HIV Flashcards
1
Q
- 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
A
- RNA retrovirus
- CD4+ T-helper cells
- CD4+ T cell count
- 200 cells/mm^3
- opportunistic infections and certain malignancies
2
Q
- 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
A
- HIV-1 and HIV-2
- HIV-1
- mutations; high replication rate; error-prone reverse transcriptase
3
Q
- 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
A
- drug resistance
- multidrug regimens
- monotherapy; resistant
4
Q
- HIV is spread through what?
- What are the two most common means of HIV transmission?
- (…) transmission may occur as well
- How does this occur?
A
- infected blood, semen, and vaginal secretions
- unprotected sex and sharing needles
- vertical transmission (from mother to child)
- during pregnancy, at birth, or through breastfeeding
5
Q
- 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?
A
- 13-64
- TB or other STIs
- annually
- injecting drug users, high-risk sexual behaviors (male to male sex)
6
Q
- 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
A
- viremia (virus in blood)
- flu-like symptoms
- anti-HIV antibodies (HIV ab); 4-8 weeks; 3-6 months
- HIV RNA and HIV p24 antigen
7
Q
What lab parameters are recommended for the evaluation and monitoring of HIV infections?
(there are 5)
A
- CD4+ count
- HIV viral load
- drug resistnace testing
- comprehensive metabolic panel
- hepatitis B and C testing
8
Q
- The CD4+ count is the key factor for determination of need for (…)
- The treatment goal is a normal CD4+ count which is what?
A
- opportunistic infection prophylaxis
- 800-1200 cells/mm^3
9
Q
- HIV viral load is the most important indicator of what?
- The treatment goal is to have an (…) HIV viral load
A
- response to antiretroviral therapy (ART)
- undetectable HIV viral load
10
Q
What describing genotypic testing that determines the specific mutations of the HIV virus?
A
drug resistance testing
11
Q
- 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?
A
- binding/attachment
- gp120; CCR5 and/or CXCR4
- CD4 receptor and a co-receptor
- CCR5 antagonist, CD4-directed post-attachment HIV-1 inhibitors
12
Q
- 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?
A
- fusion
- fusion; uncoating; HIV RNA; cytoplasm
- fusion inhibitors
13
Q
- 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?
A
- reverse transcriptase
- reverse transcriptase
- nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs); non-nucleoside reverse transcriptase inhibitors (NNRTIs)
14
Q
- 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?
A
- integration
- integrated; host cell’s DNA
- integrase strand transfer inhibitors (INSTIs)
15
Q
- 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?
A
- transcription and translation
- transcribed and translated
- no drugs target this stage
16
Q
- 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?
A
- assembly
- HIV virus
- protease enzyme
- no drugs target this stage
17
Q
- 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?
A
- budding and maturation
- buds off from host cell
- protease; proteins and enzymes
- CD4+ host cells
- protease inhibitors (PIs)
18
Q
- 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
A
- ART (antiretroviral therapy)
- ART
- 95% or higher (can’t miss more than 1 dose per month)
19
Q
What are the primary goals of ART?
(there are 5)
A
- restore and preserve immune system
- suppress HIV viral load to undetectable levels
- prevent transmission
- reduce HIV-associated morbidity
- prolong survival
20
Q
- 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
A
- expensive; funding programs
- social workers and programs
21
Q
- 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?
A
- 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
22
Q
Is maraviroc (selzentry) used often in HIV treatment? Why or why not?
A
no, there are other, more effective alternatives
23
Q
- 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?
A
- 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
24
Q
- 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?
A
- 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
