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Immune disorders: Lecture 7 (S/S of AIDS (Type 1 HIV (in the U.S. and…
Immune disorders: Lecture 7
Acquired Immune Diseases
all humans eventually have a decreased immune system over time
less effective in older individuals
both virus and cancers increase with age
severe stress can suppress cell mediated response and excess glucocorticoids
malnutrition and environmental factors can cause production of b and t cells to stop
AIDS
discovered in 1981
opportunistic infection, low CD4(+) and a presence of HIV syndrome
S/S of AIDS
not a single disease but a syndrome
have a rare several opportunistic infections along with the HIV infection
have to have a positive for HIV
different diseases and infection define AIDS
HIV can lead to AIDS if left untreated
can lie dormant in your body but might show up after an exposure risk
retrovirus uses reverse transcriptase to make DNA copy of genome
Type 1 HIV
in the U.S. and Europe more
type 2 HIV
more in West Africa and share the nucleic acid sequence half way to produce more slowly and is stronger
Structure of HIV
typical retrovirus size and component retrovirus
Gp120
primary attachment molecule for HIV
antigenicity changes during course of infection
makes harder for body to make good immune response
Gp41
smaller one that provides fusion of envelope to target cell membrane of CD4
these stop the immune system of HIV from pt
origin
likely arose from mutation of a simian virus
arrived in Africa around 1930
scientists found disease in 1959 not not documented until 1981
Replication steps
attach to 4 different cells; helper T, macrophage, smooth muscle, and dendretic
enter into cell by cytoplasmic membrane ends up forming a pocket and fluids to surround virus and form a vesicle
viral envelope fuses with vesicles membrane and capsid HIV enters cytosol
DNA reverse transcriptase to make a double strand DNA
enter nucleus and be part of human DNA and then becomes latent for a time period cell life
infected cell transcribes infected cell to make a messanger RNAand copies of viral +ssRNA for new virus
two molecules of RNA and several viral peptides leave or bud cell from host's cell membrane
HIV that budded from cells and nonvirulent (able to infection or damage) because capsid is not functional
reverse transcriptase is innactive
protease allows release of it and capsomeres
inactive in the cell and becomes active outside of the cell
leaves to go infect other cells becuase of protease
Pathogenesis
only humans replicate it
destroys immune system
destroys helper T cells related
Epidemiology
first in young men who were homosexuals in the U.S.
now it is worldwide
in blood, saliva, vaginal secretions, blood, and breast milk, and semen
blood and semen are more infectious than others
infectious fluid can be injected or encountered in a tear, lesion of the mucous membrane
behaviors can affect the infection
anal intercourse
sexual promiscuity
drug use with a dirty needle
sex with someone who is already extra active
Diagnose
based on s/s
antibodies against HIV are detected by ELISA or by western blot
the positive test doesn't indicate AIDS
if the person is a long term infected but doesn't have AIDS they can have defective virons, poor binding of HIV to cells, or well developed immune system
Treat
antiretroviral therapy reduces replication
cocktail of antiviral drugs
does not cure the infection
inhibits HIV replication
pt can live relatively normal life while on treatment
vaccine must generate antibodies and cytotoxic T cells
numerous HIV varies within each person
spreads directly from cell to cell
HIV infects cells and are #1 in combating infection
Testing involves ethical and medical problems
Prevention
abstinence and safe sex
use clean needles
provide antiviral drugs to infected pregnant women
screen blood products
protective wear to prevent blood contact
circumcision reduces infection with sexual activity
pre-exposure prophylaxis (oral-tenofovir_
vaginal application of tenofovir before and after intercourse reduces chance of infection