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IMMUNOPATHOGENESIS(L1) pt.1 - Coggle Diagram
IMMUNOPATHOGENESIS(L1) pt.1
Initiation of HIV infection
Stratified epithelium:Torn>virus enters into the internal environment(
Physical abrasion
)
Virus comes across the
Columnar/stratified epithelium
>
transmigrate
across the epithelial cell =
transcytosis
>meet with langerhans & dendritic cell>carry HIV to lymph nodes>provide initiation of immune response by T-CElls & macrophages
Inflammatory events
around epithelial cells>Cells part ways(opening for the virus to enter the epithelium tissue)
STI presence
increases the density of Langerhans cells(HIV targets) in the epithelial tissue both outer & inner NB:Interplay btwn epithelium,HIV targets & epidermal keratin layer(protect epidermis from beng infected with pathogens)
Transmission
Latent Phase(sub-clinical)>Decreased transmission
Late phase>dissolution of lymph nodes
Acute infection>high incident cases
HIV sequesters(attaches) in the
germinal centres
(follicular dendritic cells) of Lymph nodes
Within Germinal centers>passage of CD4 cells>help B cells make antibodies>get infected with the virus
CD4 cells are
minority
of population in circulation, &
majority
in lymph nodes(where HIV sequesters , & affects the cells)
Central role of CD4 t cells
Expansion required for
Production of Antibodies
, &
CD8 cytotoxic
>provide protection
Expansion of CD4 cells
(may be infected) as they are arund HIV infected dendritic cell needed to
Typical immune response to HIV
Protective immune response
(around CD8 cells)>Killer
Late arrival of n.antibodies>too late for host to prevent infection
Neutralising
antibodies take 7-9 months to be produced(takes long for antibodies to affinity)
Transmission
>
Dissemination
>
Control
(CD8+ cells ,CD4 , cytokine production>Serocoversion>Produce IgM>switches to IgG(binding antibodies)>then neutralising antibodies
Small % of people>able to be protected by CD8 cells(
ELITE individuals
)