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MBE3 > Coronaviruses (Chapter 32) > Flashcards

Coronaviruses (Chapter 32) Flashcards

1
Q

Coronaviruses (Chapter 32)

A

+ strand Virus RNA
Enveloped
Sars CoV-2

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2
Q

Cause up to 30% of common colds

A

Corona Virus

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3
Q

Covid enveloped or no?

A

Yeah Bro!

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4
Q

SARS-CoV

SARS-CoV-2

A

Jumped from animals to humans

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5
Q

SARS outbreak

A

Resperatory Syndrom

2k2-2k3

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6
Q

MERS-CoV

Mortality Rate

A

Kinda New to Hue-mons. Middle eastern resperatory syndrome

30-40%

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7
Q

CoronaVirus life cycle Viral envelope acquisition?

A

Budding of nucleocapsid into ER

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8
Q

Clinical Presentation SaRsCoV2

Moderate

A

SPO2 saturation of >= 94%

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9
Q

Clinical Presentation SaRsCoV2

Severe

A

SPO2 Sat. <94%

<30b/m

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10
Q

Covid inters cell how?

A
  1. ACE 2 receptors in the presence of TMPRSS2
  2. Dysregulation of RAAS due to down regulation of ACe2 = decreased cleavage of Ang 1 and 2.
  3. Facks app endothelial cells and thromboinflammation
  4. Cytokine release syndrome. IL6, TNFalpha.
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11
Q

ACE2 activity effect on BP

A

Lowers BP

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12
Q

ACE2 –

A

angiotensin converting enzyme (cleaves angiotensin II (vasoconstrictor) to angiotensin 1-7 (vasodialator)

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13
Q

TMPRSS2

A

transmembrane protease, serine 2 (cleaves (“primes”) Spike protein)

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14
Q

RAAS

A

renin angiotensin aldosterone system (blood pressure regulation)

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15
Q

Extrapulmonary manifestations of COVID-19

A

Pretty much every other system. Facks App.

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16
Q

Picornaviruses (Chapter 32)

A

Picornaviruses (Chapter 32)
+ stranded RNA viruses
do not have envelope
enteroviruses

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17
Q

Picornaviruses (Chapter 32)

Sub types

A

Rhinovirus
Hepatovirus
enterovirus. Polio, Coxsakievirus
Parechovirus

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18
Q

Enteroviruses:
very stable in ___________ and ______
also stable at pH ______)

A

Enteroviruses:
very stable in food and water
also stable at pH 3 (stomach)

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19
Q

Rhinoviruses:
Sensitive to ______
Replicate poorly above _____

A

Rhinoviruses:
Sensitive to acidic pH
Replicate poorly above 33 C

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20
Q

Polio Virus

Three antigen types

A

Pv1, PV2, Pv3

Capsid Differances between types

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21
Q

Poliovirus Shape

A

icosahedral

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22
Q

Poliovirus Size

A

Small AF! 30nm

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23
Q

Polio Virus + strand

A

Polio Virus + strand 7500 nt in lenght

24
Q

Poliovirus replication

A

CD155 Polio virus receptor. PVR

25
Q

lytic virus Polio Virus

A 
destruction of host cells
virus is shed into stool
up to 10,000 virus per infected cell)
even weeks to months after symptoms
gone
26
Q

Polio Virus transmission

A

transmission: fecal-oral

27
Q

Polio Virus RNA properties

A

RNA alone can cause infection

28
Q

Poliovirus IRES

A

Internal Ribosome Entry Site
IRES serves as the “cap” of the viral RNA, promoting translation of
viral RNA into viral proteins

29
Q

Because of IRES, translation starts _____ from the 5’ end of poliovirus RNA (normal mRNA translation starts ______ 5’ end)

A 
Because of IRES, translation starts far from the 5􀀁 end of
poliovirus RNA (normal mRNA translation starts near 5’ end)
30
Q

IRES serves as the…….

A

IRES serves as the “cap” of the viral RNA, promoting translation of
viral RNA into viral proteins

31
Q

Pathogenesis of poliovirus

A

central nervous system disease
flaccid paralysis
results from destruction of anterior horn cells in spinal cord
bulbar poliomyelitis
most severe form
respiratory muscle paralysis (medulla oblongata)
~25% mortality
factors increasing severity of poliovirus infections
physical exertion and trauma
tonsillectomy

32
Q

5% of polio infections

A

Multiplication in various organs

Major Viremia»»»»»>peripheral nerve ganglia/CNS=paralytic disease=1% infections

33
Q

Poliovirus vaccine

A

Live oral vaccine (Sabin) mimics the normal infection process of poliovirus
Killed parenteral vaccine (Salk) only generates serum antibodies

34
Q

group A coxsackieviruses

Type a16

A 
aseptic meningitis
herpangina
sudden onset of fever
vesicles/ulcers on tonsils and palate
coxsackievirus type A16
hand, foot, and mouth disease
blisters on hand, feet, and palate
35
Q

group B coxsackieviruses

A

heart (myocarditis)
respiratory tract (pleurodynia)
mucous membranes of eye
(hemorrhagic conjunctivitis

36
Q

Rhinoviruses

A

~100 serotypes
account for ~1/2 the cases of the common cold
bind to respiratory epithelial cells
ICAM-1 (most) or VLDL receptor (some)
replication details very similar to poliovirus
Acid sensitive and 33oC optimum for replication
no tissue destruction

37
Q

common cold

bind to respiratory epithelial cells

A

Icam mostly

38
Q

Rhinoviruses Complications.

A

sometimes infection has complications
sinusitis, otitis media
worsening of asthma (assoc. with 50% of attacks)
vaccine prospects poor (too many variants)

39
Q

Arboviruses

A

(arthropod-borne viruses) (Chapter 33)
viruses transmitted by arthropods
multiply in tissues of vector, often without producing disease

40
Q

For many arboviruses humans are
____________ hosts:
viremia of short duration
virus levels in blood are ___________

A

For many arboviruses humans are
􀀁dead-end􀀂 hosts:
viremia of short duration
virus levels in blood are low

41
Q

Togaviruses

Enveloped or No

A

plus stranded RNA (single linear molecule)

enveloped

42
Q

Togavirus

replication

A

2 phases of translation
-first produce early proteins
and then late proteins
-like coronavirus

43
Q

Toga Virus Replication:

Ribosomes bind to the
__________ RNA genome

A

Ribosomes bind to the
positive-sense RNA genome
early polyproteins are made

44
Q

Toga Virus
The
polyproteins are cleaved to produce nonstructural proteins ___ to _____ (___ to ___), which include a
polymerase to transcribe the genome into a ______ RNA template.

A

The
polyproteins are cleaved to produce nonstructural proteins 1 to 4 (NSP1 to NSP4), which include a
polymerase to transcribe the genome into a negative-sense RNA template.

45
Q

Toga virus replication: 5, The template is used to

produce a full-length _____, ______-sense mRNA genome and a late ____ mRNA for the structural proteins.

A

5, The template is used to

produce a full-length 42S positive-sense mRNA genome and a late 26S mRNA for the structural proteins.

46
Q

Toga Replication
9, _______ from the plasma membrane releases
the virus.

A

9, Budding from the plasma membrane releases

the virus.

47
Q 
Rubella virus
Member of Togavirus family
Rubivirus genus
but not \_\_\_\_\_\_\_\_-borne
Rubella = \_\_\_\_\_\_\_
one of the 5 childhood exanthems
(along with measles, roseola, chickenpox,
and fifth disease)
A 
Rubella virus
Member of Togavirus family
Rubivirus genus
but not arthropod-borne
Rubella = German measles
one of the 5 childhood exanthems
(along with measles, roseola, chickenpox,
and fifth disease)
48
Q

Flaviviruses
_______ stranded RNA (single linear molecule)
Enveloped or No?

A

Flaviviruses
plus stranded RNA (single linear molecule)
Enveloped Brah!

49
Q

Disease syndromes of
togaviruses and
flaviviruses

A

Encephalatis
yellow fever (heptitis)
Hemorric fever
DHF/DSS

50
Q

Zika virus (a Flavivirus)
mostly mild illness (Zika fever) except for _____________of fetus,
which leads to__________ and other birth defects
transmitted by _________from person to person (most common)
Aedes aegypti mosquito (worldwide distribution of A. aegypti below)

A

mostly mild illness (Zika fever) except for congenital infection of fetus,
which leads to microcephaly and other birth defects
transmitted by mosquitos from person to person (most common)
Aedes aegypti mosquito (worldwide distribution of A. aegypti below)

51
Q

Zika Virus Transmission

A

also transmitted sexually

Person to person

52
Q

Dengue fever (caused by a ______)

A

most prevalent disease caused by arboviruses
does not cause significant mortality

enerally not a zoonosis:
transmitted by mosquitos from person to person
when partial immunity exists due to prior infection
dengue hemorrhagic shock (DHS)
dengue shock syndrome (DSS)
due to immune enhancement
virus forms immune complex/readily enter macrophages
increases viral load
Activates memory T cells, which release cytokines and initiate hypersensitivity reactions.
These reactions cause weakening and rupture of vasculature, internal bleeding, loss of plasma.

53
Q

when partial ________ exists due to prior infection
dengue hemorrhagic shock (DHS)
dengue shock syndrome (DSS)
due to __________
virus forms immune complex/readily enter macrophages
increases viral load

A

when partial immunity exists due to prior infection
dengue hemorrhagic shock (DHS)
dengue shock syndrome (DSS)
due to immune enhancement
virus forms immune complex/readily enter macrophages
increases viral load

54
Q

Dengue Fever
immune enhancement
virus forms immune complex/readily enter macrophages
increases viral load

A

Activates memory T cells, which release cytokines and initiate hypersensitivity reactions.
These reactions cause weakening and rupture of vasculature, internal bleeding, loss of plasma

55
Q 
Yellow Fever (caused by a\_\_\_\_\_\_\_
• historical importance
– first human disease found \_\_\_\_\_\_\_\_\_
– first viral disease confirmed to be spread by\_\_\_\_
– Mosquito: \_\_\_\_\_\_\_\_
• spread by two methods (via mosquito)
– \_\_\_\_\_\_ to human
– \_\_\_\_\_ to human
A 
Yellow Fever (caused by a Flavivirus)
• historical importance
– first human disease found to be caused by a virus
– first viral disease confirmed to be spread by insect vector
– Mosquito: Aedes aegypti
• spread by two methods (via mosquito)
– human to human
– monkey to human
56
Q

Yellow Fever
Severe
Controll

A

Jaundice
lesions and hemorrhaging of infected organs
attenuated live vaccine and insect control measures

MBE3 (13 decks)

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