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CMBM exam 3 > Pathogenesis of AIDS > Flashcards

Pathogenesis of AIDS Flashcards

0
Q

HIV infection stage is based on

A

age specifc CD4+ T cell count

CD4 T cell % of total Lymphocytes

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1
Q

Stage 0

A

early infection
recognized by HIV-test within 180 days of the first HIV+ test
meaning test positive within 180 days of the last negative test

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2
Q

stage 1

A

No AIDS-defining condition and a CD4 cell count at or above the cells/ul indicated per age

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3
Q

stage 2

A

No AIDS defining condition and a CD4 cell count at or above the cells/ul indicated per age

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4
Q

stage 3

A

AIDS

documented AIDS defining condition or CD4 cell count less than 200, 500 or 750 cells/ul indicated per age

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5
Q

Stage unknown

A

lab confirmation of HIv infection but no information on Cd4 cell count, CD4 cell percentage, or the presence of an AIDS-defining condition

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6
Q

Staging can be bidirectional given ….

A

no AIDS defining condition is present

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7
Q

AIDS defining illness in children under 6

A

Bacterial infections, multiple or recurrent

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8
Q

AIDS defining illnesses in adults, adolescents or children over 6yo

A

cervical cancer, invasive
Mycobacterium TB of any site, pulmonary
Pneumonia, recurrent

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9
Q

Phases of HIV infection

A
  1. Acute retroviral syndrome - weeks
  2. Chronic HIV - years to decades
  3. AIDS - Months to years
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10
Q

Acute retroviral syndrome

A

primary infection of cells in blood and mucosa
infection is then established in lymphoid tissues leading to viremia
Acute HIV syndrome when spread of infection throughout body
seroconversion - Anti HIV antibodies and HIV specific CTLs
Immune response

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11
Q

Chronic HIV

A

Clinical latency
establishment of chronic infection
virus trapped in lymphoid tissues by follicular DCs, low level of viral production
other microbial infections or cytokines can lead to increased viral replication

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12
Q

AIDS - phase

A

destruction of lymphoid tissue

depletion of CD4 T cells

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13
Q

Constitutional symptoms of ARS

A

fever*
chills*
fatigue*
Night sweats, anorexia and wt loss

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14
Q

Lymphatic symptoms of ARS

A

*Swollen lymph nodes especially in groin, head and neck

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15
Q

Nose and throat symptoms of ARS

A

*Sore throat, with or without ulcers or thrush

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16
Q

GI symptoms of ARS

A

Nausea
emesis
diarrhea

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17
Q

Musculoskeletal symptoms of ARS

A

Asymmetric joint swelling and tenderness

*myalgias

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18
Q

Neurologic symptoms of ARS

A

personality changes, headache, and painful, stiff neck

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19
Q

Rash characteristics of ARS

A

Maculopapular and primarily on trunk and/or proximal extremities

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20
Q

characteristics of oral lesions in ARS

A

thrush develops commonly on soft palate

early lesions also seen along gingival border

21
Q

Reactivation in ARS

A

can reactivate HSV - cold sores

or VSZ - shingles

22
Q

How can HIV enter the body?

A

blood
colon-rectum
vagina

23
Q

What happens when HIV initially enters?

A

infects macrophages

24
Q

How does HIV affect macrophages?

A

creates virus reservoir
infects the microglial cells of the brain, Pulmonary alveolar macs and Dendritic cells in skin
Causes macrophage dysfunction, virus release and cytokine release and dysregulation of immune function

25
Q

Where do HIV travel for its latent period?

A

Lymph nodes

26
Q

What happens upon increased viral load in the blood with regards to immunopathogenesis?

A

by this time, HIV has been able to infect CD4 T cells
if crosses the BBB leads to AIDS dementia
through CD4 ctyloysis causes
-immunodeficiency
-loss of B cell control - lymphadenopathy, hypergammaglobulinemia
-Loss of DTH (delayed type hypersensitivity) function - cutaneous infection and intracellular pathogens

27
Q

what happens as a result of loss of T cell function?

A

severe systemic opportunistic infections
Kaposi’s sarcoma
Lymphoma

28
Q

HIV causes ??? and what are the outcomes

A

-Lytic and latent infection of CD4 T cells
-Persistent infection of cells of macrophage family
-Disrupts neuron function
Outcomes are:
Immunodeficiency, AIDS dementia (crosses the BBB)

29
Q

Briefly describe progression of untreated HIV

A

About 6 weeks after primary infection, CD4 T cell count falls drastically. At this same time, viral load peaks. This is acute HIV syndrome and there is wide dissemination of virus and seeding of lymphoid organs
small T cell count recovery around 12 weeks as viral load drop while virus enters latent period
over next 10-11 years, viral load slowly increases as CD4 count continues to slowly decrease
Constitutional symptoms appear 7-8 years
opportunistic infections occur as viral load increases exponentially
Death by year 10 -11

30
Q

what happens due to loss of CD4 T cells during Chronic HIV?

A

through infection and loss of CD4 cells

  • loss control of nonlymphoid cells
  • loss of growth and control of B cells
  • Growth and control of CD4 and CD8 T cells and NK cells - this leads to tumors and HIV progression
  • loss of DTH which leaves vulnerable to intracellular organisms
31
Q

what are some immunologic events affecting Macrophages and DCs during an HIV infection?

A 
Macrophages carry HIV into CNS 
Excess secretion of cytokines in lymph nodes 
Decreased antigen presentation 
Decreased MHC II expression 
Decreased chemotaxis 
Decreased phagocytic ability 
Decreased cytotoxic ability
32
Q

AIDS-dementia complex

A 
(HIV/AIDS encephalopathy) 
results of HIV entering brain via microglial transport leads to: 
-memory loss 
-impaired cognition 
-impaired motor function 
-behavioral changes 
-Apathy 
-depression 
occurs as CD4 count falls to <200 cell/microliter
33
Q

Due to Highly active anti retroviral therapy, ADC has

A

declined to <20% of those HIV+

may also improve mental function in those with ADC already

34
Q

How does HIV evade the immune system?

A
  • Antigenic drift of gp120 - evades antibody detection
  • Heavy glycosylation of gp120 - evades antibody detection
  • Infection of lymphocytes and Macrophages - inactivation of key element of immune defense
  • Inactivation of CD4 helper cells - loss of activator of immune system and delayed type hypersensitivity
35
Q

what are the possible outcomes of HIV infections?

A

rapid progression - AIDS in 2-3 yrs
typical progressors - AIDS in 10 yrs
Long-term nonprogressors - low HIV levels, normal CD4 T cells >10 yrs after HIV positive - BM transplant case (usually HIV-2 or HIV-1 ??)
Highly exposed persistently seronegative patients - infected but no HIV antibodies or HIV-RNA detected

36
Q

Describe M-Tropic (R5)

A

Initial stages of infection mediated by R5
Macs and DCs are persistently infected and major reservoirs and means of distribution (Trojan Horses)
Targeting of CCR5 expressing T cells depletes GALT of CD4 T cells - lyse
Deficient CCR5 receptor pts more resistant to HIV infection and CCR5 in binding target for antiviral drugs

37
Q

Describe T-Tropic (X4)

A

change in receptor preference to CXCR4 occurs late and correlates with progression of disease
Mutation of ENV gene for gp120 shifts tropism from R5 to X4
some viruses use both R5X4 receptors
Development of symptoms of AIDS

38
Q

what is occuring pathology wise during development of symptoms of AIDS?

A

correlates with increased release of virus into the blood
increase in X4 virus
decrease in CD4 T cells
subsequent decrease in total T cell numbers (CD3 bearing cells) due to the lack of helper function

39
Q

CD4 expressed

A

on surface of CD4 T lymphocytes (helper) and macrophages (including dendritic cells)

40
Q

CCR5 expressed

A

on CD4+ T lymphocytes and macrophages

41
Q

CXCR4 expressed on

A

CD4+ T lymphocytes and T cell lines

42
Q

HIV-2 is less _____ than HIV-1

A

pathogenic
most HIV-2 pts are long term non progressors
longer asymptomatic stage, slower decline in CD4 T cell count
lower mortality rate due to AIDS
pts with HIV-2 are less infectious in early stages but trasmission rate increases as disease progresses

43
Q

HIV-2 was more difficult to monitor but

A

in 2014, first FDA licensed viral load assay to detect HIV-2 nucleic acid was approved

44
Q

Treatment of HIV-1 vs. HIV-2

A

some drugs for HIV-1 are not effective for HIV-2

HIV-2 is intrinsically resistant to Fusion inhibitors and non-nucleoside reverse transcriptase inhibitor based regimens

45
Q

List some Antiviral therapies

A

Nucleoside Analogue reverse transcriptase inhibitors
Non nucleoside reverse transcriptase inhibitors
Protease inhibitors
Binding and Fusion inhibitors
Integrase inhibitors

46
Q

A small number of ppl are resistant to infection because

A

have mutations in genes encoding CCR5 and/or CXCR4 co receptors
CCR5delta32 mutation - leads to a truncated protein with loss of extracellular component
-Homozygous mutation - immune
-Heterozygous mutation - decreases chances of infection, slows disease progression

47
Q

Out of ppl who are naturally HIV immune, they were found to carry

A

gene called HLA B57
leads to larger production of CD8/killer cells
CTLs are cross reactive - attack more than one epitope associated with HIV including mutants that arise
contributes to strong response towards viruses that rapidly evolve
increase susceptibility to autoimmune diseases, in which T cells attack the body’s own cells

48
Q

Mucosal immunity generated by frequent ______

A

sexual exposure to HIV

meaning immunity generated by cells lining the genital membranes prevented infection

49
Q

Cells of macrophage lineage include

A 
monocytes 
macrophages 
alveolar macs of the lung 
dendritic cells of skin 
microglial cells of brain

CMBM exam 3 (24 decks)

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