Flashcards in Primary HIV Infection Deck (37):
How many of patients infected with HIV are infected with a single quasispecies?
What increases the risk of being infected with multiple HIV quasispecies?
IVDU is highest group, MSM is higher than hetersexuals
How many days after initial inoculation is virus found in the regional lymph nodes?
How long after initiail inoculation does it take to find HIV in cells?
How long does it take HIV to become disseminated across the body?
What happens to CD$ cells with active viral replication?
What happens to the lymph nodes in HIV infection?
uncontrolled viral replication leads to lymph nodes architecture desctruction and prevents immmune priming
What does a larger HIV reservoir mean for a patient?
accelerates clinical progression and predicts time to viral rebound
What does point of care HIV testing measure?
What is the 4th generation lab test for HIV
antigen (p24) and antibody
What is p24?
What does the WEstern blot HIV test test for?
antibodies against bands of different antigens
What is the Fiebig staging ssytem for acute HIV?
determines when you were HIV infected based on your positive test results
What does the Fiebig staging system allow you to do?
the likelihood of whether or not have HIV- e.g if tests that you would expect to be positive at 2 weeks are negative- unlikely
What is the avergae rate of CD4 decline without ARt?
What are htegenetic factors most strongly associated wti hnon-progressive infection?
HLA class I alleles esp. HLA-B5701
What cellular responses are associated with non-progressive infection?
CD4 and CD8 T cell repsonses with polyfunctional profile
Why are many age-associated diseases such as CVS disease or cancer thorugh to be more common in treated HIV disease than in theri HVI-negative couterparts?
chronic inflammation is thought to underlie much of this
What factors cause persistent inflammation during ARt?
HIV production and replication; ART toxicitiy; lipodystrophy; CMV and other copathogens; loss of regulatory cells
What is the eclipse phase of acute HIV infection?
HIV is replicating in the mucosa; submucosa nad draining lymphoreticular tissues and cannot be detected in the plasma
How long can the eclipse phase last?
What type of epithlelium is foudn in the rectum and endocervix?
What type of epithelium is found in the vagina and ectocervix?
What cells does HIV first infect in the vagina; ectocervix and penile foreskin?
langerhan cells and CD4 T cells
Which lymphoreticular system does HIV replication converge upon within a few days
What is the first signal of an immune response to HIV infection in the blood?
appearance of acute-phase reactants incl. alpha1 antitrypsin and amyloid A
Which cytokine does the steep rise in the HIV viral load coincide with a large burst of?
IFN-a and IL-15
Describe the initial antibody response to HIV?
its to the viral envelope; is non-neutralising and doesn't select for viral escape
When are the first neutralising antibodies to the transmitted founder virus found?
3 or more months after infection
Why are HLA types HLA-B27 and HLA-B57 associated with better viral control?
present highly conserved parts ofh te virus to T cells so that the virus can escape immune control only at the cost of replicative fitness
What have cervicovaginal transmsiions studies with SIV implicated as the earliest target cells of SIV infection?
CCR5 and CD4 T cells in the lamina propria of the endocervix
What has been a challenge with developing SHIV?
circulating HIV variants don't use the macaque CD4 receptor for entry so they have to use adapted HIV envelope variants to permi entry using this receptor
What illustrates the difficulties with acaque studies in humans?
there are differences in early events of infection between SIV and SHIV which shows there amy be unique features to each virus/host interaction and there is no way to know which findings translate to huamns
What is SHIV?
a chimera whose genome is a combo of SIV and HIV- ancode HiV envelope
What are risk factors for the transmission by more than one genetic variant?
STIs and hormonal contraceptives
What suggests that transmission resets the virus population to the less pathogenic transmissable form?
there has not been a trend of increased virulence over the course of the HIV epidemic; trnamistted viruses are not very similar to donor sequences near the time of transmission but to the donor seuences earlier in infection- archived variant?