Block 3 Flashcards by catherine perea

VIRUS PATHOGENESIS

The ability of a virus to cause disease in the host is called?

Pathogenicity

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VIRUS PATHOGENESIS

the manner/mechanism of development of a disease is called?

pathogenesis

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VIRUS PATHOGENESIS

DOSE OF THE VIRUS THAT WILL INFECT 50% OF AN
EXPERIMENTAL GROUP is called?

INFECTIOUS DOSE 50 (ID50):

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VIRUS PATHOGENESIS

DEGREE OF PATHOGENICITY (NOT AN ABSOLUTE PROPERTY OF A VIRUS).

VIRULENCE

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VIRUS PATHOGENESIS

NOT VIRULENT/NOT HARMFUL

AVIRULENT

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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

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VIRUS PATHOGENESIS

THE LOWER or HIGER THE ID50 AND LD50 THE MORE VIRULENT?

LOWER

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VIRUS PATHOGENESIS

NAME 4

THE SKIN
GI TRACT
MUCOUS MEMBRANES
RESPIRATORY TRACT

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ROUTES OF ENTRY

THE SKIN
NAME 2 WAYS

BITES OF AN ARTHROPOD/INFECTED ANIMAL
CONTAMINATED OBJECTS (EX: HEP C
CONTAMINATED NEEDLE)

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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

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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

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ROUTES OF ENTRY

RESPIRATORY TRACT
NAME 5 DEFENSES

MUCOCILIARY BLANKET
ALVEOLAR MACROPHAGES
NALT (NASAL ASSOCIATED LYMPH TISSUE)
BALT (BRONCHUS-ASSOCIATED LYMPH
TISSUE)
*** TEMPERATURE GRADIENT **

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VIRAL SPREAD IN HOST

WHAT IS INFECTION SPREADS BEYOND
PRIMARY SITE

DISSEMINATED INFECTION

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VIRAL SPREAD IN HOST

WHAT IS # OF ORGANS/TISSUES ARE
INFECTED

SYSTEMIC INFECTION

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VIRAL SPREAD IN HOST

WHAT FACILITATES DISPERSAL

APICAL RELEASE

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VIRAL SPREAD IN HOST

WHAT FACILITATES SYSTEMIC SPREAD

BASOLATERAL RELEASE:

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VIRAL SPREAD IN HOST

SPECIFICITY OR AFFINITY TO A PARTICULAR HOST
TISSUE

TROPISM

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VIRAL SPREAD IN HOST

REPLICATE IN MORE THEN ONE HOST
ORGAN/TISSUE

PANTROPIC

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VIREMIA

PRESENCE OF VIRUS IN THE BLOOD

VIREMIA

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VIREMIA

WHAT IS PRIMARY?
WHAT IS SECONDARY?

PRIMARY: INITIAL ENTRY OF VIRUS INTO BLOOD
SECONDARY: VIRUS REPLICATED IN ORGANS AND
ENTERED CIRCULATION ONCE AGAIN

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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

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VIREMIA

can mosquito bites transmit some viruses directly to the blood? is the called active viremia?

I say Yes you didn’t say

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SPREAD VIA NERVES

VIRUS THAT CAN INFECT NEURAL CELLS BY
NEURAL OR HEMATOGENOUS SPREAD

NEUROTROPIC

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SPREAD VIA NERVES

ENTERS CNS AFTER INFECTION OF PERIPHERAL
SITE

NEURO-INVASIVE

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# 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

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

# 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

# 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