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MNI (immuno path) > L22- HIV > Flashcards

L22- HIV Flashcards

1
Q

HIV: family, subfamily, genus

A

Family- retroviridae
Subfamily- orthoretroviridae
Genus- lentivirus

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2
Q

list the important properties of the Lentivirus genus

A
  • infects immune cells
  • provirus permanently in infected cells (latent infections via reverse transcriptase)
  • causes slow, progressive, chronic disease

-non-oncogenic viruses

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3
Q

HIV: group, genome make-up (include ORF), virus / core shape and structure

A

Group VI- (+)ssRNA, 2 copies
-9 open reading frames => ~15 proteins

  • enveloped, spherical shape
  • inverted cone or bullet shaped core with genome
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4
Q

(1) is the term for when HIV genome is integrated with host genome

viral mRNA codes for (2) in a (3) structure

A

1- provirus

2/3- non-structural (core) and structural (envelope, capsid) proteins each in a polyprotein form –> cleaved into proteins as final step of maturation

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5
Q

HIV main external Ags (include brief functions):

  • (1) surface
  • (2) transmembrane
  • (3) precursor to (1)/(2)
A

1- gp120- binding to CD4 receptor

2- gp41- fusion and entry (possibly binding to co-receptor)

3- gp160 –> cleaved into gp120, gp41

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6
Q

list the 3 main genes found in all retroviruses and include what they code for generally

A

gag (group specific Ag): core, matrix, capsid proteins (p17, p24)

pol (polymerase)- reverse transcriptase, protease, integrase

env (envelope)- transmembrane glycoproteins (gp120, gp41)

Note- HIV has the most accessory genes of all retroviruses
-LTRs- long terminal repeats for gene expression once integrated

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7
Q

list the modes of HIV transmission (include infected body fluids)

A
  • unprotected sex (vaginal, oral, anal)
  • shared needles/syringes
  • vertical transmission

Body fluids: blood, semen, vaginal fluids, pre-seminal fluid, rectal fluids, breast milk
-contact with mucosa, damaged tissue, or blood-to-blood

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8
Q

HIV:

  • increases the risk of getting (1) infections, note before AIDS
  • (2) may decrease heterosexual transmission of HIV
  • (3) discuss survival of HIV in environment
A

1- other STIs
2- circumcision
3- doesn’t survive outside host long

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9
Q

HIV uses (1) to bind to (2), the main receptor. (3) is the initial co-receptor found on (4). (5) is the secondary co-receptor found on (6).

A

1- gp120
2- CD4 receptors

3/4- (m-tropism, early and less aggressive phase) CCR5: macrophages, dendritic cells, CD4 T cells (APCs)

5/6- (t-tropism, late and more aggressive phase) CXCR4: CD4 T cells

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10
Q

what is unique property of reverse transcriptase in terms of genome replication

A
  • viral (+)ssRNA –> dsDNA
  • *poor proofreader –> random errors

-uses host nucleotides

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11
Q

(1) will use viral dsDNA to create provirus
(2) will cleave polyprotein translated from viral mRNA to mature viral proteins; (3) is the key sign that a HIV virus has matured

A

1- integrase

2- protease

3- change of core shape –> bullet shaped (inverted cone shape)

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12
Q

(1) is the key receptor in the brain that HIV attaches to on (2) cells, resulting in formation of (3)

A

1- CCR3
2- microglial cells
3- brain nodules

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13
Q

initially HIV viruses enter the body and bind to (1) cells, leading to (2) progression before development of acute viremia

A
  • macrophages: internalized –> goes to LNs

- dendritic cells: accumulates on surface –> goes to LNs –> CD4 T cells infected

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14
Q

what parameters lead to AIDS diagnosis

A

1) T cells count <200

2) AIDS defining opportunistic infections

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15
Q

describe the two methods HIV uses to avoid Ab detection + the method to shied HIV from the immune system in general

A

1) gp120 antigenic drift (random errors via reverse transcriptase)
2) syncytia formation –> direct cell-to-cell spread (as opposed to cell lysis)

-viral latency / provirus in T cells and APCs shield virus from immune system

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16
Q

what is the function of HIV infecting dendritic cells, macrophages, and Th cells (CD-4) // APCs

A

loss of activators and controllers of immune system

17
Q

(T/F) antiretroviral drugs are able to eliminate latent HIV

A

F- no ARV has this function

18
Q

describe the cytopathic effects or cellular changes (often seen with in the brain)

A

HIV encephalopathy:

  • syncytial fusion of macrophages, microglial cells (to bypass immune system)
  • multinucleated giant cells (as a result of this fusion)
19
Q

list the stages of HIV infection + timeline

A

1) Acute HIV (acute retrovial syndrome), 2-4wks post-exposure
2) Chronic HIV, asymptomatic latency, years
3) AIDS, T cell count <200 and or AIDS defining opportunistic infections

20
Q

Acute HIV:

  • (1) timeline
  • (2) prevalence
  • (3) symptoms
  • (4) pathogenesis
A

1- 2-4wks post-exposure
2- 50-60% of Pts (non-specific / flu-like Sxs)

3- fever, HA, rash, lymphadenopathy, **oral ulcers (+ penis, anus)

4- rapid multiplication of virus + disseminated destruction of CD4 T cells –> high viral levels in blood, high risk of transmission

21
Q

Chronic HIV:

  • (1) main occurring process
  • (2) possible signs and symptoms
A

1- progressive decline of CD4 T cells

2- generalized lymphadenopathy + greater frequency and severity of some infections (thrush, VZV/shingles, cervical dysplasia)

22
Q

describe the distribution and timeline of HIV infected patients developing AIDS (w/o treatment)

A

80%, typical progression: 7-10 yrs

5-10%, rapid progression: <2yrs

10-15%, non-progression

23
Q

describe the timeline of viral copies in plasma and T cell count in HIV infections

A

Acute HIV: massive spike in HIV viral numbers + large decline in T cell count

(viral numbers sharply dec, T cell count bounces back, but not to as high numbers)

Chronic HIV: gradual T cell count decline, gradual viral number inc

AIDS: T cell count <200 –> massive inc in viral numbers

24
Q

HIV detection:

  • (1) is the initial sign of HIV in serum, include timeline
  • (2) is the general sign of HIV in serum, include timeline
  • (3) describe window period
A

1- p24 Ag: present after 10-12 days, lasts for 2-3 months (afterwards no free Ag –> all is bound // will not inc until T cell count <200)

2- anti-HIV Ab (gp120): not detectable for first 1-2 months

3- first 1-2 mos, no detectable anti-HIV Ab

25
Q

HIV testing:

  • (1) recommendation for all people
  • (2) recommendation for high-risk individuals
  • (3) recommendation for pregnant patients
A

1- once in lifetime for everyone 13-64 y/o

2- annually (all STDs)

3- 1st trimester (+ 3rd for high risk Pts)

26
Q

describe the pre-4th generation HIV testing, including timeline (hint- 3 tests)

A

1) HIV RNA, 11-12 days post-infection
2) p24 Ag, 14-15 days post-infection
3) ELISA, HIV Abs, 3-8wks post-infection (median ~25 days)

27
Q

describe the HIV Dx algorithm with 4th generation HIV testing

A

1) 4th Gen. ELISA: detects p24 Ag and anti-HIV Ab (gp120)
- very high sensitivity/specificty

2) (if positive) HIV1/HIV2 differentiation testing –> HIV1, HIV2 or indeterminant
3) (if inderterminant) HIV1 NAT testing –> (+) HIV1 or (-) HIV2

28
Q

(1) is the main test for monitoring HIV as it is suggestive of (2). (3) levels are considered undetectable and is the goal of anti-retroviral therapy.

A

1- viral load (NOT T cell count - too expensive)

2- severity of infection, disease progression –> monitor in therapy

3- <50 copies/mL

29
Q

list the other testing that is usually completed after an initial HIV diagnosis is made

A
  • test for all other STIs + annual testing: syphilis serology, NAATs for gonorrhea, chlamydia if necessary
  • test for HepB, HepC (90% chance of infection if IV drug user with HIV)
  • test for Tb
30
Q

discuss the use of PrEP in terms of HIV

A 
Pre-exposure prophylaxis:
\+very high efficacy
\+used for HIV neg. Pts at high risk: 
-high risk and no regular condom use
-HIV+ partner
-IV drug users sharing injection equipment

MNI (immuno path) (14 decks)

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