Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Infectious Disease 2 > HIV TBL > Flashcards

HIV TBL Flashcards

(69 cards)

Start Studying
1
Q

How is HIV transmitted?

A

Blood-borne pathogen transmitted sexually, mother-to-child, or through blood (IV drug use, blood product)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is acute HIV infection?

A

Documentation of HIV acquisition prior to full seroconversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is early HIV infection?

A

Within 3-6 months of HIV acquisition; May have full seroconversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is established HIV infection?

A

> 3-6 months after HIV acquisition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is HIV diagnosed?

A

Screening using serum ELISA or rapid blood or salivary Ab tests; confirmation with Western Blot; Consent for HIV Ab testing must be obtained and be accompanied by pre-test information and post-test counselling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical characteristics of acute HIV infection?

A

50-90% of infections are symptomatic; Symptoms generally occur 5-30 days after
exposure and include Fever, fatigue, myalgias, arthralgias, headache, nausea, vomiting, diarrhea, adenopathy, pharyngitis, rash, weight loss, mucocutaneous ulcerations, aseptic meningitis, occas.
oral/vaginal candidiasis, Leukopenia, thrombocytopenia, elevated liver enzymes; Median duration of symptoms: 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the major receptor associated with HIV?

A

CD4, CCR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why is HIV infection forever?

A

The retrovirus DNA is integrated into the host genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What system does HIV infect?

A

The lymphatic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a problem with the ELISA?

A

Patients with acute HIV infection may present to a health
care facility before full antibody seroconversion; Plasma HIV-1 RNA level should be done if acute HIV
infection is suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does acute infection affect the GI tract?

A

Depletion of CD4+ cells in the lamina propria, Absence of lymphoid cell aggregates in terminal Ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where does HIV replicate (/live)?

A

Lymphatic system, gastrointestinal tract (GALT), CNS, genital tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How many virions are produced per day?

A

At least 10 X 10 to the 9 virions produced and destroyed each day; T1/2 of HIV in plasma is less than 6 h and may be as short as 30 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the different kind of progressors?

A

chronic (takes years to develop - primary HIV infection, asymptomatic, AIDS), rapid (takes months-1 year - primary infection, AIDS), controller (primary HIV infection, asymptomatic, never develop AIDS); 2 kinds of controllers: viremic (HIV RNA under 2000 c/ml), elite (less than 20-50 c/ml)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the viral factors that can determine outcome?

A
  1. Escape from immune response; 2. Attenuation (nef deleted viruses associated with slow or long-term
    nonprogression in case reports and small cohorts); 3. Tropism; 4. Subtypes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 3 parts of the virus that all retroviruses have?

A

gag, pol and env

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is HIV named?

A

Groups (M, N, O, P), subtypes (at least 9), sub-subtypes, circulating recombinant forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What host factors affect HIV infection?

A

CD8 cells (Play prominent role in control of viremia, slowing of disease progression and perhaps prevention of infection), CD4 (vital for presentation of CTL response), humoral immunity, chemokine receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What chemokine receptor is particularly relevant in HIV infection?

A

CCR5-delta32 deletion; Homozygosity associated with decreased susceptibility to R5 virus infection; Heterozygosity associated with delayed disease progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which HLA is particularly relevant to HIV infection?

A

HLA-B57 (associated with long-term non-progression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why do CD4+ numbers decreased?

A

HIV-infected cells: Direct cytotoxic effect of HIV, Lysis by CTL’s, Apoptosis (Potentiated by viral gp120, Tat, Nef, Vpu); HIV-uninfected cells: Apoptosis (Release of gp120, Tat, Nef, Vpu by neighboring, infected cells), Activation induced cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do CD4 numbers affect HIV RNA levels in untreated people?

A

Rate of CD4 decline linked to HIV RNA level in untreated persons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Are CD4 and HIV RNA levels good indicators?

A

Good but incomplete surrogate markers (for both natural history and treatment effectiveness), Thresholds are arbitrary, Treatment decisions should be individualized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When should treatment be evaluated?

A

Antiviral potency can be assessed in first 7-14 days: Should see 1-2 log declines after initiation of therapy in persons with drug susceptible virus who are adherent; HIV RNA trajectory in first 1-8 weeks can be predictive of subsequent response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are "non-AIDS" conditions?
Described to be associated with uncontrolled HIV-1 viremia, even in persons with relatively well preserved CD4 cell counts (e.g., >350/mm3): Cardiovascular events, Hepatic disease, Renal disease, Malignancies (may be associated with HIV)
26
What is the structure of HIV?
HIV is a member of the Retrovirus family. It is a single stranded RNA virus with an icosahedral nucleocapsid and a lipid envelope. The virion has two identical copies of RNA and carries a unique viral enzyme, the reverse transcriptase.
27
What are the parts of HIV?
The HIV genome is 10kB in length and consists of 3 major (Gag, Pol, Env) and 6 accessory genes: 1. Gag codes for internal structural proteins., 2. Pol codes for major enzymes of the virus – reverse transcriptase, protease and integrase, 3. Env codes for the gp120 envelope glycoprotein and the gp41 transmembrane protein. These proteins mediate attachment and entry of the virus into the cell, 4. Tat, Rev, Nef, Vif, Vpr and Vpu are accessory proteins which are involved in amplification of virus replication, infectivity and pathogenesis
28
What is the first cell that the virus encounters following deposition on mucosal surfaces?
dendritic cell interaction is the first encounter the virus has following deposition on mucosal surfaces
29
What is the warning level for CD4 cell count?
200/cubic mm
30
What is the average time of HIV infection to clinical AIDS?
typically 8-10 years
31
What are the top 10 AIDS complications?
Pneumocystis Pneumonia, Toxoplasmosis, Cryptococcal meningitis, Disseminated Mycobacterium Avium Complex, Cytomegalovirus, Kaposis sarcoma, Non Hodgkin Lymphoma, Muscosal candidiasis, Herpes Zoster, Herpes Simplex
32
How does ART affect opportunistic infections in HIV?
Immune reconstitution with anti-retroviral therapy may reverse OI susceptibility (but may also trigger an inflammatory response to active OIs)
33
What is the strongest predictor for risk of pneumocystic pneumonia?
CD4 less than 200
34
What is the microbiology of pneumocystic pneumonia (PCP)?
P jirovecii is the human pathogen; Categorized as a fungus based on nucleic acid features; Has some fungal structural features (cell wall Beta D glucan) but so far not responsive to antifungal agents; Unable to cultivate so limited data on epidemiology, transmission, drug susceptibility
35
How does PCP present?
Non AIDS cases: Usually abrupt onset of fever, cough, dyspnea. Diffuse “interstitial” infiltrates; respiratory failure. Mortality 25%; AIDS cases: Slower onset (up to 6 weeks); gradual progression from fever and cough to dyspnea, respiratory failure. Death. Mortality 10-20% with initial episodes, increases with subsequent ones
36
How is PCP diagnosed?
No reliable culture method; Diffuse “ground glass” opacities on CT, elevated serum LDH are suggestive but not specific; Staining of alveolar contents (histochemical or fluorescent) is standard method. Silver stains are definitive.; Usual specimen source is bronchoscopy with alveolar lavage. Alternatives include induced sputum, lung biopsy
37
How is PCP treated?
Two regimens well defined in pre-AIDS era: Pentamidine isethionate IM or IV and Trimethoprim-sulfamethoxazole IV or PO; Equal efficacy but pentamidine far more toxic
38
Should steroids be used for PCP?
Counter-intuitive use of steroids in desperation proved highly successful at preventing respiratory failure and decreasing mortality by 50%.
39
What should be used for PCP prophylaxis?
Trimethoprim-sulfa nearly 100% effective at preventing PCP in AIDS and leukemia patients; HIV+ Indications: CD4 under 200, or 14%; prior PCP; Unexplained fever, weight loss or diarrhea
40
What is CNS toxoplasmosis?
Commonest CNS mass lesion in AIDS. Usual presentation: “stroke” or seizure; Geographic history (Carribean, Central America) is good predictor; Reactivation in AIDS associated with CD4 under 100.
41
How is CNS taxoplasmosis diagnosed?
Focal presentation, CNS imaging and seropositivity for toxo usually adequate for presumptive diagnosis
42
How is CNS taxoplasmosis treated?
Pyrimenthamine+sulfadiazine is standard treatment
43
When is it CNS toxoplasmosis, and when is it lymphoma?
Both have mass effect, contrast enhancement and occur at low CD4. Toxo more likely to have multiple lesions
44
How does cryptococcal disease present in HIV?
Widespread fungus in environment. Reactivation in advanced HIV disease (CD4 less than 100). Meningitis commonest presentation but wide dissemination frequent. Presentation: Headache, fever. Often indolent.
45
How does CMV present in HIV?
Reactivation at CD4
46
How is CMV treated?
Ganciclovir (IV), oral valganciclovir
47
What is Disseminated Mycobacterium-avium complex (MAC) disease in AIDS?
Widespread visceral dissemination in AIDS. Diagnosis by blood culture. Absence of inflammation in tissue sites.
48
How is MAC treated?
Azithromycin+ethambutol
49
What is HAART?
Highly Active Antiretroviral Therapy - this has led to life expectancies approaching the general population
50
When was ART initiated?
1995
51
What are the types of ART?
Nucleos(t)ide reverse transcriptase inhibitors (NRTIs), Non-nucleoside reverse transcriptase inhibitors (NNRTIs), Protease Inhibitors (PIs), Fusion inhibitor, CCR5 antagonist, Integrase inhibitors
52
Where do NRTIs work? NNRTIs? PIs? Fusion inhibitors? CCR5 antagonists? Integrase inhibitors?
NRTIs: synthesis of viral DNA; NNRTI: synthesis of viral DNA; PIs: assembly of virus and budding from the cell; CCR5 antagonists: binding to the receptor; fusion inhibitors: binding to the receptor; integrase inhibitor: integration into the host DNA
53
What are side effects of NRTIs?
nausea, headache, lactic acidosis, anemia (AZT), peripheral neuropathy, pancreatitis, lipodystrophy, hypersensitivity syndrome (abacavir)
54
What are the primary Nucleoside Reverse Transcriptase Inhibitors?
Zidovudine (AZT), abacavir (ABC), lamivudine (3TC), emtricitabine (FTC)
55
What are Nucleotide Reverse Transcriptase Inhibitors?
Pretty much the same as the nucleoside RTIs. Two drugs in class: tenofovir disoproxil fumarate (TDF) and tenofovir alafenamide (TAF)
56
What is the toxicity associated with Nucleotide Reverse Transcriptase Inhibitors?
nephrotoxicity, bone demineralization; TAF has decreased renal and bone toxicity profile
57
What are NNRTIs?
Second class of antiretroviral agents developed; Inhibit reverse transcriptase by binding a hydrophobic pocket close to active site, locking it in an inactive conformation
58
What are the types of NNRTIs?
1st generation: efavirenz, nevirapine; 2nd generation: etravirine, rilpivirine; 1st gens are potent but lots of resistance
59
What are the side effects of NNRTIs?
Are either potent inducers or inhibitors of CYP3A4, Potential for major drug interactions with HIV and non-HIV drugs, including antimycobacterials; Adverse effects: rash, hepatotoxicity, neurocognitive impairment (efavirenz), teratogenicity (efavirenz)
60
What are protease inhibitors?
Third class of antiretroviral agents developed, introduced to clinical use ~1995; must be "boosted" with ritonavir
61
What are the most commonly used protease inhibitors?
lopinavir, atazanavir, darunavir
62
What are side effects of protease inhibitors?
abdominal upset, diarrhea, dyslipidemia, lipodystrophy, atherosclerosis
63
What are integrase inhibitors?
Inhibit DNA strand transfer into host-cell genome and thus prevent viral integration
64
What are the names of the integrase inhibitors?
raltegravir, elvitegravir and dolutegravir
65
What are the side effects of integrase inhibitors?
headache, nausea, rash (rare)
66
What is the goal of HIV ART?
Virological suppression measured by an undetectable viral load, Immune reconstitution as measured by a rise in CD4+ count, Clinical decrease in HIV-associated morbidity and mortality, Epidemiological evidence of decreased in HIV transmission
67
What is the ART combo typically used?
2 NRTI plus 1 of either integrase inhibitor, protease inhibitor with booster, NNRTI
68
What group of HIV is typically found in the US? In Africa?
US: B; Africa: F, G, H, J, K; HIV-2 in West Africa
69
What is the only kind of PrEP approved in the US?
Truvada - Daily routine use of systemic ART

Infectious Disease 2 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions