Primary HIV Infection Flashcards Preview

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Flashcards in Primary HIV Infection Deck (37):
1

How many of patients infected with HIV are infected with a single quasispecies?

80%

2

What increases the risk of being infected with multiple HIV quasispecies?

IVDU is highest group, MSM is higher than hetersexuals

3

How many days after initial inoculation is virus found in the regional lymph nodes?

3 days

4

How long after initiail inoculation does it take to find HIV in cells?

2 days

5

How long does it take HIV to become disseminated across the body?

25 days

6

What happens to CD$ cells with active viral replication?

they die

7

What happens to the lymph nodes in HIV infection?

uncontrolled viral replication leads to lymph nodes architecture desctruction and prevents immmune priming

8

What does a larger HIV reservoir mean for a patient?

accelerates clinical progression and predicts time to viral rebound

9

What does point of care HIV testing measure?

antibody only

10

What is the 4th generation lab test for HIV

antigen (p24) and antibody

11

What is p24?

capsid protein

12

What does the WEstern blot HIV test test for?

antibodies against bands of different antigens

13

What is the Fiebig staging ssytem for acute HIV?

determines when you were HIV infected based on your positive test results

14

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

15

What is the avergae rate of CD4 decline without ARt?

67 cells/year

16

What are htegenetic factors most strongly associated wti hnon-progressive infection?

HLA class I alleles esp. HLA-B5701

17

What cellular responses are associated with non-progressive infection?

CD4 and CD8 T cell repsonses with polyfunctional profile

18

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

19

What factors cause persistent inflammation during ARt?

HIV production and replication; ART toxicitiy; lipodystrophy; CMV and other copathogens; loss of regulatory cells

20

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

21

How long can the eclipse phase last?

7-21 days

22

What type of epithlelium is foudn in the rectum and endocervix?

columnar

23

What type of epithelium is found in the vagina and ectocervix?

stratified squamous

24

What cells does HIV first infect in the vagina; ectocervix and penile foreskin?

langerhan cells and CD4 T cells

25

Which lymphoreticular system does HIV replication converge upon within a few days

GALT

26

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

27

Which cytokine does the steep rise in the HIV viral load coincide with a large burst of?

IFN-a and IL-15

28

Describe the initial antibody response to HIV?

its to the viral envelope; is non-neutralising and doesn't select for viral escape

29

When are the first neutralising antibodies to the transmitted founder virus found?

3 or more months after infection

30

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

31

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

32

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

33

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

34

What is SHIV?

a chimera whose genome is a combo of SIV and HIV- ancode HiV envelope

35

What are risk factors for the transmission by more than one genetic variant?

STIs and hormonal contraceptives

36

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?

37

What are the differences between viruses seen at transmission vs chronic infection?

at transmission have less glycosylation and hsorter variable loops whereas viruses with more glyosylation dominate in chornic infection as can escape neutralising antibodies ; CCR5 viruses are favoured; less sensitive to inhibition by type I IFNs