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Pathology: Infectious disease section > Epidemiology and pathogenesis of AIDS > Flashcards

Epidemiology and pathogenesis of AIDS Flashcards

1
Q

most common routes of transmission of HIV in the world

A

heterosexual transmission

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2
Q

most common routes of transmission of HIV in the US

A

sexual transmission

-men: men with men

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3
Q

ethnicity/race/ and sex percentages

A
  • men: 41% black African American, 32% white, 24% Hispanic

- women: 62% black African American, 18% Hispanic, 17% white

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4
Q

top 3 transmission routes

A

60% male to male sexual contact
27% heterosexual contact
8% injection drug use

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5
Q

transmission of HIV happens when?

A
  • exchange of infected bodily fluids that allows for entry of virus across a mucosal membrane or injected parenterally
  • blood, semen, vaginal fluid, breast milk
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6
Q

What fluids have no documentation of spreading HIV?

A

-saliva and tears , sweat

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7
Q

MOST important mode of transmission

A

-unprotected sexual intercourse (80-85%) of both men and women

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8
Q

what percent of pediatric infections are perinatal transmission?

A

90%

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9
Q

what are 3 routes of perinatal transmission?

A
  • trans placental
  • infected birth canal
  • breast milk
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10
Q

what are precautious for fetus for not getting HIV?

A
  • universal HIV screening prior to week 36 or on delivery
  • risk of infection from untreated mother 30%
  • HAART treatment greatly reduces risk-> mother treated during pregnancy and infant for 6 weeks after birth
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11
Q

Genetic variability of HIV

A
  • HIV-1-> US and central Africa

- HIV-2 western Africa and India

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12
Q

Important proteins to note for HIV viral envelope

A
  • gp120: mediates binding of CD4 on macrophages, lymphocytes, glial cells
  • gp41: fusion to cell membranes
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13
Q

important core proteins to note for HIV

A

p24: major capsid proteins

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14
Q

Viral proteins

A

-proteases, intergrases, reverse transcriptases

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15
Q

where does HIV lay latent usually?

A

-in unactivated lymphocytes for long periods of time

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16
Q

what triggers proliferation of latent HIV

A
  • cell activation

- multiplication is cytotoxic to host cell

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17
Q

what is the normal ratio of CD4 to CD8 cells

A

CD4 2:1 CD8

-ratio flips in AIDS, 1:2

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18
Q

summary of progression

A

primary infection of cells in blood, mucosa-> drainage to lymph nodes-> infection established in lymphoid tissue-> VIREMIA->acute HIV syndrome, spread of infection throughout the body-> immune responses-> partial control of viral replication-> clinical latency inside lymphocyte-> extensive replication and CD4 lysis-> other microbial infections-> destruction of lymphoid tissue and depletion of CD4 cells-> CD4 count below 200-> AIDS

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19
Q

CD4 cell death by cytopathic effect of virus

A
  • chronic T cell activation ->viral replication in infected CD4 T cells-> death of infected cells
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20
Q

Death of CD4 cell by apoptosis of

A
  • chronic T cell activation -> activation of uninfected CD4 T cells-> activation induced cell death
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21
Q

HIV specific CTL death of CD4 cell

A

Chronic T cell activation-> expression of HIV peptides on infection CD4 T cells-> killing of infected cells by virus specific CTL’s

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22
Q

What does cell activation lead to?

A

cell death

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23
Q

CD4 cells with viral replication

A
  • Cytolysis by viral replication in activated CD4 cells

- killed by immune response to infected cells

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24
Q

how do uninfected CD4 cells die?

A

apoptosis

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25
Q

in HIV progression, what happens to CD8 cells and naïve T cells

A
  • CD8 cells activated by inflammation and die within lymph nodes (cytokine mediated)
  • naïve T cells die late in progress
26
Q

what are important things to approach with treatment

A
  • inhibit viral replication

- inhibit activation of cells already infected

27
Q

Most important measurement of HIV progression

A

-viral RNA levels

28
Q

what accelerates decrease in CD4 count?

A

-change in receptors, normally monotropic CCR5-> switches to CXCR4 (chemokine receptor)

29
Q

progressive loss of immune cells

A
  • loss of CD4 cells
  • inflammatory disruption of lymph nodes
  • loss of functional CD8 effector cells
30
Q

How is the virus found in the body?

A
  • within lymphocytes and in cell free state

- levels in genital secretions and plasma levels, genital levels may be higher though

31
Q

what is high efficacy of sexual transmission related to

A
  • abundant lymphoid tissue
  • abundant secretion: leucorrhea, prostatic secretions
  • concurrent infections/inflammation enhances breaks in mucosa, presence of inflammatory and immune cells
  • local reservoirs for virus-> lack of circumcision
32
Q

how does the virus enter the body?

A
  • abrasions, direct contact with bodily fluid, goes directly into blood vessels or adherence to dendritic cells in mucosa
  • parenteral transmission, IV drug use
33
Q

what does the virus require besides the receptor to enter cells?

A
  • co-receptor
  • gp120 binds CD4 molecules-> binding exposes a new recognition site for CCR5 or CXCR4
  • gp41 undergoes conformational change that results in the insertion of a fusion peptide
34
Q

Majority of virus forms require which chemokine receptor?

A

CCR5

-genital dendritic cells and GI lymphoid tissue express high amounts of CCR5

35
Q

what could happen to gp120 late in infection?

A
  • mutations in gp120 may alter its co-receptor requirement from CCR5 to CXCR4
  • monocytotropic-> CCR5 is expressed on monocytes and lymphocytes
  • lymphotropic-> CXCR4 is expression only on T-lymphocytes
36
Q

CXCR4-dependent viruses causes what?

A
  • syncytia formation in lymphoid tissue
  • bind to wider range of T cells, including naïve T cells and thymocytes
  • poor prognosis, rapid loss of lymphoid tissue
37
Q

what naturally blocks viral uptake early on with infection

A
  • inflammatory chemokines-> block binding of CCR5

- once switch occurs to CXCR4-> blockade is bypassed

38
Q

can CD4 negative cells still get infected?

A

Yes, actually enhance virus uptake by CD4 receptor negative cells

39
Q

establishment of viral reservoir

A
  • CCR5/CD4 positive cells in mucosa membranes-> local lymphoid tissue
  • virus undergoes limited proliferation in non-activated cells-> severe disease associated with an increase in virus proliferation and cytotoxicity in activated lymphocytes
  • virus mainly in lymphoid tissue (not peripheral lymphocytes)
40
Q

macrophages as a viral reservoir

A

virus proliferates in macrophages

  • provide transport of virus throughout body, including CNS (glial cells)
  • mucosal dendritic cells-> entry and transport
  • follicular dendritic cells-> viral reservoir
41
Q

Viremia with HIV

A

-significant viremia leading to seeding of lymphoid tissues throughout the body

42
Q

what causes the second slower phase of virus clearing

A
  • initially 100 billion virions are produced each day with destruction and replacement of nearly 2 billion CD4 lymphocytes each day
  • initial decay-> virus specific CD8 T cell response-> destroys virally infected cells and terminates early infection
  • DUE TO: loss of longer lived viral reservoirs
43
Q

because there is a low level of plasma viral RNA, the virus is still_____

A

-HIV continues to proliferate in lymphoid tissue reservoirs

44
Q

definition of latent phase

A

-period between acute infection with establishment of reservoir and eventual loss of immune function

45
Q

what is one goal of therapy?

A

prolong latent phase

46
Q

What results from progression of infection?

A
  • results in loss of adequate immune function

- death usually from overwhelming infection

47
Q

what are 3 main factors for progressive development of immune deficiency?

A
  • continued loss of CD4 cells
  • associated loss of CD8 functions
  • evolutionary changes in virus
  • “productive infection of T cells and viral replication in infected cells is the major mechanism by which HIV causes lysis of CD4 T cells”
48
Q

what stays continual with progression of infection?

A

replication of virus in CD4 cells

49
Q

what is progressive of immune function is associated with disruption of?

A
  • lymph node function and architecture
  • increased inflammatory activation of macrophages retention of effector CD8 cells within lymph nodes
  • bystander injury of cells by inflammatory lymphokines and monokines
  • immune and inflammatory activation of lymphocytes and macrophages which leds to further replication of virus
50
Q

what causes “burn out”

A

chronic inflammation with eventual cell loss of fibrosis of lymph nodes

51
Q

what does concurrent infection result in?

A

-immune activation and speeds progression immune cell loss

52
Q

what does extensive early loss of CD4 cells from peyer’s patches lead to?

A
  • products from gut pathogens are released into blood stream-> resulting in Ag released and non-specific activation of these cells
  • binding to toll like receptors activates inflammation
  • increased production of immunoglobulins
  • increased cells entering into proliferative phase leading to cytolysis or apoptosis
53
Q

progression of infection in relation to CD8 cells

A
  • chronic inflammation and immune activation of both CD4 and CD8 cells
  • increased viral replication and cytolysis
  • enhanced apoptosis of non-infected cells
  • disruption of CD8 effector mechanism
54
Q

what does it mean when CD8 T cells become “sticky”

A

-with activation, effector CD8 T cells become “sticky” by expressing CD69-> retained within lymph nodes

55
Q

what are some other mechanisms of decreased immune function?

A
  1. apoptosis of uninfected lymphocytes mediated by soluble gp120 bound to CD40, also killing by CD8 cells specific for gp120
  2. blocking of immune function by binding of gp120 to CD4 molecules-> interferes with antigen presentation and cell-cell interactions
  3. production of toxic lymphokines by infected cells
56
Q

what qualitative defects still happen in asymptomatic individuals?

A
  • defects in T cell function
  • decrease in T cell proliferation
  • decrease Th1 responses
  • loss of memory CD4 subsets
57
Q

what evolutionary changes have evolved to help the virus in progression of infection?

A
  • virus can change envelope proteins
  • evolution from CCR5 to CXCR4 co-receptor form associated with syncytia formation
  • virus evolves for drug resistant strains
58
Q

two current treatment maxiums formed from drug resistant strains

A
  1. maximal inhibition of virus replication should result in a decrease in the frequency of drug resistance
  2. treatment should always include multiple agents
59
Q

immunological demise summary

A
  • initially activation of immune cells by both specific and innate (TLR) mechanisms results in lymphadenopathy and hyperammaglobulinemia
  • corresponds to germinal center hyperplasia in lymph nodes
  • further systemic activation of immune response (M and CD8 cells) leads to inflammatory cytokine-mediated immune dysfunction-> architectural and functional disruption of lymph nodes, burn out
60
Q

progressive defects in immune function

A

loss of memory T cells, CD4

disruption of effector T cells (CD8)-mediated processes

61
Q

clinical features of disease related to progression loss of immune function?

A
  • Opportunistic infections
  • neoplastic proliferation and endothelial cells and lymphoid tissues-> mostly associated with infectious organisms such as HHV8, EBV, HTLV, papilloma virus

Pathology: Infectious disease section (11 decks)

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