95

what does antiretroviral tx do to the liver and kidney

Back 95

TOXIC!!!!

can have non AIDS related morbidity bc of the drugs that treat it.

Front 96

A 28 y/o man presents c/o flu‐like symptoms.
He has lymphadenopathy, fever and a diffuse
 rash.
A monotest is negative.
He gives a history of “recreational” drug use
and unprotected sex with several partners in the
past year.
HIV antibody is positive and confirmed.
CD4 count is 550/ml
HIV RNA level is 735,000 copies/ml

what is it HIV stage

Back 96

CD4- 550
RNA Virus- SUPER HIGH

acute retroviral syndeome

Front 97

A 22 y/o woman in the 1st trimester of her
first pregnancy is in good health w/o
complaints. She is tested for HIV as part of
the antepartum evaluation.
 HIV antibody test is positive and confirmed.
CD4+ T cell count is 275 copies/mL
Plasma HIV RNA level is 127,000 copies/mL

WHat HIV stage, will her baby be infected

C‐section indicated if HIV RNA copies >1000 at
term
‐ Study: c‐section reduced rate of neonatal HIV
by up to 5x
• Infant should receive zidovudine (oral syrup)
for 6 weeks
‐ If mother’s HIV has no resistance to this drug

Back 97

CD4- 275, close to AIDS, end of clinical latency
RNA high

**with a high viral load its 50% you will oass it. maternal viral load is the strongest predictor

Front 98

A 34 y/o man presents to the ER with a chest
rash typical of herpes zoster. The physician
believes the patient to be unusually young for
this diagnosis and obtains a history of
 recreational cocaine use.
Patient denies having thrush or pneumonia.
HIV antibody test is positive and confirmed.
CD4+ T cell count done 5 weeks later: 425/mL
HIV RNA: 70,000 copies/mL
What is his stage of HIV infection?

Back 98

CD4- 425.
VIral RNA-

Latency, but bc we are getting zooster we think its the end of latency

Front 99

Mrs. A suffered a perforated viscus in 1980.
• She received blood transfusions during the
surgery and contracted HIV. She had been
actively and continuously treated for her infection
and was taking AZT*, Epivir*, Invirase+,
and Norvir*. (+ protease inhibitor; *reverse
transcriptase inhibitor).
• She was hospitalized in 2005 with fever,
confusion, severe dehydration and difficulty
swallowing. She had type II diabetes mellitus

Mrs. A, Labs
• WBC 1,200/dL (5000‐10,000)
• Hb 9.6g/dL (12‐14) Hct 28%
• Platelets 34,000 (>150,000)
• B2microglobulin 9.7 (<1.85)
• Absolute lymphocyte count: 368 (1500‐4500)
• CD4 49 (500‐1740)
• CD8 186 (180‐1170)
• CD4/CD8 ratio 0.25 (0.86‐5.00)
• HIV RNA quantitation by bDNA <75 copies/ml
• What stage of HIV infection?

Back 99

leukopenic, thrombocytopenic, anemia- common in AIDS

B2 microglobulin- lots of inflammation

CD4:CD8 is <1 so inverted (normal is 1)

CD4 <200 so AIDS

Front 100

Mrs. B is a 33 y/o female with HIV x13 yrs.
• She has a history of IV drug abuse and
continued ETOH abuse. She smokes tobacco.
She has valvular disease from IE and end stage
renal disease. She is G4P4
• She presents with nausea, vomiting, weakness.
• Her ARV therapy is Epivir, Zerit, Acyclovir.
• She takes diflucan for candida and bactrim for
Pneumocystis jiroveci/carinii prophylaxis.

WBC 6,300 (5,000‐10,000)
• Hb 11.5 gm (12‐14) Hct 34 %
• MCV 103 (80‐100)
• Platelets 18,000 >150,000
• Diff: 83% segs; 1% lymphs; 8% bands; 4% eos
1% basos, 2% metamyelos, 1% myelo, 3NRBC
• Absolute lymphocyte count 106
• CD4 count < 20; helper/suppressor ratio 0.24
• HIV Quant by PCR 64,900 copies
• Hepatitis C positive What stage of HIV

Back 100

AIDS CD4 was 20 , its AIDS even wo opprotunistic infection

common to be co infected with hep C

Front 101

Mr. C is a 38 y/o male. HIV by EIA test
performed 3 yrs. ago was negative.
• First hospitalization: He presented with weight
loss, chronic diarrhea and shortness of breath.
• He had fever, night sweats and a 40 # wt. loss
in 2 mon. HIV infection was suspected.
• HIV by EIA was positive and confirmed by
Western blot
Pneumocystis jiroveci‐ carinii pulmonary
infection was diagnosed and successfully treated.
Respiratory cultures for CMV returned
positive wks. later.
• He was started on antiretroviral therapy and
discharged to recover in a skilled nursing
facility. Diarrhea persisted.
• He was readmitted and intestinal CMV and
Cryptosporidiosis were diagnosed.
What stage of HIV?

What would you predict his CD4 count to be?
• WBC 2100 (5,000‐10,000)
• Hb 12.3g (14‐16), Hct 35.4%
• Platelets 98,000 (>150,000)
• Diff: 67% segs, 15% bands, 18% lymphs

Back 101

rapid progression, AIDS defining

**T cells will be LOW

HIV RNA quantitation by bDNA
• 9/5 371,000 log 5.57
• 9/15 67,200 log 4.83
• 10/15 <500 < log 2.6