HIV and AIDS Flashcards
HIV and AIDS
- chronic, progressive retroviral infection (prognosis gets better, but most ppl w HIV will develop AIDS, takes ~10 yrs)
- HIV leads to immunodeficiency
- complx of HIv results in AIDS
- retrovirus targets immune system (Th cells destroy defenses)
- no cure
how does HIV lead to immunodeficiency?
virus incorporates itself into host cell to replicate (happens to target immune cells = ID)
discuss how the retrovirus targets the immune system
- usually DNA transcribes into RNA and that forms proteins, but here the viruses take RNA and put it into DNA of the host
- this results in profound immunosuppression -> develop CA and infections very readily
etiology
- HIV-1 and HIV-2 (strains of virus)
- 3 stages: primary infection, latency, overt AIDS (8-12 yrs)
transmission
- sexual (semen can contain virus)
- contaminated blood, blood products, organs
- placenta, delivery (severed bv and baby is in contact
- lactation (through breast milk)
- needle stick injury (0.3% risk if precautions taken)
how do you determine the degree of risk with a needle stick injury?
viral load, depth, and site of injury
primary infection
- wks to months
- window period and seroconversion
- increased viral load (# of viral particles)
- decreased CD4 count
window period
- time it takes for Abs to form
- dependent on microbe, individual, and dx test
seroconversion
formation of Abs
CD4
- cluster of differentiation 4
- surface protein on T helper cells, macrophages, and some epithelial cells
- CD4 count is an indirect measure of the # of T cells
- can’t be used for dx in primary stage
- CD4 and viral load are inversely proportionate
latency
- could be asympt for yrs
- lymphadenopathy
- recurrent resp infections
why do you have recurrent resp infections in the latency stage?
bc its through this system that most microbes and viruses enter via inhalation, but are usually fought off by a functioning immune system
overt AIDS
- typically 60-70% of cases in 10 yrs (typical progressors)
- ~5yrs = rapid progressors
- ~15 yrs = slow progressors
- long term non-progressors (2-5%) -> don’t develop AIDS
patho
- targets T helper cells (CD4)
- targets macrophages and B cells (Ab formation inhibited)
- destroys immune system -> decreased immunity and defenses -> many new systemic infections and via latent pathogens
what happens when the virus targets T helper cells (CD4)?
responsible for cell-mediated response, if these cells are damaged then cytokines aren’t generated for immune cells to communicate with each other and the immune system is compromised
diagnosis
- presentation and labs
- ELISA
- western blot assay
- PCR
- CD4 counts and viral loads (viral load not recommended for screening or dx)
- newer blood and saliva tests (P24 antigen)
ELISA
- serology, Ab test
- Enzyme Linked Immunosorbant Assay
- body’s prod of Abs measured against entire virus using an enzymatic method
- if it’s positive, you confirm using a western blot
western blot assay
- Abs prod to a specific part of the HIV virus
- more specific test
PCR
- polymerase chain reaction
- amplifies genetic material and measures the viral particle itself
- not a routine test, but a research test
P24 antigen
protein found in viral core and makes its appearance early (between infection and seroconversion, when Abs are detectable)
manifestations
- many, systemic
- opportunistic infections that impact the resp tract, GI, nervous system
- opportunistic CA (Kaposi’s sarcoma, cervical CA, non-Hodgkin’s lymphoma)
how do opportunistic infections impact the resp tract?
defense compromised so recurrent infection can not be prevented
ex.)TB and pneumonia
how is the GI system impacted?
infections from normal flora and ingested microbes
ex.) diarrhea
how is the nervous system impacted?
dementia, encephalopathy (impairment of CNS fx d/t various infections and the presence of the virus)
opportunistic CA
malignant cells in the early stage are controlled by the immune system
Kaposi’s sarcoma
mesenchyme origin (non-epithelial) -> arises in endothelial cells (lining bv), forms malignant lesions (appear in skin, mucosa of mouth, lymph nodes)
why might you be at risk for cervical CA?
d/t HPV infection
treatment
- no cure
- HAART
HAART
- Highly Active Anti-Retroviral Therapy
- therapy targets reverse transcription used by the virus
- at least 3 antivirals are used -> each target a different step
what are examples of antivirals that can be used in HAART?
- reverse transcriptase inhibitors
- protease inhibitors
- entry inhibitors
- integrase inhibitors
entry inhibitors
inhibit entry into host cell, if the virus cannot get into the cell it can’t damage it
integrase inhibitors
enzyme inhibited -> prevents the viral particle from integrating its RNA into the host’s DNA
reverse transcriptase inhibitors
inhibit viral RNA replicating DNA and the multiplication of the virus
protease inhibitors
inhibits the enzyme that breaks down proteins -> protease breaks up polypeptides in host cells
