- HIV is an (...) that attackes the immune system, maining the (...) cells - It causes a progressive decrease in the (...) cell count - Once this count falls below (...), the person becomes more susceptible to (...) and (...) 1. type of virus

- RNA retrovirus - CD4+ T-helper cells - CD4+ T cell count - 200 cells/mm^3 - opportunistic infections and certain malignancies

- HIV has 2 subtypes, what are they? - Which subtype causes the vast majority of infections and is the predominant subtype in the US? - Because HIV is a retrovirus, it is very susceptible to (...); it has a (...) replication rate and (...) transcriptase enzymes

- HIV-1 and HIV-2 - HIV-1 - mutations; high replication rate; error-prone reverse transcriptase

- Rapid mutations allow HIV to evolve and develop (...) very rapidly - Because mutations can develop so rapidly, (...) regiments are the standard of care - You never want to give (...) for HIV treatment because HIV will becomes (...) to it very quickly

- drug resistance - multidrug regimens - monotherapy; resistant

- HIV is spread through what? - What are the two most common means of HIV transmission? - (...) transmission may occur as well - How does this occur?

- infected blood, semen, and vaginal secretions - unprotected sex and sharing needles - vertical transmission (from mother to child) - during pregnancy, at birth, or through breastfeeding

- The CDC recommends routine screening for patients ages (...) in all healthcare settings - Pregnant women and patients initiating treatment for (...) or (...) should also be tested for HIV - Persons at high risk should be tested for HIV (...) - Who are people in these high risk groups?

- 13-64 - TB or other STIs - annually - injecting drug users, high-risk sexual behaviors (male to male sex)

- An acute HIV infection is characterized by an initial burst of (...) - A person experiencing acute HIV infection may experience (...) symptoms - (...) are undetectable initially; may show positive results at (...) weeks but may take (...) months - If trying to detect HIV before these time frames, you can test for (...) and (...) because they will be present

- viremia (virus in blood) - flu-like symptoms - anti-HIV antibodies (HIV ab); 4-8 weeks; 3-6 months - HIV RNA and HIV p24 antigen

- The CD4+ count is the key factor for determination of need for (...) - The treatment goal is a normal CD4+ count which is what?

- opportunistic infection prophylaxis - 800-1200 cells/mm^3

- HIV viral load is the most important indicator of what? - The treatment goal is to have an (...) HIV viral load

- response to antiretroviral therapy (ART) - undetectable HIV viral load

- What is the first stage of the HIV life cycle? - HIV attaches with (...) to a CD4 receptor and the co-receptors (...) on the surface of the CD4+ host cell - The virus must bind/attach to both a (...) and a (...) in order for the next step of viral replication to occur - What drug classes target this stage?

- binding/attachment - gp120; CCR5 and/or CXCR4 - CD4 receptor and a co-receptor - CCR5 antagonist, CD4-directed post-attachment HIV-1 inhibitors

- What is the second stage of the HIV life cycle? - (...) of the HIV viral envelope with the CD4+ host cell membrane allows HIV to enter the host cell, where (...) of the virus releases (...) and viral proteins and enzymes needed for HIV replication into host cell's (...) - What drug classes target this stage?

- fusion - fusion; uncoating; HIV RNA; cytoplasm - fusion inhibitors

- What is the third stage in the HIV life cycle? - Once inside the cell, the single-stranded HIV RNA is converted to double-stranded HIV DNA by (...) - What drug classes target this stage?

- reverse transcriptase - reverse transcriptase - nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs); non-nucleoside reverse transcriptase inhibitors (NNRTIs)

- What is the fourth stage in the HIV life cycle? - HIV is transported across the host cell nuclear membrane and is (...) into the host cell's (...) - What drug classes target this stage?

- integration - integrated; host cell's DNA - integrase strand transfer inhibitors (INSTIs)

- What is the fifth stage in the HIV life cycle? - HIV DNA is (...) and (...) into new HIV RNA as well as new viral proteins (envelope proteins and non-functional long-chain proteins) - What drug classes target this stage?

- transcription and translation - transcribed and translated - no drugs target this stage

- What is the sixth stage of the HIV life cycle? - New HIV RNA viral envelope proteins, and non-functional long-chain proteins migrate to the host cell surface and begin forming new, immature (...) - (...) enzyme is also incorporated into this newly forming HIV virus - What drug classes target this stage?

- assembly - HIV virus - protease enzyme - no drugs target this stage

- What is the seventh stage of the HIV life cycle? - Newly formed, immature HIV virus (...) from the host cell - During the maturation process, (...) cleaves the long-chain viral proteins into smaller, functional viral (...) and (...) - The mature HIV viruse is now able to move on and infect other (...) cells - What drug classes target this stage?

- budding and maturation - buds off from host cell - protease; proteins and enzymes - CD4+ host cells - protease inhibitors (PIs)

- Combination (...) has dramatically reduced HIV morbidity and mortality - (...) is recommended in all HIV-infected individuals - With this treatment, patients must have an adherence rate of (...) in order for it to be effective long-term

- ART (antiretroviral therapy) - ART - 95% or higher (can't miss more than 1 dose per month)

- ART can be very (...), but there are many (...) available - It is important to leverage (...) and (...) to ensure patients can obtain and maintain access to ART

- expensive; funding programs - social workers and programs

- How to CCR5 antagonists work? - What drugs are CCR5 antagonists? - Patients must undergo a tropism test to determine the type of (...) present because this drug, (...), only works in (...) disease and patients may have (...), (...), or both receptors - In the tropic test, patients must be negative for what?

- inhibits binding to the CCR5 co-receptor and prevents HIV from entering the cell - Maraviroc (selzentry) - co-receptor; maraviroc; CCR5 tropic disease; CCR5, CDCR4 - CXCR4 or dual/mixed tropisms

- What drug is a post-attachment HIV-1 inhibitor? - This is the first new class of (...) for HIV - How does this drug work? - How is it administered? - This is approved for use in (...) who are failing their current ART - Is this drug used often?

- Ibalizumab - monoclonal antibody - binds to domain 2 of CD4 and blocks entry of HIV into host cells - IV - heavily treatment-experienced (with multidrug resistant HIV or MDR-HIV) - no, not used often

- What do fusion inhibitors do? - What drug is a fusion inhibitor? - How is this drug given (dosage, ROA)? - Typically, this drug is only used in what type of patients? - Is this drug used often?

- block fusion of the HIV virus with the CD4+ cells by blocking the conformational change in gp41 required for membrane fusion - enfuvirtide (fuzeon) - 90 mg subcutaneous injection BID - patients who are treatment-experiences with resistance to multiple other ARTs - not used often

HIV Flashcards by Brittany Christmas

HIV is an (…) that attackes the immune system, maining the (…) cells
It causes a progressive decrease in the (…) cell count
Once this count falls below (…), the person becomes more susceptible to (…) and (…)

1. type of virus

RNA retrovirus
CD4+ T-helper cells
CD4+ T cell count
200 cells/mm^3
opportunistic infections and certain malignancies

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HIV has 2 subtypes, what are they?
Which subtype causes the vast majority of infections and is the predominant subtype in the US?
Because HIV is a retrovirus, it is very susceptible to (…); it has a (…) replication rate and (…) transcriptase enzymes

HIV-1 and HIV-2
HIV-1
mutations; high replication rate; error-prone reverse transcriptase

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Rapid mutations allow HIV to evolve and develop (…) very rapidly
Because mutations can develop so rapidly, (…) regiments are the standard of care
You never want to give (…) for HIV treatment because HIV will becomes (…) to it very quickly

drug resistance
multidrug regimens
monotherapy; resistant

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HIV is spread through what?
What are the two most common means of HIV transmission?
(…) transmission may occur as well
How does this occur?

infected blood, semen, and vaginal secretions
unprotected sex and sharing needles
vertical transmission (from mother to child)
during pregnancy, at birth, or through breastfeeding

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The CDC recommends routine screening for patients ages (…) in all healthcare settings
Pregnant women and patients initiating treatment for (…) or (…) should also be tested for HIV
Persons at high risk should be tested for HIV (…)
Who are people in these high risk groups?

13-64
TB or other STIs
annually
injecting drug users, high-risk sexual behaviors (male to male sex)

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An acute HIV infection is characterized by an initial burst of (…)
A person experiencing acute HIV infection may experience (…) symptoms
(…) are undetectable initially; may show positive results at (…) weeks but may take (…) months
If trying to detect HIV before these time frames, you can test for (…) and (…) because they will be present

viremia (virus in blood)
flu-like symptoms
anti-HIV antibodies (HIV ab); 4-8 weeks; 3-6 months
HIV RNA and HIV p24 antigen

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What lab parameters are recommended for the evaluation and monitoring of HIV infections?

(there are 5)

CD4+ count
HIV viral load
drug resistnace testing
comprehensive metabolic panel
hepatitis B and C testing

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The CD4+ count is the key factor for determination of need for (…)
The treatment goal is a normal CD4+ count which is what?

opportunistic infection prophylaxis
800-1200 cells/mm^3

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HIV viral load is the most important indicator of what?
The treatment goal is to have an (…) HIV viral load

response to antiretroviral therapy (ART)
undetectable HIV viral load

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What describing genotypic testing that determines the specific mutations of the HIV virus?

drug resistance testing

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What is the first stage of the HIV life cycle?
HIV attaches with (…) to a CD4 receptor and the co-receptors (…) on the surface of the CD4+ host cell
The virus must bind/attach to both a (…) and a (…) in order for the next step of viral replication to occur
What drug classes target this stage?

binding/attachment
gp120; CCR5 and/or CXCR4
CD4 receptor and a co-receptor
CCR5 antagonist, CD4-directed post-attachment HIV-1 inhibitors

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What is the second stage of the HIV life cycle?
(…) of the HIV viral envelope with the CD4+ host cell membrane allows HIV to enter the host cell, where (…) of the virus releases (…) and viral proteins and enzymes needed for HIV replication into host cell’s (…)
What drug classes target this stage?

fusion
fusion; uncoating; HIV RNA; cytoplasm
fusion inhibitors

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What is the third stage in the HIV life cycle?
Once inside the cell, the single-stranded HIV RNA is converted to double-stranded HIV DNA by (…)
What drug classes target this stage?

reverse transcriptase
reverse transcriptase
nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs); non-nucleoside reverse transcriptase inhibitors (NNRTIs)

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What is the fourth stage in the HIV life cycle?
HIV is transported across the host cell nuclear membrane and is (…) into the host cell’s (…)
What drug classes target this stage?

integration
integrated; host cell’s DNA
integrase strand transfer inhibitors (INSTIs)

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What is the fifth stage in the HIV life cycle?
HIV DNA is (…) and (…) into new HIV RNA as well as new viral proteins (envelope proteins and non-functional long-chain proteins)
What drug classes target this stage?

transcription and translation
transcribed and translated
no drugs target this stage

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What is the sixth stage of the HIV life cycle?
New HIV RNA viral envelope proteins, and non-functional long-chain proteins migrate to the host cell surface and begin forming new, immature (…)
(…) enzyme is also incorporated into this newly forming HIV virus
What drug classes target this stage?

assembly
HIV virus
protease enzyme
no drugs target this stage

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What is the seventh stage of the HIV life cycle?
Newly formed, immature HIV virus (…) from the host cell
During the maturation process, (…) cleaves the long-chain viral proteins into smaller, functional viral (…) and (…)
The mature HIV viruse is now able to move on and infect other (…) cells
What drug classes target this stage?

budding and maturation
buds off from host cell
protease; proteins and enzymes
CD4+ host cells
protease inhibitors (PIs)

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Combination (…) has dramatically reduced HIV morbidity and mortality
(…) is recommended in all HIV-infected individuals
With this treatment, patients must have an adherence rate of (…) in order for it to be effective long-term

ART (antiretroviral therapy)
ART
95% or higher (can’t miss more than 1 dose per month)

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What are the primary goals of ART?

(there are 5)

restore and preserve immune system
suppress HIV viral load to undetectable levels
prevent transmission
reduce HIV-associated morbidity
prolong survival

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ART can be very (…), but there are many (…) available
It is important to leverage (…) and (…) to ensure patients can obtain and maintain access to ART

expensive; funding programs
social workers and programs

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How to CCR5 antagonists work?
What drugs are CCR5 antagonists?
Patients must undergo a tropism test to determine the type of (…) present because this drug, (…), only works in (…) disease and patients may have (…), (…), or both receptors
In the tropic test, patients must be negative for what?

inhibits binding to the CCR5 co-receptor and prevents HIV from entering the cell
Maraviroc (selzentry)
co-receptor; maraviroc; CCR5 tropic disease; CCR5, CDCR4
CXCR4 or dual/mixed tropisms

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Is maraviroc (selzentry) used often in HIV treatment? Why or why not?

no, there are other, more effective alternatives

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What drug is a post-attachment HIV-1 inhibitor?
This is the first new class of (…) for HIV
How does this drug work?
How is it administered?
This is approved for use in (…) who are failing their current ART
Is this drug used often?

Ibalizumab
monoclonal antibody
binds to domain 2 of CD4 and blocks entry of HIV into host cells
IV
heavily treatment-experienced (with multidrug resistant HIV or MDR-HIV)
no, not used often

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What do fusion inhibitors do?
What drug is a fusion inhibitor?
How is this drug given (dosage, ROA)?
Typically, this drug is only used in what type of patients?
Is this drug used often?

block fusion of the HIV virus with the CD4+ cells by blocking the conformational change in gp41 required for membrane fusion
enfuvirtide (fuzeon)
90 mg subcutaneous injection BID
patients who are treatment-experiences with resistance to multiple other ARTs
not used often

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Regarding the MOA of nucleoside/nucleotide transcriptase inhibitors: - NRTIs are inhibitors of (...) - They are analogs of (...) (nucleosides or nucleotides containing ribose) which all lack (...) - Once they enter the cell, they are (...) by cellular enzymes, which is then encorporated into the viral DNA by (...) - Because of the missing (...), the growing DNA chain is terminated

- HIV reverse transcriptase - ribosides; 3'-hydroxyl group - phosphorylated; reverse transcriptase - 3'-hydroxyl group

What drugs are NRTIs?

- abacavir - lamivudine - **emtricitabine** - **tenofovir** | (bold are most common)

- All NRTIs are administered (...) - Tenofovir has two salt forms, what are they? - Which achieves better anti-HIV activity at lower dose, and has a lower side effect profile - All NRTIs are (...) excreted, except (...)

- orally - tenofovir disoproxil fumarate (TDF) and tenofovir alafenamide (TAF) - tenofovir alafenamide (TAF) - renally excreted except for abacavir

- What are the boxed warnings for all NRTIs? - Abacavir is associated with (...), so patients must test negative for (...) allele to safely take - Tenofovir (TDF or TAF) is associated with (...) and (...) - What can Tenofovir cause? - What is the preferred NRTI?

- lactic acidosis and severe hepatomegaly with steatosis (fat accumulation) - hypersensitivity reaction; HLA-B*5701 allele - kidney damage and decreased bone density - AKI, CKD, proximal tubular injury (Fanconi syndrome) - TAF

What drugs are non-nucleoside reverse transcriptase inhibitors (NNRTIs)? | ("-vir-")

- nevirapine - efavirenz - etravirine - relpivirine - doravirine

- What is the MOA of non-nucleoside reverse transcriptase inhibitors (NNRTIs)? - Most NNRTIs are (...) inducers, so there are many (...) - Efavirenz is safe to use in which patients? Why? - What does Rilpivirine require in order to be absorbed? What should you avoid taking this with?

- noncompetitive inhibitors of HIV reverse transcriptase - CYP450 inducers; drug interactions - patients coinfected with TB because lower potential for drug interaction (lower CYP induction compared to others) - acidic stomach; avoid proton-pump inhibitors (PPIs)

What are the adverse effects of NNRTIs?

- serious psychiatric symptoms (suicidal ideation, depression) - CNS symptoms (usually resolve 2-4 weeks; includes impaired concentration, dizziness, vivid dreams)

What drugs are integrase strand transfer inhibitors (INSTI)? | ("-tegravir")

- raltegravir - elvitegravir - dolutegravir - bictegravir - cabotegravir

- What is the MOA of integrase strand transfer inhibitors? - Oral INSTIs are subject to (...) - What should you avoid taking oral INSTIs with? - Elvitegravir has a short half life of (...) and is often given with (...) to "boost" its half-life to allow once daily dosing - What is a CYP3A4 inhibitor that has no retrovial activity by itself?

- blocks integrase; inhibits the insertion of viral DNA into the host genome - chelation with cations - avoid antacids - 3 hours; cobicistat - cobicistat (Tybost)

What are the mainstay of initial treatment for HIV?

INSTIs

- How can resistance occur with INSTIs? - Which drugs have cross resistance? - Which drugs have limited cross-resistance to other INSTIs?

- mutations within the inetrase gene - cross-resistance between raltegravir and elvitegravir - dolutegravir and bictegravir

- What is the mainstay for initial HIV therapy (general combo)? - What is the best initial option (actual drugs)?

- INSTI + 2 NRTIs (dual NRTI backbone) - biktarvy (bictegravir + emtricitabine, TAF)

- What is a long-acting injection approved for the treatment of HIV? - What is the general combo for this?

- Cabenuva (cabotegravir, rilpivirine) - INSTI + NNRTI

What drugs are protease inhibitors? | ("-navir")

- atazanavir - durunavir - lopinavir/r (boosted) - nelfinavir - saquinavir - tipranavir

- What is the MOA of protease inhibitors? - It is recommended that all PAs be (...)

- inhibit HIV protease; prevents assembly of viral proteins and maturation of virus - boosted

- What are the different boosting agents for HIV drugs? - Where are all PIs metabolized in? - PIs are (...) substrates - Most PIs are also (...) inhibitors - Therefore, there are many (...)

- ritonavir and cobicistat - liver - CYP3A4 substrates - CYP3A4 inhibitors - drug interactions

What are the different drugs that protease inhibitors may have drug interactions with?

- CYP3A4 inhibitors (rifampin, St. Johns Wort) - antiarrhythmics (dronedarone, amiodarone) - anticoagulants/antiplatelets (apixaban, edoxaban, rivaroxaban, ticagrelor, warfarin) - hormonal conraceptives - methadone - PDE-5 inhibitors (sildenafil, tadalafil) - statins (lovastatin, simvastatin)

Because of long list of contraindicated or dose-adjustments required, PIs are not typically recommended at what?

first line agent for HIV treatment

What are the adverse effects of protease inhibitors?

- hepatotoxicity - metabolic abnormalities (hyperlipidemia, lipohypertrophy, insulin resistance/hyperglycemia) - GI upset (N/V/D) - fat redistribution (buffalo hump)

Which protease inhibitor has the highest risk for hepatotoxicity?

tipranavir

- What agents can act as boosters for HIV drugs? - Do they have antiviral activity? - Which one is difficult to co-formlate with other ARVs?

- ritonavir, cobicistat - ritonavir does (protease inhibitor), cobicistat does not - ritonavir

- INSTI-based regimens are recommended as (...) therapy for most patients - An INSTI-based regimen is an (...) - What can the 2 NRTIs be referred to as?

- initial therapy - an INSTI + 2 NRTIs - dual NRTI backbone

- What drugs make up truvada? - What is truvada given with?

- emtricitabine/TDF - dolutegravir (tivicay)

- What drugs make up descovy? - What is descovy given with? - What patients can this combo be used in?

- emtricitabine/TAF - dolutegravir (tivicay) - pregnant patients

- What is the most popular INSTI+2NRTI regiment at this time? - What does the use of abacavir require? - What drug should be used with caution in patients with renal insufficiency? - Single tablet regimens offer no flexibility in (...)

- biktarvy - testing pts for HLA-B*5701 allele - tenofovir disproxil fumarate (TDF) - renal dosing

- What is an HIV prevention method in people who do not have HIV in high-risk groups? - What types of individuals would be in this group?

- Pre-exposure Prophylaxis (PrEP) - men who have sex with men (MSM), sex with an HIV positive partner, persons who inject drugs

What are the principles of PrEP?

- must be HIV negative - no documented hepatitis B virus - normal renal function

What is the surveillance during PrEP use?

- must have follow up visit every 3 months - this includes: HIV test, renal funtion test, evaluation for bacterial STDs

What are the different PrEP regimens and their ROA?

**truvada** - emtricitabine/tenofovir disproxil fumarate - oral - 1 tablet daily **descovy** - emtricitabine/tenofovir alafenamide - oral - 1 tablet daily **apretude** - cabotegravir - long-acting injection (1 month) | (truvada mostly used, better efficacy and cheaper)

- What is PEP? - When must a patient start PEP to prevent HIV? - What is the length of PEP treatment?

- post exposure prophylaxis - taking ART to prevent HIV after possible exposure - within 72 hours - 28 days

What are the recommended PEP regimens?

- biktarvy (bictegravir/emtricitabine/TAF) - dolutegravir + TDF or TAF - raltegravir + TDF or TAF

- Which PEP regimen is usually what is prescribed? - Which PEP regimen is not recommended due to twice daily dosing?

- Biktarvy - Raltegravir

What are some complications of ART?

- lactic acidosis and severe hepatomegaly with steatosis - immune reconstitution inflammatory syndrome (IRIS)

- Lactic acidosis and severe hepatomegaly with steatosis is a complication most common with (...) - If this happens, (...) treatment

- NRTIs - stop treatment

- What is the paradoxical worsening of a pre-existing opportunistic infection or malignany once ART is initiated? - What common pathogens are associated with this?

- immune reconstitution inflammatory syndrome (IRIS) - M. tuberculosis, M. avium, Pneumocystis jirovecii pneumonia (PCP), herpes viruses

How is IRIS managed?

- treat underlying opportunistic pathogen - continue ART

HIV Flashcards

(60 cards)