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Case 7: HIV > Virology: HIV > Flashcards

Virology: HIV Flashcards

1
Q

What is a retrovirus

A

A RNA virus that requires host DNA to replicate causing a life long infection w/ or w/o clinical disease

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2
Q

What is the morphology of a retrovirus

A

Lipid envelope w/ lipid proteins (protein spikes) called gp160 that cleaves into gp120 to attach to T cell & gp41 that fuse & enters into T cell
2+ sense ssRNA w/ p24 protein surrounded by conical core
Contains key enzymes like reverse transcriptase, protease & integrase

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3
Q

What is the 3 main genes that encodes for the virus

A

GAG: p24
Pol: enzymes
Env: envelope proteins

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4
Q

What does HIV use to enter a cell

A

CCR5: monocytes, macrophages & dendritic cells going to lymph nodes
CXCR4: replicate in T cells (occurs later in infection)

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5
Q

What is HTLV-1, how does it spread & replication rate

A

Chronic infection & clonal expansion causing T cell leukaemia
Spread via: sexual transmission, parental & vertical
Low replication rate causing low infectivity

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6
Q

What is the 3 complications of HTLV-1

A
  1. Infective dermatitis: in children w/ chronic severe impetigo
  2. Adult T cell leukaemia: infection acquired in childhood causing an aggressive tumour in skin & brain
  3. Tropical spastic para-paresis: infection in adulthood causing difficulty walking because of either affects the spinal cord
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7
Q

What is the origin of HIV & what is causing the pandemic

A

A cross species infection w/ group M causing current pandemic

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8
Q

What HIV 1 subtypes is causing the majority of the infection

A

Type C

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9
Q

What is the significance of the different subtypes

A

Different antigens influence the development of vaccines & diagnosis BUT same pathogenesis

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10
Q

How is HIV transmitted

A

Sexual transmission (w/ STI increasing risk of transmission)
Parental/horizontal via blood or needle
Vertical via mother to child transmission

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11
Q

Describe the pathogenesis/life cycle of HIV

A
  1. GP120 binds to CD4+ receptor
  2. GP41 binds to CCR5/CXCR4 for entry
  3. In host cytoplasm, viral RNA transcribed via reverse transcriptase into cDNA then dsDNA
  4. dsDNA is transported into the nucleus & integrase fuse host & viral DNA establishing infection (infection can remain dormant or replicate)
  5. Lytic infection & DNA transcription occur producing viral RNA & protein
  6. Virus particles assemble in cytoplasm & buds off
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12
Q

Give 2 reasons why HIV have variations

A
  1. High mutation due to RT misread
  2. Recombination of a cell w/ 2 viruses leading to a new virus
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13
Q

Why is it complicated to produce antibodies against HIV

A

Due to GP120 that mutates rapidly

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14
Q

Describe the course of the infection w/ a graph

A

Look at graph
1. Transmission:
a. HIV penetrates the epithelial surface
b. Epidermal Langerhans cells bind to GP120 via CD207 to internalise & degrade virus particles
c. Activated Langerhans cells move to lymph nodes for antigen presentation to CD4/8+ T cells & produces pro-inflammatory cytokines causing a fever (increase permeability & dilation - increased local blood flow)
d. CD4+ T cells can be trans infected & LC can infect themself
2. Dissemination:
a. Lymphadenopathy: B lymphocytes enlarge
b. HIV infected T cells move to mucosal tissue (dissemination) increasing viral replication in lymph nodes = increase viral load in blood
c. Decrease in CD4+ T cells especially gut lymphoid
d. Tissue macrophages become infected (express CD4/CCR5)
e. DC captures HIV on surface via CD209 & mediate CD4+ T cell trans infection = increasing viral load further
3. Control of viraemia:
a. Partial resolution at acute stage due to T cell interactions
b. Tissue DC engulf extracellular virus & present Ag via MHC1/2 to CD4/8+ T cells in lymph tissue
c. Activated HIV specific CD8+ T cells kill HIV infected cells that decrease viral replication & increase CD4+ Th cell
do not eradicate infection or increase CD4+ T cell count back to baseline
4. Seroconversion:
a. Presence of antibodies appear 4-6 weeks after transmission
b. HIV specific antibodies requires sufficient HIV Ag presentation to B lymphocytes via follicular DC in lymph follicles in lymph nodes
c. + HIV specific CD4+ T cells required to send activation signals for B cells differentiation into plasma cells

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15
Q

What & why is the effect of HIV on the gut

A

The gut is rich in lymphoid tissue & expresses integrin a4b7 where HIV env protein binds to causing MALT destruction due to increased inflammation, cell apoptosis & engulfed dead cells causing further inflammation having long term consequences
This leads to more Ag being able to access the systemic circulation increasing the antigenic load reaching the lymph nodes further increasing inflammation & increase CD4+ T cell susceptibility to infection

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16
Q

How long does clinical latency take

A

Can take up to 8 years

17
Q

What is 2 requirement to it classify as AIDS

A
  1. CD4+ T cells count is less than 200
  2. Opportunistic infections begin
18
Q

What is a elite controller

A

Individuals who maintain low/undetectable viral load & preserve immune function w/o ARV

19
Q

Name 2 ways the T cell pool maintained w/ HIV

A
  1. Replaced by the thymus & cell division of mature cell in primary lymphoid organs
  2. In HIV the T cell death rate is so high to maintain T cell pool replaced by maturation of secondary lymphoid organs
20
Q

What is the connection between CTL response & HIV outcome

A

Stronger cytotoxic T lymphocyte response leads to increased survival due to quicker response to kill infected cells before it spreads the virus that decreases viral load

21
Q

What is the 3 ways of T cell death

A
  1. Viral lysis: release of new virus particle kills cell
  2. CTL lysis: CD8+ T cell recognise antigen on MHC1 of infected cell & kill before released
  3. Pyroptosis: cell suicide due to unsuccessful HIV infection due to incomplete reverse transcriptase causing the cell to burst & cause severe inflammation
22
Q

Why does the immune system fail

A

Due to chronic immune activation
The combination of pyroptosis & damaged MALT leads to disease progression

23
Q

3 effects of immune system failure

A
  1. Immune cells dysfunction
  2. Lymphoid tissue structure destruction
  3. Impaired cell replacement of dying cells
24
Q

When does the HIV infection becomes a persistent viral infection

A

When the viral DNA is integrated into host DNA & can not me cleared

25
Q

Give 5 reasons why the HIV virus is persistent

A
  1. Sanctuary sites: hides in the brain that can not mount an specific immune response
  2. Latency: hide from immune system & ARV by not expressing Ag
  3. Interfering w/ Ag presentation: HIV encodes proteins that change Ag presenting pathways & down regulate MHC molecule
  4. Ag variation: point mutation of gp120 & evade CTLR
  5. Ab failure: requires time to develop Ab & HIV already established (early Ab fails to neutralise)
26
Q

What is the 2 ways HIV is diagnosed in

A
  1. Antibody detection
  2. Virus detection
27
Q

How does the ELISA test work

A

Tests for antibodies
Perform 2 test from 2 different samples to increase sensitivity & specificity

28
Q

2 instances who antibodies HIV diagnosis tests not performed

A

Early infections (first 4-6 weeks)
Babies as they have antibodies from mothers

29
Q

How does a rapid antibodies test work

A

Detects antibodies & IgG on a strip w/ HIV Ag
Both strip colour needs to change = +

30
Q

What is the 3 virus detection tests

A
  1. p24 Ag
  2. PCR
  3. Viral load
31
Q

What is the 2 antibody detection tests

A
  1. ELISA
  2. Rapid test
32
Q

How does the p24 antigen virus detection test work

A

Detects virus at initial peak & disappear after Ag-Ab complexes form
EARLY DETECTION

33
Q

For who is the PCR test & why

A

Used in babies/children
As they have maternal antibodies & very expensive but sensitive test

34
Q

What is used to monitor infection & why

A
  1. Viral load: monitor effect of drug therapy & assess prognosis
  2. CD4+ T cell: monitor response to ARV & indicate prophylaxis

Case 7: HIV (6 decks)

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