13_HIV/AIDs Flashcards

1
Q

What is underlying pathological cause of immunosuppression?

A
  • depletion of CD4 T cells
  • isolation of HIV retrovirus occurred in 1984 –> shown to be CD4 T tropic key link
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2
Q

when did symptoms develop for HIV in the US?

A
  • there’s a delay between HIV-1 infection and development of sxs (clinical latency), such as secondary infections –> indicates HIV-1 infections in US begain in early to mid-1970S
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3
Q

epidemiology of HIV in US

A
  • 1.2M people w/ HIV in the US, at diff’t stages
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4
Q

HIV virion:

  • structure
  • prevalence
  • origin for HIV-1
A
  • structure: mature HIV type 1 –> elongated internal cores
  • most prevalent in Africa, but still a global concern
    • sub-saharan Africa
    • 40M worldwide
  • primate origin for HIV-1
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5
Q

Describe the origin of HIV virus

A
  • Lentivirus from primates made the adaptation to humans in mid-1900s –>
  • gave rise to HIV-1 and HIV-2
  • how?
    • monkeys destined for local market place or export
    • some pet monkeys
    • monkeys as food source
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6
Q

how is HIV transmitted?

A
  • unprotected sexual intercourse w/ infected partner
  • vertical transmission (mother to child)
  • injection drug use (rare)
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7
Q

describe the replication cycle for HIV-1

A
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8
Q

how is the HIV-1 genome organized?

A
  • structural proteins
  • enzymes
  • coat proteins

Includes Gag, Pol, and envelope genes

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9
Q

two different tropic strains of HIV-1

fuction of each?

A
  • M-tropic = “macrophage-tropic strain of HIV-1”
  • T-tropic = “T-cell-line-tropic strain of HIV-1”

M tropic infxn is followed by switch to T tropic –> depletes CD4 T cells –> resulting in AIDS

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10
Q

At what point can HIV-1 lead to T cell depletion?

A

after HIV-1 infects monocytes –> can genetically change to tropic T cells –> leading to T-cell depletion

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11
Q

what is the suggested meghanisms for depletion of CD4 cells?

A
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12
Q

what are the functions of T helper cells?

A
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13
Q

what confers genetic plasticity to HIV-1?

A
  1. Reverse Transcription (RT) error prone lacks proof-reading 1 in 10,000
  2. Stand switching from one genome to another during replication, co-infection, or following super-infection (HIV-1 is diploid)
  3. recombination following co-infection and superinfection
  4. transcription of integrated proviral DNA by host RNA polymerase II error prone
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14
Q

what are the consequences of HIV-1’s genetic plasticity?

A
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15
Q

disease course of HIV/AIDS

relationship b/w CD4+ lymphocyte count and HIV RNA copies?

A
  • as HIV RNA copies increase, the CD4 T cell cound decreases
  • Once CD4 count is below 200/mL, considered AIDS
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16
Q

what is the acute phase of HIV syndrome?

Timing and sxs?

A
  • T cells appear to be targets of infxn even early on; high levels of circulating virus (10^8 viral particles/mL)
    • viral population may double every 6-10 hours
    • each infected cell can resul tin infxn of about 20 cells;
    • seeding of lymphoid organs and CNS
  • Sxs occur days-wks after infxn w/ HIV
    • sxs: fever, fatigue/lack of energy and motivation
    • rash (maculopapular)
    • lymphadenopathy
    • pharyngitis
    • thrush (candida)
17
Q

disease progression of HIV

(acute vs. long)

A
18
Q

How does AIDS affect the clinical presentation of diseases?

A

clinical presentation of any of these conditions is much worse (due to fever CD4 T cell count)

19
Q

What are the early sxs in secondary infections?

last symptom of secondary HIV infxn?

A
  • Early sxs:
    • Thrush, and
    • Oral Hairy Leukoplakia
  • Late sxs: Mycobacterium avium complex disease
20
Q

Oral hairy leukoplakia (OHL):

what is it a sign of?

A

sign of EBV replication in epithelial cells

if not already diagnosed w/ HIV, this is an indiction for testing

21
Q

Mycobacterium avium complex:

prevalence

when does it develop?

A
  • organisms are ubiquitous; but commonly found in water/soil
  • develops when CD4 count is lower than 75
    • usually, organism is ingested –> disseminates to rest of the body
22
Q

What virus is associated w/ the following malignancies?

A
23
Q

what is the following skin lesion?

A
24
Q

progressive multifocal leukoencephalopathy (PML)

define

A

caused by Human polyomavirus JC

25
Q

HIV-1 Associated Neurological DIsease (HAND)

define

A

HIV-1 Infxn can often lead to neurological sxs directly or by inducing the reactivation and infection of the brain by other agents –

common to develop neuro conditions

26
Q

How to diagnose AIDS?

How to diagnose HIV-1?

A
  • AIDS: dx by depleted immune system (<200 CD4 cells/mL)
  • HIV-1
    • Primary infxn:
      • infectious mono-like illness, viral syndrome, flu-like sxs
      • enzyme-linked immune sorbent assay (ELISA) TO P24
      • western blotting gp120, gp160, gp41, p24
    • Late onset –> beginning of AIDS: Oral hairy leukoplakia & lymphadenopathy
      1. CD4+ T cell numbers and HIV RNA load in plasma
      2. Sequencing of HIV-1 pol gene, or phenotyping to determine sensitivity to HAART is cost effective
27
Q

what is the optimal management of HIV-1 positive patients?

A
28
Q

how to prevent HIV-1 infection?

A
  • HAART Therapy: highly active anti-retroviral therapy
    • only therapy available for HIV-1/AIDS pts;
    • consists of reverse transcriptase, fusion/entry, and proteast inhibitors
  • AND CONDOM USE
  • (combined, the 2 can reduce transmission risk to near 0% risk)
29
Q

when to start tx after HIV infxn?

what effect does it have on breastfeeding?

A
  • w/in a year of seroconversion – w/in a few weeks of HIV infxn when Abs to the virus are first produced and their concentration reaches a detectable level (tx should be as soon as possible)
  • 10-15% of HIV-negative babies will become infected by breastfeeding mother; can be prevented by ART of newborn