Block 3 Flashcards
VIRUS PATHOGENESIS
The ability of a virus to cause disease in the host is called?
Pathogenicity
VIRUS PATHOGENESIS
the manner/mechanism of development of a disease is called?
pathogenesis
VIRUS PATHOGENESIS
DOSE OF THE VIRUS THAT WILL INFECT 50% OF AN
EXPERIMENTAL GROUP is called?
INFECTIOUS DOSE 50 (ID50):
VIRUS PATHOGENESIS
DEGREE OF PATHOGENICITY (NOT AN ABSOLUTE PROPERTY OF A VIRUS).
VIRULENCE
VIRUS PATHOGENESIS
NOT VIRULENT/NOT HARMFUL
AVIRULENT
VIRUS PATHOGENESIS
DOSE OF VIRUS REQUIRED TO CAUSE DEATH IN 50% OF ANIMALS
is this exact? or approximate?
LETHAL DOSE (LD50):
* THIS IS ONLY AN ESTIMATION
VIRUS PATHOGENESIS
- THE LOWER or HIGER THE ID50 AND LD50 THE MORE VIRULENT?
LOWER
VIRUS PATHOGENESIS
NAME 4
THE SKIN
GI TRACT
MUCOUS MEMBRANES
RESPIRATORY TRACT
ROUTES OF ENTRY
THE SKIN
NAME 2 WAYS
- BITES OF AN ARTHROPOD/INFECTED ANIMAL
- CONTAMINATED OBJECTS (EX: HEP C
CONTAMINATED NEEDLE)
ROUTES OF ENTRY
THE SKIN
WHAT ARE 6 DEFENSES OF THE SKIN?
- DENSE OUTER LAYER OF THE KERATIN
- LOW PH
- PRESENCE OF FATTY ACIDS
- BACTERIAL FLORA
- DRYNESS
- COMPONENTS OF INNATE AND ADAPTIVE
IMMUNITY
ROUTES OF ENTRY
GI TRACT
WHAT ARE 9?
HINT: MUCUS MEMBRANE OF WHAT?
ACIDITY OF WHAT?
ALKALINITY OF WHAT?
LAYER OF MUCUS COVERING WHAT?
LIPOLTIC ACTIVITY OF WHAT
PROTEOLYTIC ACTIVITY OF WHAT
CYSTEINE RICH PROTIENS CALLED WHAT?
2 OTHERS …
- MUCOUS MEMBRANES OF ORAL CAVITY AND
ESOPHAGUS - ACIDITY OF STOMACH
- ALKALINITY OF INTESTINES
- LAYER OF MUCOUS COVERING THE GUT
- LIPOLYTIC ACTIVITY OF BILE
- PROTEOLYTIC ACTIVITY OF PANCREATIC ENZYMES
- DEFENSINS
- IGA
- SCAVENGING MACROPHAGES
ROUTES OF ENTRY
RESPIRATORY TRACT
NAME 5 DEFENSES
- MUCOCILIARY BLANKET
- ALVEOLAR MACROPHAGES
- NALT (NASAL ASSOCIATED LYMPH TISSUE)
- BALT (BRONCHUS-ASSOCIATED LYMPH
TISSUE)
*** TEMPERATURE GRADIENT **
VIRAL SPREAD IN HOST
WHAT IS INFECTION SPREADS BEYOND
PRIMARY SITE
DISSEMINATED INFECTION
VIRAL SPREAD IN HOST
WHAT IS # OF ORGANS/TISSUES ARE
INFECTED
SYSTEMIC INFECTION
VIRAL SPREAD IN HOST
WHAT FACILITATES DISPERSAL
APICAL RELEASE
VIRAL SPREAD IN HOST
WHAT FACILITATES SYSTEMIC SPREAD
BASOLATERAL RELEASE:
VIRAL SPREAD IN HOST
SPECIFICITY OR AFFINITY TO A PARTICULAR HOST
TISSUE
TROPISM
VIRAL SPREAD IN HOST
REPLICATE IN MORE THEN ONE HOST
ORGAN/TISSUE
PANTROPIC
VIREMIA
PRESENCE OF VIRUS IN THE BLOOD
VIREMIA
VIREMIA
WHAT IS PRIMARY?
WHAT IS SECONDARY?
- PRIMARY: INITIAL ENTRY OF VIRUS INTO BLOOD
- SECONDARY: VIRUS REPLICATED IN ORGANS AND
ENTERED CIRCULATION ONCE AGAIN
VIREMIA
what is active?
what is passive?
ACTIVE: VIREMIA FOLLOWING INITIAL VIRUS REPLICATION
(MOSQUITOS BITES CAN TRANSMIT DIRECTLY TO BLOOD)
* PASSIVE: DIRECT INOCULATION (BITE OR SYRINGE)- NO
PRIOR REPLICATION
VIREMIA
can mosquito bites transmit some viruses directly to the blood? is the called active viremia?
I say Yes you didn’t say
SPREAD VIA NERVES
VIRUS THAT CAN INFECT NEURAL CELLS BY
NEURAL OR HEMATOGENOUS SPREAD
- NEUROTROPIC
SPREAD VIA NERVES
ENTERS CNS AFTER INFECTION OF PERIPHERAL
SITE
NEURO-INVASIVE
SPREAD VIA NERVES
CAUSES DISEASE OF NERVOUS TISSUE,
MANIFESTED BY NEUROLOGICAL SYMPTOMS/ DEATH
NEURO-VIRULENT
SPREAD VIA NERVES
OLFACTORY AND BBB
SPREAD TO CNS
SPREAD VIA NERVES
TRAVELS OPPOSITE IMPULSE FLOW,
INVADING AXON TERMINAL THEN TO CELL BODY.
RETROGRADE SPREAD
SPREAD VIA NERVES
TRAVELS WITH IMPULSE FLOW,
INVADES CELL BODY THEN TO AXON TERMINAL.
ANTEROGRADE SPREAD
EXAMPLES OF VIRUS SPREAD VIA
NERVES
How does Herpes simplex virus work?
neuroinvasiveness?
neurovirulence?
which nervous system?
what result?
EXHIBITS **LOW NEUROINVASIVENESS **OFTHE CENTRAL NERVOUS SYSTEM, BUT HIGH NEUROVIRULENCE.
ALWAYS ENTERS THE PERIPHERAL NERVOUS SYSTEM, RARELY THE
CENTRAL NERVOUS SYSTEM. IF IT DOES-CONSEQUENCES ARE
ALWAYS SEVERE SOMETIMES FATAL.
EXAMPLES OF VIRUS SPREAD VIA
NERVES
MUMPS VIRUS
neuroinvasiveness?
neurovirulence?
invasive?
MUMPS VIRUS EXHIBITS NEUROINVASIVENESS BUT LOW
NEUROVIRULENCE. MOST INFECTIONS LEAD TO INVASION OF THE
CNS, BUT NEUROLOGICAL DISEASE IS MILD.
EXAMPLES OF VIRUS SPREAD VIA
NERVES
RABIES VIRUS
NEUROINVASIVENESS?
NEUROVIRULENCE?
RABIES VIRUS EXHIBITS HIGH NEUROINVASIVENESS AND HIGH
NEUROVIRULENCE. IT READILY INFECTS THE PNS AND SPREADS TO
THE CNS WITH 100% LETHALITY UNLESS ANTIVIRAL THERAPY IS
ADMINISTERED SHORTLY AFTER INFECTION.
Viruses can enter the CNS from blood by?
a-Monocyte trafficking
b-breaking the cementing at endothelial junctions
c-increase permeability of endothelium
d-all of the above
Important features of localized and systemic acute viral infections
Site of pathology
localized acute infections?
systemic acute infections?
portal of entry
distant sites
Important features of localized and systemic acute viral infections
Incubation period(IP)
localized acute infections?
systemic acute infections?
relatively short
relatively long
Important features of localized and systemic acute viral infections
Virema
localized acute infections?
systemic acute infections?
no
yes
Important features of localized and systemic acute viral infections
Duration of immunity
localized acute infections?
systemic acute infections?
variable, may be short
mostly lifelong
Important features of localized and systemic acute viral infections
Secretory IgA
localized acute infections?
systemic acute infections?
very important
not important
VIRUS SHEDDING
USUALLY INTENSIVE SHEDDING OVER
SHORT PERIOD OF TIME is from a ? infection
ACUTE INFECTION
VIRUS SHEDDING
- CAN BE SHED AT LOW TITERS FOR
MONTHS TO YEARS - CAN BE CONTINUOUS OR INTERMITTENTLY
is from a ? infection?
PERSISTENT INFECTIONS
VIRAL TROPISM
THE AFFINITY OF A VIRUS FOR A PARTICULAR
HOST TISSUE
*dog–> liver
TROPISM
VIRAL TROPISM
CAN REPLICATE IN MORE THAN ONE
HOST ORGAN/TISSUE
*dog–> liver, heart, spleen
PANTROPIC VIRUS
A family of viruses may prefer a particular organ for effective replication. the term used to describe same is ?
a-affinity
b-pathogenicity
c-tropism
d-virulence
VIRUS INJURY TO
THE SKIN
FLUID FILLED SAC/ELEVATIONS
VESICLES
VIRUS INJURY TO
THE SKIN
OPENING CAUSED BY SLOUGHING OF NECROTIC TISSUE
ULCER
VIRUS INJURY TO
THE SKIN
SOLID, ELEVATED MASS WITH DISTINCT BORDERS EXTENDING
DEEP INTO DERMIS
- NODULE
VIRUS INJURY TO
THE SKIN
BENIGN, SKIN GROWTH THAT INFECTS TOP LAYER OF SKIN
WARTS
VIRUS INJURY TO
THE SKIN
SOLID ELEVATION WITHOUT FLUID WITH SHARP BORDERS
PAPULE
VIRUS INJURY TO
THE SKIN
reddening of skin, usually consequence from systemic viral infection
ERYTHEMA
VIRUS INJURY TO THE GI
TRACT
what 2 ways?
INGESTION OR HEMATOGENOUS SPREAD
VIRUS INJURY TO THE GI
TRACT
what happens to ENTEROCYTES
why?
DESTRUCTION OF ENTEROCYTES DUE TO VIRAL
REPLICATION
VIRUS INJURY TO THE GI
TRACT
5 results?
MALABSORPTION, DIARRHEA
DEHYDRATION, ACIDOSIS, HEMOCONCENTRATION
(increased concentration of cells and solids in the bloof)
VIRUS INJURY TO THE RESPIRATORY TRACT
what are 9 possible results?
- LOSS OF CILIARY ACTIVITY
- LOSS OF INTEGRITY OF THE MUCUS LAYER
- MULTIFOCAL DESTRUCTION OF EPITHELIUM
- INFLAMMATION
- EXUDATION
- INFLUX OF INFLAMMATORY CELLS
- OBSTRUCTION OF AIR PASSAGES
- HYPOXIA & RESPIRATORY DISTRESS
- SECONDARY BACTERIAL INFECTION
VIRUS INJURY TO THE CNS
- NEURONAL NECROSIS
- NEURONOPHAGIA (PHAGOCYTOSIS OF NEURONS)
- PERIVASCULAR CUFFING (INFILTRATION OF INFLAMMATORY
CELLS)
are characteristics of what?
- ENCEPHALITIS OR ENCEPHALOMYELITIS IS CHARACTERIZED
BY:
VIRUS INJURY TO THE CNS
from path… too much apoptosis is…
PROGRESSIVE DEMYELINATION (CANINE DISTEMPER)
VIRUS INJURY TO THE CNS
name 3
-ENCEPHALITIS OR ENCEPHALOMYELITIS
-PROGRESSIVE DEMYELINATION(CANINE DISTEMPER)
- NEURONAL VACUOLATION (PRION DISEASE)
Damage to Endothelim
what 4 results
-petechial and ecchymotic hemorahages
-Disseminated intravascular coagulation (DIC)
-edema
-infarction
–>ischemic necrosis
VIRUS INJURY TO THE
ENDOTHELIUM
PIN-POINT HEMORRHAGE
PETECHIAE
VIRUS INJURY TO THE
ENDOTHELIUM
LARGER AREA OF HEMORRHAGE, ILL-
DEFINED MARGINS
ECCHYMOSES
VIRUS INJURY TO THE
ENDOTHELIUM
- DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
what 2 results?
- CLOTS FORM IN SMALL BLOOD VESSELS THROUGHOUT
THE BODY. IF ORGANS DON’T GET BLOOD, THIS LEADS
TO ORGAN FAILURE - CLOT MATERIAL EXHAUSTED DUE TO OVERUSE LEADING
TO NO CLOT FORMATION IN LATER STAGES AND
HEMORRHAGES THROUGHOUT THE BODY
TERATOGENESIS
how does a teratogenic virus pass?
what result?
motherTHIS IS THE ABNORMAL DEVELOPMENT OR ARRESTS IN
DEVELOPMENT OF THE EMBRYO OR FETUS
* MAY RESULT IN DEATH OR MALFORMATIONS DURING THE
ANTENATAL PERIOD. to fetus
Virus injury to organs/tissue
what is virus-induced immunopathology?
defined as tissue injury mediated by host immune response to virus infection. if is the price paid by the host to clear a viral infection
Virus injury to organs/tissue
virus-induced immunopathology, what does it depend on?
delicate balance between the protective and destructive effets of the host immune response to viruses
Virus injury to organs/tissue
virus-induced immunopathology is often the cause of what?
damage with viruses that are relatively non-cytolytic and persistent, ie. infected cells are not immediately destroyed and immune response becomes chronic
Virus injury to organs/tissue
virus-induced immunopathology, if the immune response clears the infection by destroying a small number of virus-infeted cells… then what
the host survives with minimal symptoms and no premanent damage
Virus injury to organs/tissue
virus-induced immunopathology, if a large number of cells are infected before immune induction then what?
the same immune mediated destruction can cause severe or fatal pathological consequences.
VIRUS INDUCED
IMMUNOPATHOLOGY
what is it?
TISSUE INJURY FROM HOST IMMUNE SYSTEM FIGHTING INFECTION
VIRUS INDUCED
IMMUNOPATHOLOGY
what kind of reactions?
HYPERSENSITIVITY REACTIONS
VIRUS INDUCED
IMMUNOPATHOLOGY
4 examples
hint
what is moon blindness in horses?
what is fibrosis?
what possible disorder?
what is infectious bursal disease?
- AUTOIMMUNE DISEASE (MOON BLINDNESS IN HORSES)
- INFLAMMATION MEDIATED TISSUE DAMAGE (FIBROSIS)
- IMMUNODEFICIENCY DISORDER
- IMMUNOSUPPRESSION
- IBD(INFECTIOUS BURSAL DISEASE): REPLICATION CAUSES ATROPHY
TO THE BURSA AND SEVERE DEFICIENCY TO B CELLS.
VIRUS INDUCED IMMUNOPATHOLOGY
T CELLS
2 possible responses
- CYTOTOXIC CELL MEDIATED LYSIS
- RELEASE OF CYTOKINES from t cells (CD4+ AND CD8+) THAT
CAUSE INFLAMMATION AND TISSUE DAMAGE THAT
WILL BECOME CHRONIC AGAINST PERSISTENT
INFECTIONS.
VIRUS INDUCED IMMUNOPATHOLOGY
TLRS
2 possible responses
- PERSISTENT ACTIVATION OF THESE RECEPTORS OF
INNATE HOST CELLS BY VIRUSES CAUSES
PRODUCTION OF PRO-INFLAMMATORY
CYTOKINES AND INTERFERONS, AS WELL AS
SIGNALS THAT RECRUIT AND ACTIVATE CELLS
INVOLVED IN INFLAMMATION. - INJURY CAN ALSO BE MEDIATED BY FREE RADICALS,
SUCH AS NITRIC OXIDE AND SUPEROXIDE
VIRUS INDUCED IMMUNOPATHOLOGY
Toxicity from antibody responses to viruses may also contribute to…
tissue damage
Virus injury to organs/tissues
Some mechanisms of virus induced immunopathology (toxicity from anitbody responses)
Antibody responses to viruses may also contribute to…
tissure damage
Virus injury to organs/tissues
Some mechanisms of virus induced immunopathology (toxicity from anitbody responses)
Antibody responses to viruses may also contribute to tissue damage when antibody binds to what? and what happens?
to an infected cell, activates complement and causes an inflammatory reaction
Virus injury to organs/tissues
Some mechanisms of virus induced immunopathology (toxicity from anitbody responses)
Antibody responses to viruses may also contribute to tissue damage when antibody binds to infected cell or antibody mediated inflammatory reactions involving what?
when does it occur?
toxicity followning:
-engagement of IgG with Fc receptors on inflammatory cells, which causes inflammatory mediator release
-following deposition of viral antigen-antibody complexes in capillary beds, leading to activation of the complement cascade.
Virus induced immunopathology
Immunosupression
Avian immune sustem
where does t cell development occur?
where does b cell development occur?
how is the splieen, liver and lymph nodes similar as in mammals?
where do blood cells develop
Virus induced immunopathology
Virus replication causing artophy of the bursa and a severe deficiency of B lymphocytes, resulting in immuno-suppression. As a result, infected birds become susceptible to other pathogens is called what
infectious Bursal disease
Virus induced immunopathology
what are 4 immunodeficiency viruses that infect and destroy different, but specific cells of the immune system, resulting in immunosuppression?
HIV
SIV
BIV
FIV
Virus induced immunopathology
systemic infection with many other viruses, especially those infecting the mononuclear phagocytes and/or lymphocytes, hace resulted in temporary suppression of both ….
humoral and cell-mediated immune system
TYPES OF VIRAL INFECTIONS
- CS AND SYMPTOMS NOT EVIDENT
- TOO FEW CELLS MAY BE INFECTED
- STIMULATE HOST IMMUNE RESPONSE
- POSSIBLE SOURCE OF SPREAD
what is this called
INAPPARENT INFECTIONS
TYPES OF VIRAL INFECTIONS
- SHORT CLINICAL COURSE
- RAPID CLEARANCE FROM HOST IMMUNE
RESPONSE
what is this called?
ACUTE INFECTIONS
PERSISTENT INFECTIONS
- NOT DEMONSTRABLE EXCEPT WHEN
REACTIVATION OCCURS. - REACTIVATION IS OFTEN STIMULATED BY
IMMUNOSUPPRESSION AND/OR BY THE ACTION
OF A CYTOKINE OR HORMONE
are called?
LATENT INFECTIONS
PERSISTENT INFECTIONS
- ACUTE INFECTION FOLLOWED BY CHRONIC
- VIRUS IS CONTINUOUSLY SHED OR PRESENT IN
INFECTED TISSUE
is called?
CHRONIC
PERSISTENT INFECTIONS
- PROLONGED INCUBATION PERIOD, LASTING
MONTHS-YEARS - SLOW PROGRESSIVE LETHAL DISEASE
is called?
SLOW INFECTION/PERSISTENT INFECTION
which of the following is not usually a feature of a persisitent viral infection?
a-virus may remain dormant in host cell
b-reactivation (clinical desease) offurs durring stress
c-intermittent sedding of virus for long periods
d-rapid clearance from host immune response
D
(acute)
EFFECTS OF VIRUSES ON HOST
CELLS
CELL DEATH BY LYSIS OR APOPTOSIS
CYTOCIDAL
EFFECTS OF VIRUSES ON HOST
CELLS
PERSISTENT INFECTION
NON-CYTOCIDAL
EFFECTS OF VIRUSES ON HOST
CELLS
TUMOR CELLS
CELL TRANSFORMATION
EFFECTS OF VIRUSES ON HOST
CELLS
(CPE) REFERS TO DAMAGE OR
MORPHOLOGICAL CHANGES TO HOST CELLS DURING VIRUS INVASION
CYTOPATHIC EFFECT/CYTOPATHOGENIC EFFECT
CELL FUSION (SYNCYTIUM OR
POLYKARYON FORMATION
what is it?
FUSION OF 4 OR MORE CELLS = PRODUCES ENLARGED
CELL WITH 4 OR MORE NUCLEI
CELL FUSION (SYNCYTIUM OR
POLYKARYON FORMATION
PRONE TO ?
PRONE TO PREMATURE CELL DEATH
CELL FUSION (SYNCYTIUM OR
POLYKARYON FORMATION
USUALLY A RESULT FROM ?
USUALLY A RESULT FROM FUSION WITH A SURROUNDING
INFECTED CELL
INCLUSION
BODIES
ABNORMAL STRUCTURE IN CELL NUCLEUS OR CYTOPLASM
INCLUSION
BODIES
INCLUSION
BODIES
HELPS TO IDENTIFY
HELPS TO IDENTIFY CERTAIN VIRAL INFECTION
INCLUSION
BODIES
describe, what do they look like?
- ROUND/IRREGULAR, SMALL/LARGE, SINGLE/MULTIPLE,
INCLUSION
BODIES
ACID DYE, STAINS PINK
which one?
EOSINOPHILIC/ACIDOPHILIC:
INCLUSION
BODIES
BASIC DYE, STAINS PURPLE
which one
BASOPHILIC
INCLUSION
BODIES
AGGREGATES OF PROTEINS FROM
name 3
AGGREGATES OF PROTEINS FROM
* ACCUMULATION OF VIRAL COMPONENTS
* DEGENERATIVE CHANGES IN CELL
* CRYSTALLINE AGGREGATES OF VIRIONS
In tissue Culture, visible morphological changes/damages to monolayer cells resulting from teh virus infection is also known as ?
a- teratogenic effect
b-cytopathic efffect
c-lethal effect
d-somatopathic effect
b
GENERAL MECHANISMS OF VIRUS-
INDUCED CELL INJURY AND DEATH
CELL NUCLEIC ACID SYNTHESIS
INHIBITION OF HOST
GENERAL MECHANISMS OF VIRUS-
INDUCED CELL INJURY AND DEATH
CELL RNA TRANSCRIPTION (MRNA PRODUCTION AND
PROCESSING)
INHIBITION OF HOST
GENERAL MECHANISMS OF VIRUS-
INDUCED CELL INJURY AND DEATH
CELL SYNTHESIS
INHIBITION OF HOST
GENERAL MECHANISMS OF VIRUS-
INDUCED CELL INJURY AND DEATH
SOME VIRUSES CAUSE LYSOSOMES TO RELEASE THEIR HYDROLYTIC ENZYMES,
causing what?
SOME VIRUSES CAUSE LYSOSOMES TO RELEASE THEIR HYDROLYTIC ENZYMES,
WHICH THEN DESTROY THE HOST CELL.
GENERAL MECHANISMS OF VIRUS-
INDUCED CELL INJURY AND DEATH
what relationship to cellular membrane function?
INTERFERENCE WITH CELLULAR MEMBRANE FUNCTION
APOPTOSIS
what is it?
when does it occur?
what is activated to start it?
- PROGRAMMED CELL DEATH AS LAST RESORT
- BEFORE PROGENY VIRUS PRODUCTION IS COMPLETE
- ACTIVATION OF CASPASE ENZYMES FOR DEGRADATION OF CELL’S OWN
DNA AND PROTEINS
APOPTOSIS
what is:
INTRINSIC PATHWAY
EXTRINSIC PATHWAY
- INTRINSIC PATHWAY (MITOCHONDRIAL)
- INCREASED PERMEABILITY OF MITOCHONDRIAL MEMBRANE
- EXTRINSIC PATHWAY (DEATH RECEPTOR)
- TNF RECEPTOR FAMILY AND CYTOKINE BINDING TRIGGERS APOPTOSIS.
APOPTOSIS
what role CYTOTOXIC T AND NK CELLS
CYTOTOXIC T AND NK CELLS
* PERFORIN AND GRANZYMES ÀDIRECTLY ACTIVATES CASPASES
TARGETS FOR APOPTOSIS
what are the 4 steps?
- AB CELL MEDIATED CYTOTOXICITY
- AB BINDS AG ON TARGET CELLS
- FC RECEPTORS ON NK CELLS RECOGNIZE AB
- CROSS LINK SIGNALS FOR DEGRANULATION EQUALS
APOPTOSIS
VIRUS INDUCED CELL TRANSFORMATION
THE CHANGING OF A NORMAL CELL INTO A CANCER CELL
CELL TRANSFORMATION
VIRUS INDUCED CELL TRANSFORMATION
DESCRIPTIVE TERM THAT DENOTES AN ABNORMAL TISSUE OVERGROWTH THAT CAN BE LOCALIZED
OR DISSEMINATED.
NEOPLASIA
VIRUS INDUCED CELL TRANSFORMATION
STUDY OF NEOPLASIA AND NEOPLASMS
ONCOLOGY
VIRUS INDUCED CELL TRANSFORMATION
GROWTH PRODUCED BY ABNORMAL CELL PROLIFERATION THAT REMAINS LOCALIZED AND DOES
NOT INVADE ADJACENT TISSUE
BENIGN
VIRUS INDUCED CELL TRANSFORMATION
LOCALLY EXTENSIVE AND MAY ALSO BE SPREAD TO OTHER PARTS OF THE BODY
(METASTASIS)
MALIGNANT
VIRUS INDUCED CELL TRANSFORMATION
VIRUSES THAT CAUSE OR GIVE RISE TO TUMORS.
ONCOGENIC VIRUSES
VIRUS INDUCED CELL TRANSFORMATION
SPREAD OF CANCER CELLS FROM THE PART OF THE PRIMARY SITE TO OTHER PARTS OF THE BODY
METASTASIS
REGULATING THE CELL CYCLE
ENCODE PROTEINS THAT FUNCTION IN NORMAL CELLULAR
GROWTH AND DIFFERENTIATION. HELPS WITH CELL DIVISION
PROTO-ONCOGENES
REGULATING THE CELL CYCLE
PLAYS A ROLE IN KEEPING CELL DIVISION IN CHECK.
ENCODES PROTEINS THAT REGULATES AND INHIBITS UNCONTROLLED GROWTH.
RB AND P53 ARE IMPORTANT TUMOR SUPPRESSOR GENES
TUMOR SUPPRESSOR GENES
REGULATING THE CELL CYCLE
BLOCKS E2F AND KEEPS CELL DIVISION IN
CHECK. E2F FACILITATES CELL DIVISION
RB (RETINOBLASTOMA PROTEIN)
REGULATING THE CELL CYCLE
PREVENTS CELLS WITH DAMAGING DNA FROM ENTERING INTO CELL
DIVISION. TRIES TO MEDIATE REPAIRING OF THE DAMAGED HOST CELL
DNA. IF THE DAMAGED DNA CANNOT BE REPAIRED, P53 MEDIATES
APOPTOSIS OF THE CELL WITH DAMAGED DNA.
P53
Which of the following is a tumor suppressor gene/protein
a-CDK
b-E2F
c-Rb
d- all of the above
c
ONCOGENIC VIRUSES
what are they?
what do they do?
what do they cause?
- USUALLY DNA GENOME OR GENERATES A DNA
PROVIRUS AFTER INFECTION (RETROVIRUS). - HAS VIRAL ONCOGENES IN THE VIRAL DNA
- THESE CAUSE CANCER AND AIDS IN REPLICATION.
ONCOGENIC DNA VIRUSES
DNA TUMOR VIRUSES INTERACT WITH CELLS IN ONE OF
TWO WAYS
what are they?
productive?
non-productive?
DNA TUMOR VIRUSES INTERACT WITH CELLS IN ONE OF
TWO WAYS
1. PRODUCTIVE INFECTION IN PERMISSIVE CELL: IN WHICH
THE VIRUS COMPLETES ITS (if you have permission to come in, you are safe-no cancer) REPLICATION CYCLE, RESULTING
IN CELL LYSIS. NO CANCER.
2. NON
-PRODUCTIVE INFECTION IN NONPERMISSIVE CELL: (is you do not have permission to come in, you are dngerous) IN
WHICH THE VIRUS TRANSFORMS THE CELL WITHOUT
COMPLETING ITS REPLICATION CYCLE. CANCER
*does not use hort onco gene
