Lesson 12 Flashcards
pathogens
agents capable of producing disease
pathogens include
- viruses
- bacteria
- fungi
first line of defense against pathogens
skin and mucous membranes which serve as barriers
second line of defense
protections against pathogens that break the skin, mucous membrane barriers
what is included in the second line of defense?
- leukocytes
- macrophages
- antimicrobial proteins
- natural killer cells
- fever
- inflammation
third line of defense
adaptive immunity, mechanisms that defeat a specific pathogen and leave the body with a memory of it
immune system
widely distributed population of cells diverse chemical, physical barriers, and physiological responses
what are the two types of immune defenses?
- innate
- adaptive
innate immunity
- defenses we are born with
- protect us from broad spectrum of disease agents
innate immunity has a ___ effect
local
local effect of innate immunity
defends at point of invasion but there are exceptions
what in an exception to the local effect of innate immunity?
fever
innate immunity is _____
nonspecific
non-specificity of innate immunity
defenses are against a broad spectrum of disease agents rather than one particular pathogen
innate immunity lacks ____
memory
memory lacking in innate immunity
does not remember exposure to a specific pathogen
adaptive immunity
defenses against specific pathogens developed only upon exposure and maintain immune memory
protective features of the skin
- toughness of keratin, difficult to penetrate
- too dry and nutrient-poor to support much microbial growth
- acid mantle
- peptides that kill microbes present
what happens to microbes that are adhered to the skin
skin is continually shed with dead keratinocytes of the stratum corneum of the epithelium
acid mantle
thin filament of lactic and fatty acids from sweat and sebum that inhibits bacterial growth
what peptides are present in the skin that kill microbes
- dermcidin
- defensins
- cathelicidins
what protects all tracts open to the exterior
mucous membranes
protective features of mucous membranes
- sticky mucus physically traps microbes
- presence of lysozyme
lysozyme
enzyme that destroys bacterial cell walls
____ is in skin and mucous membranes
subepithelial areolar tissue
subepithelial areolar tissue of skin and mucous membranes contain
viscous barrier of hyaluronic acid in ground substance
hyaluronic acid
large glycosaminoglycan
pathogens can release
hyaluronidase
hyaluronidase
enzyme to make hyaluronic acid less viscous
what is waiting when skin and mucous membranes are penetrated?
- phagocytes
- leukocytes
what are the five types of leukocytes?
- neutrophils
- eosinophils
- basophile
- monocytes
- lymphocytes
neutrophils
- wander in connective tissue
- function to kill bacteria
neutrophils can ensnare bacteria by releasing
neutrophil extracellular trap
neutrophil extracellular trap (NET)
web of nuclear chromatin and proteins
how can neutrophils kill
phagocytizing and digesting microbe or by releasing bactericidal chemicals to create killing zone around neutrophil
eosinophils found especially in
mucous membrane
eosinophils guard against
large parasites like tapeworms and roundworms
eosinophil participate in
inflammation and allergic reactions
basophils secrete chemicals that do what?
aid mobility and action of other leukocytes
leukotrienes
- vasodilator
- increases blood flow and speeds delivery of leukocytes to the area
heparin
inhibits clot formation that would impede leukocyte mobility
mast cells
secrete histamine and heparin like basophils but in connective tissues
lymphocytes include
- B cells
- T cells
- NK cells
T cells and B cells are apart of ___ immunity
adaptive
NK cells participate in ____ immunity
innate
monocytes
emigrate from blood into connective tissues and transform into macrophages
macrophage system
all the body’s avidly phagocytic cells except leukocytes
what is included in the macrophgae system
- monocytes
- macrophages
- dendritic cells
some macrophages are ____ while others are _____
- wandering
- fixed
examples of specialized forms of macrophages in specific locations (3)
- microglia (CNS)
- alveolar macrophages (lungs)
- stellate macrophages (liver)
blood-borne antimicrobial proteins
- interferons
- complement system
interferons
proteins secreted by virally infected cells and immune cells
interferons serve as
alarm to nearby cells
interferons bind to receptors on nearby cells and do what?
stim their synthesis of defensive antiviral proteins to prevent their infection
interferons activate ____ to do what?
- NK cells and macrophages
- better destroy infected cells or cancer cells
complement system
group of 30 or more globular proteins that contribute to both innate immunity and adaptive immunity
complement system synthesized mainly by
liver
complement system circulate in the blood in ___ form
inactive
what do activated complements participate in?
- inflammation (C3a)
- immune clearance (C3b)
- phagocytosis (C3b)
- cytosis (C3b)
three pathways of complement system activation
- classical pathway
- alternative pathway
- lectin pathway
classical complement activation pathway is ___ than alternative pathway
faster
classical complement activation pathway requires
antibody binding to microbe
what happens in the classical pathway when the antibody binds to the microbe?
changes the antibody shape and exposes complement-binding sites on the antibody
binding of the ____ to the antibody sets off reaction cascade
complement C1
complement fixation
complement C1 binding on the antibody that sets off a reaction cascade
alternative complement activation pathway
complement C3b binds to microbe surface activating reaction cascade
lectins
plasma proteins that bind to carbohydrates on the pathogen’s surface activating reaction cascade
lectin complement activation cascade is dependent on
lectins
four outcomes of complement activation
- inflammation
- immune clearance
- phagocytosis
- cytolysis
inflammation as an outcome of complement activation
C3a stims mast cells and basophils to secrete histamine and other inflammatory chem which activate and attracts neutrophils and macrophages
immune clearance as an outcome of complement activation
C3b binds the antigen-antibody complexes to red blood cells that then circulate to the liver and spleen where macrophages strip off and destroy the Ag-Ab complexes leaving RBC unharmed
phagocytosis as an outcome of complement activation
C3b coats microbial cells and serves as binding sites for phagocyte attachment
what is it called when the microbial cell gets coated by C3b in phagocytosis after complement activation?
opsonization
cytolysis as an outcome of complement activation
- complement C3b initiates formation C5b
- C5b aggregates with other complement proteins within plasma membrane of microbe which forms the membrane attack complex
membrane attack complex
a hole in the target cell membrane
what does the membrane attack complex do
- electrolytes leak out
- water flows in rapidly
- target cell ruptures
natural killer cells continually
patrol body looking for pathogens and diseased host cells
immunological surveillance
continually being on patrol for pathogens and diseased cells
what do NK cells do?
attack and destroy microbes, transplanted cells, cells infected with viruses, and cancer cells
how do NK cells destroy microbes
recognize infected cell and bind to it and release perforins
perforins
polymerize to form a ring to create a hole in the target’s plasma membrane
granzymes
group of protein-degrading enzymes
granzymes function
enter through pore and degrade intracellular enzymes and induce apoptosis
apoptosis
programmed cells death
cancer cells exhibit
tumor specific antigens
where are tumor-specific antigens located?
cell’s plasma membrane
cancer cells are identified as abnormal by
NK cells
immunological escape
cancer cells that destroy NK cells that detect them or avoid detection by not displaying tumor-specific antigens or masking them
in viral infections cells infected with virus present
abnormal proteins on their plasma membrane which allows NK cells to identify and destroy them
fever aka
pyrexia
fever
abnormal elevation of body temp
fever results from
- trauma
- infections
- drug reactions
- brain tumors
what does a fever do? (3)
- promote interferon activity
- elevates metabolic rate and accelerates tissue repair
- inhibits reproduction of bacteria and viruses
recovery from fever is faster when
you let the fever take its course
antipyretics
fever reducing medications
stages of fever (3)
- onset
- stadium
- defervescence
what the six steps of the course of a fever?
- infection and pyrogen secretion
- hypothalamic thermostat is reset to higher set point
- onset
- stadium
- infection ends, set point returns to normal
- defervescence
onset of fever
body temp rises
stadium of fever
body temp oscillates around set point
defervescence of fever
body temp returns to normal
reye syndrome
serious disorder in children younger than 15 following an acute viral infection such as chickenpox or flu
what can trigger reye syndrome
use of aspirin to control fever
what happens in reye syndrome
- swelling of brain neurons
- pressure of swelling brain
- fatty infiltration of liver and other viscera
what are the symptoms of pressure of swelling brain (5)
- nausea
- vomiting
- disorientation
- seizures
- coma
____ die of reye syndrome
30%
what happens to most survivors of reye syndrome
suffer intellectual disabilities
inflammation
local defensive response to tissue injury, trauma, or injury
general purposes of inflammation
- limit spread of pathogens and destroy them
- remove debris from damaged tissue and initiate tissue repair
four cardinal symptoms/signs of inflammation
- redness
- swelling
- heat
- pain
inflammation involves numerous
cytokines
cytokines
small proteins that function in chemical communication between cells
cytokines do what during inflammation
alter physiology of receiving cell
cytokines include
- interferon
- interleukins
- tumor necrosis factor
- chemotactic factors
most immediate requirement after tissue injury is
get defensive leukocytes to the site quickly
how are leukocytes moved to injury spot quickly?
local hyperemia
hyperemia
increased blood flow
what chemicals cause hyperemia?
- histamine
- leukotrienes
- cytokines
what are vasodilators secreted by?
- basophils
- mast cells
- cell damaged by trauma, toxins, or organisms triggering inflammation
hyperemia other function
washes toxins and metabolic waste from the site more rapidly
vasoactive chemicals stim
endothelial cells to contract
what happens when endothelial cells contract
widens gaps between them
what happens when gaps widen between endothelial cells?
- increase capillary permeability
- fluid, leukocytes, and plasma proteins leave bloodstream
cell adhesion molecules are made by
endothelial cells
what do cell adhesion molecules aid in
recruitment of leukocytes
how do cell adhesion molecules aid in recruitment of leukocytes
make membranes sticky so leukocytes adhere to vessel wall
margination
leukocytes adhering to vessel walls
diapedesis
- emigration
- leukocytes crawl through gaps in the endothelial cells and enter tissue fluid
extravasated
term for cells and chemicals that have left the bloodstream
what is the heat of inflammation caused by
hyperemia
what is the redness of inflammation caused by
- hyperemia
- extravasated RBCs in the tissue
what is swelling in inflammation caused by?
increased fluid filtration from the capillaries
what is pain in inflammation caused by?
- direct injury to the nerves
- pressure on the nerves from edema
- stim of pain receptors by prostaglandins
- bacterial toxins
- bradykinin
other priority of inflammation
prevent pathogens from spreading throughout body
____ filters into tissue fluid and clots to form stick mesh that walls off microbes
fibrinogen
heparin prevents
clotting at site of injury
pathogens are in fluid pocket surrounded by
clot
pathogens are attacked by
antibodies, phagocytes, and other defenses
neutrophils accumulate at the injury site within
an hour
after leaving bloodstream neutrophils exhibit
chemotaxis
chemotaxis
attraction to chemicals that guide them to injury site
____ quickly respond to and kill bacteria
neutrophils
how do neutrophils kill bacteria
phagocytosis
respiratory burst
neutrophils absorb O2 to form H2O2 an release hypochlorite
hypochlorite
highly toxic and forms killing zone around cell
neutrophils secrete ____ for what function?
- cytokines
- recruitment of macrophages and additional neutrophils
____ and ___ secrete colony-stimulating factor
macrophages and T cells
what do colony-stimulating factors from macrophages and t cells do
stim leukopoiesis and raise WBC count
neutrophilia
5000 cells/uL to 25000 cells/uL in bacterial infection
eosinophilia
elevated eosinophil count in allergy or parasitic infection
tissue cleanup and repair primarily involves
monocytes
monocytes arrive in ____ and become macrophages
8-12 hours
how do macrophages assist in tissue cleanup and repair
engulf and destroy bacteria, damages host cells, and dead and dying neutrophils
____ contributes to tissue cleanup
edema
how does edema contribute to tissue cleanup?
swelling compresses veins and reduces venous drainage
forces of edema open valves of lymphatic capillaries, promoting
lymphatic drainage of bacteria, dead cells, and debris
pus
yellow accumulation of dead neutrophils, bacteria, cellular debris, and tissue fluid
abscess
accumulation of pus in a tissue cavity
platelet-derived growth factor
secreted by blood platelets and endothelial cells in injured areas
platelet-derived growth factor stims ___ to multiply and ____
- fibroblasts
- synthesize collagen
hyperemia delivers oxygen, amino acids, and other necessities for ___
protein synthesis
increased heat
- increases metabolic rate
- speeds mitosis
- tissue repair
_____ forms a scaffold for tissue reconstruction
fibrin clot
pain does what for tissue repair
makes us limit the use of body part so it has chance to rest and heal
_____ serves as the third line of defense
adaptive immunity
what are the three characteristics that distinguish adaptive immunity and innate immunity?
- systemic affect
- specificity
- memory
systemic effect in adaptive immunity
acts throughout the body
specificity in adaptive immunity
generates protection and immunity to specific pathogens on an individual basis
memory in adaptive immunity
- when re-exposed to the same pathogen
- the body reacts so quickly that there is no noticeable illness
two types of adaptive immunity
- cellular
- humoral
what happens in cellular immunity
T lymphocytes directly attack and destroy foreign cells or diseased host cells
cellular immunity aka
cell mediated
what is the function of cellular immunity
rids the body of pathogens that reside in human cells where they are inaccessible to antibodies
what does cellular immunity work against other than pathogens in cells?
- parasitic worms
- cancer cells
- transplanted cells
humoral immunity aka
antibody mediated
what happens in humoral immunity
mediated by B cells that become plasma cells that release antibodies that do not directly destroy a pathogen but tag it for destruction
humoral immunity is effective against
- extracellular viruses
- bacteria
- yeasts
- protozoans
- molecular diseases agents
what are molecular disease agents
- toxins
- venoms
- allergens
other forms of classifying immunity
- natural active immunity
- artificial active immunity
- natural passive immunity
- artificial passive immunity
natural active immunity
production of one’s own antibodies or T cells as a result of infection or natural exposure to antigen
example of natural active immunity
catching the flu and gaining immunity to that strain
artificial active immunity
production of one’s own antibodies or T cells as a result of vaccination against disease
vaccine
consists of dead or attenuated pathogens that stim the immune response without causing the disease
booster shots
may be given to re-stim immune memory to maintain a high level of protection
example of artificial active immunity
shots
natural passive immunity
temporary immunity that results from antibodies produced by another person
example of natural passive immunity (2)
- fetus acquires antibodies from mother through placenta
- baby acquires them during breast feeding
artificial passive immunity
temporary immunity that results from the injection of immune serum from another person or animal
immune serum
antibodies
example of artificial passive immunity
emergency treatment for snakebite, botulism, tetanus, rabies, and other diseases
antigen
any molecule that can bind an antibody
most antigens have ___ MW
high
what are antigens usually composed of?
- proteins
- polysaccharides
- glycoproteins
- glycolipids
characteristics enable body to distinguish between
self and non self
epitopes
certain regions of an antigen molecule that stim immune responses
epitopes aka
antigenic determinants
haptens
too small to be antigenic in themselves
hapten aka
incomplete antigens
haptens may trigger immune responses by
combining with a host molecule, creating a complex that the body recognizes as foreign
examples of haptens
- cosmetics
- detergents
- industrial chemical
- poison ivy
- animal dander
- penicillin
antibodies aka
immunoglobulins
antibodies
defensive proteins that play a variety of defensive roles
human immune system capable of ____ different antibodies
1 trillion
soluble antibodies are dissolvable in what? (8)
- blood plasma
- tissue fluids
- lymph
- mucus
- saliva
- intestinal secretions
- tears
- breast milk
antibody monomer
basic structural unit of an antibody
antibody monomer composed of
four polypeptide chains linked by disulfide bonds
what are the four polypeptide chains in antibody monomers called?
two heavy and two light chains
all four polypeptide chains have ___ that give antibody its uniqueness
variable region
antigen binding site formed from
the V regions of the heavy and light chain on each arm
where does the antigen binding site attach
the epitope of an antigen molecule
constant region has the ___ amino acid sequence as variable region
same
what does the constant region determine
mechanism of antibody action
antigen classes (5)
- IgM
- IgG
- IgD
- IgA
- IgE
IgA as monomer in
plasma
IgA as dimer in
- mucus
- saliva
- tears
- breast milk
- intestinal secretions
IgA prevent
pathogen adherence to epithelia and penetrating underlying tissues
IgA provides ____ immunity to newborns
passive
IgD
- monomer
- B cell transmembrane antigen receptor
IgD functions in
B cell activation by antigens
IgE
- monomer
- bound to receptors on basophils and mast cells
IgE stims what two things
- release of histamine and other chemical mediators of inflammation and allergy
- eosinophil defensive actions against parasites
IgG
- monomer
- constitutes 80% of circulating antibodies
IgG is the predominant antibody in ___
secondary immune response
IgG is capable of
- complement fixation
- crossing placenta to fetus
IgM
pentamer in plasma and lymph
IgM is predominant antibody in ____
primary immune response
IgM is capable of
- strong agglutinating
- complement fixing abilities
three types of lymphocytes
- NK cells
- T cells
- B cells
NK cells are a part of ___ immunity
innate
T and B cells are part of ___ immunity
adaptive
T cell production
produced in red bone marrow but migrate to thymus to complete their maturation process
positive selection
cortical epithelial cells test developing T cells to ensure they have the proper receptors
what happens when positive selection does not occur
T cells die
T cells can fail by
reacting to self antigen
what happens to T cells that react to self antigen
they’re eliminated to ensure the immune system is self tolerant
self tolerant
will not attack one’s own tissues
anergy
self reactive T cells remain alive but unresponsive
with proper receptors T cells become _____
immunocompetent
immunocompetent
capable of recognizing antigens presented to them
B cells development
develop entirely in red bone marrow
what happens to B cells that react to self anitgens
undergo either anergy or clonal deletion
self tolerant B cells do what?
synthesize antigen surface receptors, divide rapidly, produce immunocompetent clones
B cells leave bone marrow and do what?
colonize lymphoid tissues and organs as T cells
T cells can only recognize antigens presented by
antigen presenting cells
APCs include
dendritic cells, macrophages, and B cells
function of APCs depend on
MHC proteins
MHC proteins are encoded by
major histocompatibility complex genes
MHC proteins act as
cell identification tags
cell identification tags
label every cell of your body as belonging to you
what is the only instance that MHC proteins are not structurally unique
identical twins
MHCs are displayed on ___ of APCs along with ___
- surface
- fragment of presented antigen
antigen processing
APC encounters antigen, internalizes it by endocytosis, digests it into fragments, and attaches it to the MHC protein
what happens after antigen processing
cell displays MHC protein with the antigen in its plasma membrane
if APC displays a self antigen to a T cell
the T cell disregard it
if an APC displays a non-self antigen to a T cells
the appropriate T cell will initiate an immune response against the source of that antigen
APCs and lymphocytes communicate to cytokines called
interleukins
cellular immunity
form of specific defense in which the T lymphocytes directly attack and destroy diseased or foreign cells
classes of T cells
- cytotoxic T cells
- helper T cells
- memory T cells
cytotoxic T cells
carry out attack
helper T cells
promote activities of other immune cells
memory T cells
responsible for memory in cellular immunity
what happens when APC encounters and processes an antigen
migrates to the hearest lymph node and displays it to the T cells
when T cells encounter a displayed antigen on the MHC protein
they initiate an immune response
what are the two classes of MHC T cells respond to
- MHC-I
- MHC-II
MHC-I proteins
- occur on all nucleated cells
- internal peptides are presented on cell surface including virus-infected cells
- cancer cells
MH-II proteins
- occur on APCs
- external antigens are presented on cell surface
cytotoxic T cells respond only to
MHC-I proteins
helper T cells respond only to
MHC-II
T cell activation begins when
Tc or Th cell binds to an MHC protein displaying an epitope that the T cell is programmed to recognize
costimulation
additional signaling processes required for T cell activation
in addition to MHC and antigen binding T cells must also bind
signaling proteins on surface of APCs in damaged/infected tissues
what is the purpose of T cells binding to signaling proteins?
helps to ensure the immune system doesn’t launch an attack in the absence of an enemy
what happens if T cells don’t bind to the signaling proteins
autoimmune disorders
successful T cell activation will trigger
clonal selection
activated T cell undergoes
repeated mitosis
repeated mitosis of activated T cells gives rise to
clone of identical T cells programmed against the same epitope
what do the clones of T cells become?
- effector cells
- cytotoxic cells
- memory cells
- helper cells
T cell recall response
immune memory follows the primary response in cellular immunity
why does the T cell recall response occur?
- memory cells are long-lived
- memory cells are more numerous than naive T cells
- memory cells have fewer steps to be activated
what are the four main steps of T cell activation?
- antigen recognition
- costimulation
- clonal selection
- attack
____ play central role in coordinating both cellular and humoral immunity
helper T cells
what are the three effects that occur when helper T cells secrete interleukins
- attract neutrophils and NK cells
- attract macrophages, stim their phagocytic activity, and inhibit them from leaving area
- stim T and B cell nitosis and maturation
what happens when T cell recognizes MHC-II
secrete interleukins
_____ only T cells that directly attack other cells
cytotoxic T cells
when cytotoxic T cells recognize complex of an antigen and MHC-I what happens
it docks on those cells
after cytotoxic T cells dicks what happens?
cell delivers a lethal hit of chemicals
what are the chemicals in a lethal hit?
- perforins and granzymes
- interferons
- tumor necrosis factor
perforins and granzymes
kill cells in the same manner as NK cells
interferons
inhibit viral replication and recruit and activate macrophages
tumor necrosis factor
aids in macrophage activation and kills cancer cells
what happens after a cytotoxic T cell delivers lethal hit?
cell goes off in search of another enemy cell while chemicals do their work
B cell activation begins when
an antigen binds to B cell receptors
___ has thousands of surface receptors for one antigen
immunocompetent B cells
receptor mediated endocytosis
antigen binds to several receptors, links them together, and is taken into the cell
What do B cell processes do after the antigen is taken into the cell
B cell processes digests the antigen then displays antigen fragments with MHC-II on surface
what happens after MHC-II is displayed on surface of B cell
secretes interleukins that activate the B cell
____ triggers clonal selection
B cell activation
B cell mitosis gives rise to
clones of identical B cells programmed against the same antigen
most clonal B cells differentiate into
plasma cells
what else can B cells become other than plasma cells
memory B cells
plasma cells secrete
antibodies at a rate of 2000 molecules per second
what is the lifespan of a plasma cell
4-5 days
antibodies travel through body in
blood and other body fluids
first exposure of a plasma cell to antigen triggers
production to IgM and a slower production of IgG
later exposure of a plasma cell to the same antigen does what?
rapid production of IgG
antibody assist the immune response in four ways
- neutralization
- complement fixation
- agglutination
- precipitation
neutralization as an immune response
masking active regions of an antigen
complement fixation as immune response
activating complement by the classical pathway
agglutination as immune response
clumping of enemy cells to immobile them
agglutination and precipitation cleared by
phagocytes
precipitation assisting in immune responses
antigen molecules are clumped by antibodies
primary response
immune reaction brought about by the first exposure to an antigen
protective antibodies are delayed for ____. Why?
- 3-5 days
- naive B cells multiply and differentiate into plasma cells
as plasma cells produce antibodies what happens?
antibody titer rises
antibody titer
level in the blood plasma
what happens to the antibody titer when IgM appears
peaks in about 10 days and then soon declines
___ levels rise as ___ declines in the primary response
- IgG
- IgM
how long does it take for the IgG level to drop to a low level
within a month
primary response leaves one with
immune memory of the antigen
during clonal selection some B cells become
memory B cells
secondary response
immune response when re-exposed to the same antigen
memory B cells become plasma cells within hours of
reexposure
IgG titer does what in secondary response
rises sharply an dpeaks in a few days
are there symptoms for a secondary response? why?
no because response is to rapid that the antigen has little chance to exert noticeable effect on the body
IgG remian elevated for how long after secondary response
for weeks to years
why do IgG remain elevated for so long?
long-lasting protection
autoimmune diseases
- failure to self tolerance
- immune system does not correctly distinguish self sntigens from foreign ones and produces auto-antobodies that attack body’s own tissues
reasons for failure of self tolerance
- cross-reactivity
- abnormal exposure of self anitgens to the blood
- changes in structure of self antigens
cross reactivity as a reason for failure to self tolerance
some antibodies against foreign antigens react to similar self antigense
example of cross reactivity as a reason for failure to self tolerance
rheumatic fever where strep antibodies attack the heart valves
abnormal exposure to slef antigen in the blood as reason fro failure of self tolerance
some of our native antigens are not normally exposed to the blood
what is an exmaple of abnormal exposure to slef antigen in the blood as reason fro failure of self tolerance
blood testes barrier keep sperm from getting in to the blood
changes in structure of self-antigens as reason for failure of self tolerance
viruses and drugs may change the structure of self antigens or cause the immune system to perceive them as foreign
immunodeficienies are characterized by
an immune system that fails to react vigorously enough
severe combined immunodificiency disease
hereditary lack of T and B cells
SCID leaves people vulnerable to
oppotunistsic infection
aquired immunideficiency syndrome
non-hereditary diseases contracted after birth caused by HIV
hwo does HIV cause AIDS
HIV invades helper T cells, macrophages, and dendritic cells by tricking them to internalize viurses by receptor mediated endocytosis
HIV is a
retrovius
retrovirus
uses the viral enzyme reverse transcriptase to convert its viral RNA genome into DNA which can then insert into host cell DNA
HIV cripples entire immune system by
destorying helper T cellsh
host with HIV is most volnerable to
opportunistic infections
early signs and symptoms of AIDS
flu-like symptoms of chills and fever
signs and symptoms of AIDS progress into
- night sweats
- fatigue
- headache
- extreme weight loss
- lymphadenitis
what is the normal T helper cell count
600-1200 cells/uL
what is the T helper cell count in AIDS
200 cells/uL
what are some opportnistic infections people with AIDS are susceptible to?
- toxoplasma
- pneumocystis
- herpes simplex virus
- cytomegalovirus
- TB
HIV transmitted through
- blood
- semen
- veginal secretions
- breast milk
- across placenta
is there a cure for AIDS
no but there is antiretroviral therapy that maintains near normal life expectancy
COVID 19
global pandemic oc 2020-2021 caused bu SARS-CoV-2
viral structure of COVID 19
single strand of RNA stabilized by RNA-binding nucleocapsid protein surrounded outer lipid envelope studded with spike proteins
how many genes are in the RNA strand of COVID 19
14
infection cycle of COVID 19
- virus inhaled and invades lung cells
- virus replicated within host cell
- new virus released to infect new cells
what cells do COVID 19 cells infect and how
great (type II) alveolar cells by invading their ACE2 receptors
mechanism of COVID 19
- other vody cells with ACE2 receptors also infected
- cytokines released by immune cells activate inflammation
what other body cells have ACE2 receptors
- heart
- kidneys
- digestive tract
- blood vessels
- brain
COVID 19 has the potential to induce a
cytokine storm
cytokine storm
produces excessive hyperinflammatory response
common symptoms of COVID 19
- flu-like symptoms
- loss of smell and taste
- possible breathing difficulty and low blood oxygen
some patients infected by COVID 19 experience
- respiratory failure
- shock
- multiorgan dysfunction
____ most effective way to prevet critial illness and helt spread fo COVID 19
vaccination
