HIV Flashcards

1
Q

Hallmark of AIDS

A

profound immuno deficiency

affecting cell mediated immunity

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2
Q

loss of CD4+ T cells is from

A

infection of cells

direct cytopathic effect

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3
Q

most CD4+ T cells are found in

A

mucosal and peripheral lymphoid organs

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4
Q

steady attrition of CD4 cells

A

productive infection in a fraction of latently infection by cytokines and Ags

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5
Q

Direct cytopathic effect of replicating virus

A

inc plasma mem permeability
– budding
virus replication interferes with cell protein synthesis

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6
Q

does virus kill or infect more T cells

A

kill>infect

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7
Q

type of apoptosis

A

activation induced apoptosis

due to chronic activation of UNinfected cells by HIV

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8
Q

infection leads to cell death called what?

A

Pyroptosis

infl cytokines, cell contents released for recruitment of new cells for infection

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9
Q

progressive destruction of architecture seen in

A

spleen
lymph nodes
tonsils

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10
Q

qualitative defercts of CD4+ T cells

A

Dec in Th1 type response
defect in intracellular signaling
selevtive loss of memory subset

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11
Q

an important featuer of HIV

where is it found

A

latent infection
CD4+T cells, Macs in lymph nodes

protects from antiviral therapy, persistent reservoir

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12
Q

Monocytes vs Macs, which are more infected

A

Macs in TISSUE&raquo_space; Monocytes in Blood

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13
Q

which cell becomes a virus factory later in infection when CD4+ counts are low?

A

Macs

  • few viruses bud
  • store large number of virus particles
  • allow replication, but resistant to cytopathic effects
  • protected from host defenses
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14
Q

what plays an important role in CNS infection

A

Monocytes

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15
Q

What are the functional defects seen in UNinfected Macs?

A
  • impaired microbicidal activity
  • dec chemotaxis
  • dec secretion of IL-1
  • Inapp secretion of TNF
  • poor capacity to present Ag
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16
Q

Which DC are initially infected by virus

A

Mucosal

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17
Q

Mucosal DC transport virus to

A

regional LN —> CD4 T cells

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18
Q

what are the two reservoirs of HIV

A

Macs

Follicular DC

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19
Q

how do follicular DC trap HIV virions

A

receptor for Fc of Ig coating HIV

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20
Q

Do B lymphocytes get infected?

A

No, only affected

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21
Q

How are B lymphs affected?

A
  • hyperplasia due to polyclonal activation
  • BM plasmacytosis
  • Hypergammaglobulinemia
  • circulating immune complex
  • can’t mount Ab resp to new Ag, lack of T helper/ intrinsic defect
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22
Q

Impaired humoral immunity renders ptns vulnerable to what

A

disseminated inf caused by encapsulated bacteria

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23
Q

Major target of HIV infection

A

Nervous system

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24
Q

predominant cell types infected in CNS

A

macs

microglia

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25
Q

what carries HIV to brain

A

monocytes

26
Q

are neurons infected?

A

no

27
Q

Is the CNS involvement direct or indirect?

A

indirect

28
Q

CNS damage is caused by cytokines:

A

IL1
TNF
IL6

29
Q

Early infection characterized by

A

inf of memeory CD4 T cells - mucosal Lymphoid tissue and death

30
Q

After early infection

A

dissemination to LN by infected DC

31
Q

Virus enters thru

A

mucosal epithelia

32
Q

how does virus pass to CD4 t cells in LN

A

direct cell-cell contact

33
Q

what leads to viremia

A

replication in LN

34
Q

what corresponds to drop in serum titers? how long after exposure

A

Seroconversion

3-7 wks

35
Q

Acute retroviral syndrome

A

40-90% ptns
3-6 wks after inf, resolves in 2-4 wks

= sore throat, myalgias, fever/sweats, weight loss, fatigue
= rash, cervical adenopathy, diarrhea, vomiting

36
Q

what characterizes Primary infection

A

virus dissemination and retroviral syndrome

37
Q

what characterizes Chronic inefction

A

clinical latency

38
Q

Sites of continuous HIV replication/destruction

A

LN, Spleen

39
Q

opportunistic infections

A

candidiasis, herpes zoster, TB

40
Q

Diagnosis of AIDS

A
  • opportunistic infections/ cancer

- CD4+

41
Q

AIDS presents w/

A

fatigue
weight loss
diarrhea

42
Q

majority of deaths in untreated AIDS ptns

A

opportunistic infections

43
Q

Candidiasis

A

most common fungal infection

oral cavity, vagina, esophagus

44
Q

CMV

A

dissemintaed

eyes and GI

45
Q

Toxoplasmosis gondii

A

encephalitis

cerebral abscess

46
Q

JC virus

A

human papovavirus

progressive multifocal leukoencephalopathy

47
Q

Oncogenic DNA virus

A

seen with AIDS

48
Q

most common cancer in AIDS ptn

A

Kaposi’s sarcoma

  • vascular neoplasm
  • purple skin lesions/disseminated disease in LN, skin, GI, lungs
  • HHV8
49
Q

Co-factor of kaposi’s sarcoma

A

immunosuppression

50
Q

which canceri s often in late in disease course of IADS pt

A

High grade B cell lymphomas

peripheral LN, brain, body cavities
EBV assoc
risk inc with low CD4

51
Q

High risk of ____ in women, ____ in men assoc with _____ infection

A

cervical dysplasia
anal cancer
HPV

52
Q

Long term side effects of antiretroviral therapy

A
  • lipoatrophy - loss of facial fat
  • excess fat deposition centrally
  • premature cardiovascular, kidney, liver disease
53
Q

Major cause of morbidity in AIDS ptn

A

premature cardiovascular, kidney, liver disease

54
Q

what anatomic changes are seen in HIV/AIDS

A

none

55
Q

Lesions are characteristic of

A

opportunistici nfections

56
Q

Morphology of LN:

A
  • follicular hyperplasia (early)
  • follicular involution (later) - depletion of cells/disrupted org network of follicular DC
  • trapped virus; small burnt out lymph nodes, spleen, thymus
57
Q

Rapid HIV test

A

simultaneous detection of HIV-1 p24 ag/Ab to both HIV

Ag provides earlier detection than Ab

58
Q

Ab studies

A

Ab develops w/in 3 months

59
Q

CD4+ T cell count

A
  • absolute levels are prognostic
  • disease progression
  • used for CDC classification
60
Q

Viral load test

A
  • level of HIV-1 RNA
  • predicts clinical outcome
  • effectiveness of antiviral therapy
61
Q

CDC algorith for HIV diagnostic testing

A

1 Ag (HIV1 p24) in blood ( Ab appears later)
2 immunoassay to differentiate HIV1 and 2 ab
3 positive Ag, but neg or indeterminate Ab diff - use HIV-1 nucleic acid testing