HIV infection and immune system Flashcards
Primary ID
Inherited/acquired - genetic basis (mutations) and are relatively rare
Secondary ID
Always acquired, more common, caused by extrinsic factors (HIV, extreme age, drugs)
Cell mediated immunity
Why is it bad not to have a thymus
No maturation of T cells and B cells
Mutation disorder causing primary ID
Affects adaptive immunity
Leads to defect on chromosome 22 - DiGeorge syndrome
More susceptible to intracellular pathogens
Absent thymus
Polymorphism disorder causing primary ID
Innate immunity
HLA disorder
Affects antigen presentation
More susceptible to viruses
Polygenic disorder and primary ID
Adaptive immunity
IgA deficiency
More susceptible to some bacteria
HIV causing secondary ID
Adaptive immunity affected, causes HIV infection -> AIDS -> eliminates CD4 cells -> viral/fungal/protozoa
Extreme age causing secondary ID
Adaptive immunity affected -> lack of maternal antibodies -> premature baby susceptible to infection
Drugs causing secondary ID
Adaptive immunity affected -> T and B cell deficiency -> cytotoxic cell damage -> opportunistic infections rise
How does HIV infect a cell
gp120 binds to cd4
viral genome enters cell
reverse transcriptase catalyses ssRNA forming RNA-DNA
Ribonuclease H degrades the RNA to form dsDNA
dsDNA enters genome
Transcription factors generate proviral DNA into ssRNA
ssRNA -> cytoplasm
Ribosomes catalyse the production of precursor proteins
Virus assembled in cytoplasm
Virions bud
Mature virus infects other cells
Which cytokine plays a key role in inflammation
IL-6
HIV and CXCR4 and CCR5
- Chemokine receptor: CXCR4 and CCR5 which responds to chemokines to facilitate response
- HIV changes whether it attacks cells with CXCR4 or CCR5
- CCR5 antagonist used if particular HIV variant only uses CCR5 co-receptor on T cell - if it uses just CXCL4 or both then it will be useless
Cycle of HIV killing CD4
HIV infects
Pyroptosis (kills CD4)
Causes inflammation
Recruits more healthy CD4 cells
Humoral immune response
- Occurs later in infection so level of antibodies in acute infection is very low
- Non-neutralising antibodies to structural proteins (P17 and P24)
- Later neutralising bodies anti-gp120 and anti-binding molecules