13_HIV/AIDs Flashcards
What is underlying pathological cause of immunosuppression?
- depletion of CD4 T cells
- isolation of HIV retrovirus occurred in 1984 –> shown to be CD4 T tropic key link
when did symptoms develop for HIV in the US?
- there’s a delay between HIV-1 infection and development of sxs (clinical latency), such as secondary infections –> indicates HIV-1 infections in US begain in early to mid-1970S
epidemiology of HIV in US
- 1.2M people w/ HIV in the US, at diff’t stages
HIV virion:
- structure
- prevalence
- origin for HIV-1
- structure: mature HIV type 1 –> elongated internal cores
- most prevalent in Africa, but still a global concern
- sub-saharan Africa
- 40M worldwide
- primate origin for HIV-1
Describe the origin of HIV virus
- Lentivirus from primates made the adaptation to humans in mid-1900s –>
- gave rise to HIV-1 and HIV-2
- how?
- monkeys destined for local market place or export
- some pet monkeys
- monkeys as food source
how is HIV transmitted?
- unprotected sexual intercourse w/ infected partner
- vertical transmission (mother to child)
- injection drug use (rare)
describe the replication cycle for HIV-1
how is the HIV-1 genome organized?
- structural proteins
- enzymes
- coat proteins
Includes Gag, Pol, and envelope genes
two different tropic strains of HIV-1
fuction of each?
- M-tropic = “macrophage-tropic strain of HIV-1”
- T-tropic = “T-cell-line-tropic strain of HIV-1”
M tropic infxn is followed by switch to T tropic –> depletes CD4 T cells –> resulting in AIDS
At what point can HIV-1 lead to T cell depletion?
after HIV-1 infects monocytes –> can genetically change to tropic T cells –> leading to T-cell depletion
what is the suggested meghanisms for depletion of CD4 cells?
what are the functions of T helper cells?
what confers genetic plasticity to HIV-1?
- Reverse Transcription (RT) error prone lacks proof-reading 1 in 10,000
- Stand switching from one genome to another during replication, co-infection, or following super-infection (HIV-1 is diploid)
- recombination following co-infection and superinfection
- transcription of integrated proviral DNA by host RNA polymerase II error prone
what are the consequences of HIV-1’s genetic plasticity?
disease course of HIV/AIDS
relationship b/w CD4+ lymphocyte count and HIV RNA copies?
- as HIV RNA copies increase, the CD4 T cell cound decreases
- Once CD4 count is below 200/mL, considered AIDS
what is the acute phase of HIV syndrome?
Timing and sxs?
- T cells appear to be targets of infxn even early on; high levels of circulating virus (10^8 viral particles/mL)
- viral population may double every 6-10 hours
- each infected cell can resul tin infxn of about 20 cells;
- seeding of lymphoid organs and CNS
- Sxs occur days-wks after infxn w/ HIV
- sxs: fever, fatigue/lack of energy and motivation
- rash (maculopapular)
- lymphadenopathy
- pharyngitis
- thrush (candida)
disease progression of HIV
(acute vs. long)
How does AIDS affect the clinical presentation of diseases?
clinical presentation of any of these conditions is much worse (due to fever CD4 T cell count)
What are the early sxs in secondary infections?
last symptom of secondary HIV infxn?
- Early sxs:
- Thrush, and
- Oral Hairy Leukoplakia
- Late sxs: Mycobacterium avium complex disease
Oral hairy leukoplakia (OHL):
what is it a sign of?
sign of EBV replication in epithelial cells
if not already diagnosed w/ HIV, this is an indiction for testing
Mycobacterium avium complex:
prevalence
when does it develop?
- organisms are ubiquitous; but commonly found in water/soil
- develops when CD4 count is lower than 75
- usually, organism is ingested –> disseminates to rest of the body
What virus is associated w/ the following malignancies?
what is the following skin lesion?
progressive multifocal leukoencephalopathy (PML)
define
caused by Human polyomavirus JC
