Primary HIV Infection

Question 1

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

Answer 1

80%

Question 2

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

Answer 2

IVDU is highest group, MSM is higher than hetersexuals

Question 3

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

Answer 3

3 days

Question 4

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

Answer 4

2 days

Question 5

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

Answer 5

25 days

Question 6

What happens to CD$ cells with active viral replication?

Answer 6

they die

Question 7

What happens to the lymph nodes in HIV infection?

Answer 7

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

Question 8

What does a larger HIV reservoir mean for a patient?

Answer 8

accelerates clinical progression and predicts time to viral rebound

Question 9

What does point of care HIV testing measure?

Answer 9

antibody only

Question 10

What is the 4th generation lab test for HIV

Answer 10

antigen (p24) and antibody

Question 11

What is p24?

Answer 11

capsid protein

Question 12

What does the WEstern blot HIV test test for?

Answer 12

antibodies against bands of different antigens

Question 13

What is the Fiebig staging ssytem for acute HIV?

Answer 13

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

Question 14

What does the Fiebig staging system allow you to do?

Answer 14

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

Question 15

What is the avergae rate of CD4 decline without ARt?

Answer 15

67 cells/year

Question 16

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

Answer 16

HLA class I alleles esp. HLA-B5701

Question 17

What cellular responses are associated with non-progressive infection?

Answer 17

CD4 and CD8 T cell repsonses with polyfunctional profile

Question 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?

Answer 18

chronic inflammation is thought to underlie much of this

Question 19

What factors cause persistent inflammation during ARt?

Answer 19

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

Question 20

What is the eclipse phase of acute HIV infection?

Answer 20

HIV is replicating in the mucosa; submucosa nad draining lymphoreticular tissues and cannot be detected in the plasma

Question 21

How long can the eclipse phase last?

Answer 21

7-21 days

Question 22

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

Answer 22

columnar

Question 23

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

Answer 23

stratified squamous

Question 24

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

Answer 24

langerhan cells and CD4 T cells

Question 25

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

Answer 25

GALT

Question 26

What is the first signal of an immune response to HIV infection in the blood?

Answer 26

appearance of acute-phase reactants incl. alpha1 antitrypsin and amyloid A

Question 27

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

Answer 27

IFN-a and IL-15

Question 28

Describe the initial antibody response to HIV?

Answer 28

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

Question 29

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

Answer 29

3 or more months after infection

Question 30

Why are HLA types HLA-B27 and HLA-B57 associated with better viral control?

Answer 30

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

Question 31

What have cervicovaginal transmsiions studies with SIV implicated as the earliest target cells of SIV infection?

Answer 31

CCR5 and CD4 T cells in the lamina propria of the endocervix

Question 32

What has been a challenge with developing SHIV?

Answer 32

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

Question 33

What illustrates the difficulties with acaque studies in humans?

Answer 33

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

Question 34

What is SHIV?

Answer 34

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

Question 35

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

Answer 35

STIs and hormonal contraceptives

Question 36

What suggests that transmission resets the virus population to the less pathogenic transmissable form?

Answer 36

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?

Question 37

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

Answer 37

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