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Virology RUSVM > Block 3 > Flashcards

Block 3 Flashcards

1
Q

VIRUS PATHOGENESIS

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

A

Pathogenicity

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2
Q

VIRUS PATHOGENESIS

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

A

pathogenesis

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3
Q

VIRUS PATHOGENESIS

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

A

INFECTIOUS DOSE 50 (ID50):

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4
Q

VIRUS PATHOGENESIS

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

A

VIRULENCE

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5
Q

VIRUS PATHOGENESIS

NOT VIRULENT/NOT HARMFUL

A

AVIRULENT

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6
Q

VIRUS PATHOGENESIS

DOSE OF VIRUS REQUIRED TO CAUSE DEATH IN 50% OF ANIMALS

is this exact? or approximate?

A

LETHAL DOSE (LD50):
* THIS IS ONLY AN ESTIMATION

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7
Q

VIRUS PATHOGENESIS

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

LOWER

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8
Q

VIRUS PATHOGENESIS

NAME 4

A

THE SKIN
GI TRACT
MUCOUS MEMBRANES
RESPIRATORY TRACT

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9
Q

ROUTES OF ENTRY

THE SKIN
NAME 2 WAYS

A
  • BITES OF AN ARTHROPOD/INFECTED ANIMAL
  • CONTAMINATED OBJECTS (EX: HEP C
    CONTAMINATED NEEDLE)
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10
Q

ROUTES OF ENTRY

THE SKIN
WHAT ARE 6 DEFENSES OF THE SKIN?

A
  • 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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11
Q

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 …

A
  • 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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12
Q

ROUTES OF ENTRY

RESPIRATORY TRACT
NAME 5 DEFENSES

A
  • MUCOCILIARY BLANKET
  • ALVEOLAR MACROPHAGES
  • NALT (NASAL ASSOCIATED LYMPH TISSUE)
  • BALT (BRONCHUS-ASSOCIATED LYMPH
    TISSUE)
    *** TEMPERATURE GRADIENT **
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13
Q

VIRAL SPREAD IN HOST

WHAT IS INFECTION SPREADS BEYOND
PRIMARY SITE

A

DISSEMINATED INFECTION

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14
Q

VIRAL SPREAD IN HOST

WHAT IS # OF ORGANS/TISSUES ARE
INFECTED

A

SYSTEMIC INFECTION

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15
Q

VIRAL SPREAD IN HOST

WHAT FACILITATES DISPERSAL

A

APICAL RELEASE

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16
Q

VIRAL SPREAD IN HOST

WHAT FACILITATES SYSTEMIC SPREAD

A

BASOLATERAL RELEASE:

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17
Q

VIRAL SPREAD IN HOST

SPECIFICITY OR AFFINITY TO A PARTICULAR HOST
TISSUE

A

TROPISM

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18
Q

VIRAL SPREAD IN HOST

REPLICATE IN MORE THEN ONE HOST
ORGAN/TISSUE

A

PANTROPIC

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19
Q

VIREMIA

PRESENCE OF VIRUS IN THE BLOOD

A

VIREMIA

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20
Q

VIREMIA

WHAT IS PRIMARY?
WHAT IS SECONDARY?

A
  • PRIMARY: INITIAL ENTRY OF VIRUS INTO BLOOD
  • SECONDARY: VIRUS REPLICATED IN ORGANS AND
    ENTERED CIRCULATION ONCE AGAIN
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21
Q

VIREMIA

what is active?
what is passive?

A

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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22
Q

VIREMIA

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

A

I say Yes you didn’t say

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23
Q

SPREAD VIA NERVES

VIRUS THAT CAN INFECT NEURAL CELLS BY
NEURAL OR HEMATOGENOUS SPREAD

A
  • NEUROTROPIC
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24
Q

SPREAD VIA NERVES

ENTERS CNS AFTER INFECTION OF PERIPHERAL
SITE

A

NEURO-INVASIVE

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25
Q

SPREAD VIA NERVES

CAUSES DISEASE OF NERVOUS TISSUE,
MANIFESTED BY NEUROLOGICAL SYMPTOMS/ DEATH

A

NEURO-VIRULENT

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26
Q

SPREAD VIA NERVES

OLFACTORY AND BBB

A

SPREAD TO CNS

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27
Q

SPREAD VIA NERVES

TRAVELS OPPOSITE IMPULSE FLOW,
INVADING AXON TERMINAL THEN TO CELL BODY.

A

RETROGRADE SPREAD

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28
Q

SPREAD VIA NERVES

TRAVELS WITH IMPULSE FLOW,
INVADES CELL BODY THEN TO AXON TERMINAL.

A

ANTEROGRADE SPREAD

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29
Q

EXAMPLES OF VIRUS SPREAD VIA

NERVES

How does Herpes simplex virus work?

neuroinvasiveness?
neurovirulence?
which nervous system?
what result?

A

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.

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30
Q

EXAMPLES OF VIRUS SPREAD VIA

NERVES

MUMPS VIRUS

neuroinvasiveness?
neurovirulence?
invasive?

A

MUMPS VIRUS EXHIBITS NEUROINVASIVENESS BUT LOW
NEUROVIRULENCE. MOST INFECTIONS LEAD TO INVASION OF THE
CNS, BUT NEUROLOGICAL DISEASE IS MILD.

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31
Q

EXAMPLES OF VIRUS SPREAD VIA

NERVES

RABIES VIRUS

NEUROINVASIVENESS?
NEUROVIRULENCE?

A

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.

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32
Q

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

A
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33
Q

Important features of localized and systemic acute viral infections

Site of pathology

localized acute infections?

systemic acute infections?

A

portal of entry

distant sites

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34
Q

Important features of localized and systemic acute viral infections

Incubation period(IP)

localized acute infections?

systemic acute infections?

A

relatively short
relatively long

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35
Q

Important features of localized and systemic acute viral infections

Virema
localized acute infections?

systemic acute infections?

A

no
yes

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36
Q

Important features of localized and systemic acute viral infections

Duration of immunity
localized acute infections?

systemic acute infections?

A

variable, may be short
mostly lifelong

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37
Q

Important features of localized and systemic acute viral infections

Secretory IgA

localized acute infections?

systemic acute infections?

A

very important
not important

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38
Q

VIRUS SHEDDING

USUALLY INTENSIVE SHEDDING OVER
SHORT PERIOD OF TIME is from a ? infection

A

ACUTE INFECTION

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39
Q

VIRUS SHEDDING

  • CAN BE SHED AT LOW TITERS FOR
    MONTHS TO YEARS
  • CAN BE CONTINUOUS OR INTERMITTENTLY
    is from a ? infection?
A

PERSISTENT INFECTIONS

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40
Q

VIRAL TROPISM

THE AFFINITY OF A VIRUS FOR A PARTICULAR
HOST TISSUE
*dog–> liver

A

TROPISM

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41
Q

VIRAL TROPISM

CAN REPLICATE IN MORE THAN ONE
HOST ORGAN/TISSUE
*dog–> liver, heart, spleen

A

PANTROPIC VIRUS

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42
Q

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

A
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43
Q

VIRUS INJURY TO

THE SKIN

FLUID FILLED SAC/ELEVATIONS

A

VESICLES

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44
Q

VIRUS INJURY TO

THE SKIN

OPENING CAUSED BY SLOUGHING OF NECROTIC TISSUE

A

ULCER

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45
Q

VIRUS INJURY TO

THE SKIN

SOLID, ELEVATED MASS WITH DISTINCT BORDERS EXTENDING
DEEP INTO DERMIS

A
  • NODULE
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46
Q

VIRUS INJURY TO

THE SKIN

BENIGN, SKIN GROWTH THAT INFECTS TOP LAYER OF SKIN

A

WARTS

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47
Q

VIRUS INJURY TO

THE SKIN

SOLID ELEVATION WITHOUT FLUID WITH SHARP BORDERS

A

PAPULE

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48
Q

VIRUS INJURY TO

THE SKIN

reddening of skin, usually consequence from systemic viral infection

A

ERYTHEMA

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49
Q

VIRUS INJURY TO THE GI

TRACT

what 2 ways?

A

INGESTION OR HEMATOGENOUS SPREAD

50
Q

VIRUS INJURY TO THE GI

TRACT

what happens to ENTEROCYTES
why?

A

DESTRUCTION OF ENTEROCYTES DUE TO VIRAL
REPLICATION

51
Q

VIRUS INJURY TO THE GI

TRACT

5 results?

A

MALABSORPTION, DIARRHEA
DEHYDRATION, ACIDOSIS, HEMOCONCENTRATION
(increased concentration of cells and solids in the bloof)

52
Q

VIRUS INJURY TO THE RESPIRATORY TRACT

what are 9 possible results?

A
  • 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
53
Q

VIRUS INJURY TO THE CNS

  • NEURONAL NECROSIS
  • NEURONOPHAGIA (PHAGOCYTOSIS OF NEURONS)
  • PERIVASCULAR CUFFING (INFILTRATION OF INFLAMMATORY
    CELLS)
    are characteristics of what?
A
  • ENCEPHALITIS OR ENCEPHALOMYELITIS IS CHARACTERIZED
    BY:
54
Q

VIRUS INJURY TO THE CNS

from path… too much apoptosis is…

A

PROGRESSIVE DEMYELINATION (CANINE DISTEMPER)

55
Q

VIRUS INJURY TO THE CNS

name 3

A

-ENCEPHALITIS OR ENCEPHALOMYELITIS
-PROGRESSIVE DEMYELINATION(CANINE DISTEMPER)
- NEURONAL VACUOLATION (PRION DISEASE)

56
Q

Damage to Endothelim

what 4 results

A

-petechial and ecchymotic hemorahages
-Disseminated intravascular coagulation (DIC)
-edema
-infarction
–>ischemic necrosis

57
Q

VIRUS INJURY TO THE

ENDOTHELIUM

PIN-POINT HEMORRHAGE

A

PETECHIAE

58
Q

VIRUS INJURY TO THE

ENDOTHELIUM

LARGER AREA OF HEMORRHAGE, ILL-
DEFINED MARGINS

A

ECCHYMOSES

59
Q

VIRUS INJURY TO THE

ENDOTHELIUM

  • DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

what 2 results?

A
  • 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
60
Q

TERATOGENESIS

how does a teratogenic virus pass?
what result?

A

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

61
Q

Virus injury to organs/tissue

what is virus-induced immunopathology?

A

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

62
Q

Virus injury to organs/tissue

virus-induced immunopathology, what does it depend on?

A

delicate balance between the protective and destructive effets of the host immune response to viruses

63
Q

Virus injury to organs/tissue

virus-induced immunopathology is often the cause of what?

A

damage with viruses that are relatively non-cytolytic and persistent, ie. infected cells are not immediately destroyed and immune response becomes chronic

64
Q

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

A

the host survives with minimal symptoms and no premanent damage

65
Q

Virus injury to organs/tissue

virus-induced immunopathology, if a large number of cells are infected before immune induction then what?

A

the same immune mediated destruction can cause severe or fatal pathological consequences.

66
Q

VIRUS INDUCED

IMMUNOPATHOLOGY

what is it?

A

TISSUE INJURY FROM HOST IMMUNE SYSTEM FIGHTING INFECTION

67
Q

VIRUS INDUCED

IMMUNOPATHOLOGY

what kind of reactions?

A

HYPERSENSITIVITY REACTIONS

68
Q

VIRUS INDUCED

IMMUNOPATHOLOGY

4 examples
hint
what is moon blindness in horses?
what is fibrosis?
what possible disorder?
what is infectious bursal disease?

A
  • 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.
69
Q

VIRUS INDUCED IMMUNOPATHOLOGY

T CELLS
2 possible responses

A
  • 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.
70
Q

VIRUS INDUCED IMMUNOPATHOLOGY

TLRS
2 possible responses

A
  • 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
71
Q

VIRUS INDUCED IMMUNOPATHOLOGY

Toxicity from antibody responses to viruses may also contribute to…

A

tissue damage

72
Q

Virus injury to organs/tissues

Some mechanisms of virus induced immunopathology (toxicity from anitbody responses)

Antibody responses to viruses may also contribute to…

A

tissure damage

73
Q

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?

A

to an infected cell, activates complement and causes an inflammatory reaction

74
Q

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?

A

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.

75
Q

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

A
76
Q

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

A

infectious Bursal disease

77
Q

Virus induced immunopathology

what are 4 immunodeficiency viruses that infect and destroy different, but specific cells of the immune system, resulting in immunosuppression?

A

HIV
SIV
BIV
FIV

78
Q

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 ….

A

humoral and cell-mediated immune system

79
Q

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

A

INAPPARENT INFECTIONS

80
Q

TYPES OF VIRAL INFECTIONS

  • SHORT CLINICAL COURSE
  • RAPID CLEARANCE FROM HOST IMMUNE
    RESPONSE

what is this called?

A

ACUTE INFECTIONS

81
Q

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?

A

LATENT INFECTIONS

82
Q

PERSISTENT INFECTIONS

  • ACUTE INFECTION FOLLOWED BY CHRONIC
  • VIRUS IS CONTINUOUSLY SHED OR PRESENT IN
    INFECTED TISSUE

is called?

A

CHRONIC

83
Q

PERSISTENT INFECTIONS

  • PROLONGED INCUBATION PERIOD, LASTING
    MONTHS-YEARS
  • SLOW PROGRESSIVE LETHAL DISEASE

is called?

A

SLOW INFECTION/PERSISTENT INFECTION

84
Q

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

A

D

(acute)

85
Q

EFFECTS OF VIRUSES ON HOST

CELLS

CELL DEATH BY LYSIS OR APOPTOSIS

A

CYTOCIDAL

86
Q

EFFECTS OF VIRUSES ON HOST

CELLS

PERSISTENT INFECTION

A

NON-CYTOCIDAL

87
Q

EFFECTS OF VIRUSES ON HOST

CELLS

TUMOR CELLS

A

CELL TRANSFORMATION

88
Q

EFFECTS OF VIRUSES ON HOST

CELLS

(CPE) REFERS TO DAMAGE OR
MORPHOLOGICAL CHANGES TO HOST CELLS DURING VIRUS INVASION

A

CYTOPATHIC EFFECT/CYTOPATHOGENIC EFFECT

89
Q

CELL FUSION (SYNCYTIUM OR

POLYKARYON FORMATION

what is it?

A

FUSION OF 4 OR MORE CELLS = PRODUCES ENLARGED
CELL WITH 4 OR MORE NUCLEI

90
Q

CELL FUSION (SYNCYTIUM OR

POLYKARYON FORMATION

PRONE TO ?

A

PRONE TO PREMATURE CELL DEATH

91
Q

CELL FUSION (SYNCYTIUM OR

POLYKARYON FORMATION

USUALLY A RESULT FROM ?

A

USUALLY A RESULT FROM FUSION WITH A SURROUNDING
INFECTED CELL

92
Q

INCLUSION

BODIES

ABNORMAL STRUCTURE IN CELL NUCLEUS OR CYTOPLASM

A

INCLUSION
BODIES

93
Q

INCLUSION

BODIES

HELPS TO IDENTIFY

A

HELPS TO IDENTIFY CERTAIN VIRAL INFECTION

94
Q

INCLUSION

BODIES

describe, what do they look like?

A
  • ROUND/IRREGULAR, SMALL/LARGE, SINGLE/MULTIPLE,
95
Q

INCLUSION

BODIES

ACID DYE, STAINS PINK
which one?

A

EOSINOPHILIC/ACIDOPHILIC:

96
Q

INCLUSION

BODIES

BASIC DYE, STAINS PURPLE
which one

A

BASOPHILIC

97
Q

INCLUSION

BODIES

AGGREGATES OF PROTEINS FROM

name 3

A

AGGREGATES OF PROTEINS FROM
* ACCUMULATION OF VIRAL COMPONENTS
* DEGENERATIVE CHANGES IN CELL
* CRYSTALLINE AGGREGATES OF VIRIONS

98
Q

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

A

b

99
Q

GENERAL MECHANISMS OF VIRUS-

INDUCED CELL INJURY AND DEATH

CELL NUCLEIC ACID SYNTHESIS

A

INHIBITION OF HOST

100
Q

GENERAL MECHANISMS OF VIRUS-

INDUCED CELL INJURY AND DEATH

CELL RNA TRANSCRIPTION (MRNA PRODUCTION AND
PROCESSING)

A

INHIBITION OF HOST

101
Q

GENERAL MECHANISMS OF VIRUS-

INDUCED CELL INJURY AND DEATH

CELL SYNTHESIS

A

INHIBITION OF HOST

102
Q

GENERAL MECHANISMS OF VIRUS-

INDUCED CELL INJURY AND DEATH

SOME VIRUSES CAUSE LYSOSOMES TO RELEASE THEIR HYDROLYTIC ENZYMES,

causing what?

A

SOME VIRUSES CAUSE LYSOSOMES TO RELEASE THEIR HYDROLYTIC ENZYMES,
WHICH THEN DESTROY THE HOST CELL.

103
Q

GENERAL MECHANISMS OF VIRUS-

INDUCED CELL INJURY AND DEATH

what relationship to cellular membrane function?

A

INTERFERENCE WITH CELLULAR MEMBRANE FUNCTION

104
Q

APOPTOSIS

what is it?
when does it occur?
what is activated to start it?

A
  • 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
105
Q

APOPTOSIS

what is:
INTRINSIC PATHWAY
EXTRINSIC PATHWAY

A
  • INTRINSIC PATHWAY (MITOCHONDRIAL)
  • INCREASED PERMEABILITY OF MITOCHONDRIAL MEMBRANE
  • EXTRINSIC PATHWAY (DEATH RECEPTOR)
  • TNF RECEPTOR FAMILY AND CYTOKINE BINDING TRIGGERS APOPTOSIS.
106
Q

APOPTOSIS

what role CYTOTOXIC T AND NK CELLS

A

CYTOTOXIC T AND NK CELLS
* PERFORIN AND GRANZYMES ÀDIRECTLY ACTIVATES CASPASES

107
Q

TARGETS FOR APOPTOSIS

what are the 4 steps?

A
  • AB CELL MEDIATED CYTOTOXICITY
  • AB BINDS AG ON TARGET CELLS
  • FC RECEPTORS ON NK CELLS RECOGNIZE AB
  • CROSS LINK SIGNALS FOR DEGRANULATION EQUALS
    APOPTOSIS
108
Q

VIRUS INDUCED CELL TRANSFORMATION

THE CHANGING OF A NORMAL CELL INTO A CANCER CELL

A

CELL TRANSFORMATION

109
Q

VIRUS INDUCED CELL TRANSFORMATION

DESCRIPTIVE TERM THAT DENOTES AN ABNORMAL TISSUE OVERGROWTH THAT CAN BE LOCALIZED
OR DISSEMINATED.

A

NEOPLASIA

110
Q

VIRUS INDUCED CELL TRANSFORMATION

STUDY OF NEOPLASIA AND NEOPLASMS

A

ONCOLOGY

111
Q

VIRUS INDUCED CELL TRANSFORMATION

GROWTH PRODUCED BY ABNORMAL CELL PROLIFERATION THAT REMAINS LOCALIZED AND DOES
NOT INVADE ADJACENT TISSUE

A

BENIGN

112
Q

VIRUS INDUCED CELL TRANSFORMATION

LOCALLY EXTENSIVE AND MAY ALSO BE SPREAD TO OTHER PARTS OF THE BODY
(METASTASIS)

A

MALIGNANT

113
Q

VIRUS INDUCED CELL TRANSFORMATION

VIRUSES THAT CAUSE OR GIVE RISE TO TUMORS.

A

ONCOGENIC VIRUSES

114
Q

VIRUS INDUCED CELL TRANSFORMATION

SPREAD OF CANCER CELLS FROM THE PART OF THE PRIMARY SITE TO OTHER PARTS OF THE BODY

A

METASTASIS

115
Q

REGULATING THE CELL CYCLE

ENCODE PROTEINS THAT FUNCTION IN NORMAL CELLULAR
GROWTH AND DIFFERENTIATION. HELPS WITH CELL DIVISION

A

PROTO-ONCOGENES

116
Q

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

A

TUMOR SUPPRESSOR GENES

117
Q

REGULATING THE CELL CYCLE

BLOCKS E2F AND KEEPS CELL DIVISION IN
CHECK. E2F FACILITATES CELL DIVISION

A

RB (RETINOBLASTOMA PROTEIN)

118
Q

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.

A

P53

119
Q

Which of the following is a tumor suppressor gene/protein
a-CDK
b-E2F
c-Rb
d- all of the above

A

c

120
Q

ONCOGENIC VIRUSES

what are they?
what do they do?
what do they cause?

A
  • 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.
121
Q

ONCOGENIC DNA VIRUSES

DNA TUMOR VIRUSES INTERACT WITH CELLS IN ONE OF
TWO WAYS
what are they?
productive?
non-productive?

A

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

Virology RUSVM (7 decks)

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