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microbiology > Corona-picorna-arbo viruses > Flashcards

Corona-picorna-arbo viruses Flashcards

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1
Q 
corona
RNA/DNA?
strand?
envelope? 
agent of
A

+ strand RNA viruses
enveloped
SARS-CoV-2 is agent of COVID-19

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2
Q

what causes up to 30% common colds

A

corona virus

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3
Q

• SARS-CoV is agent of:

A

severe acute respiratory syndrome (SARS)= atypical pneumonia

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4
Q

middle east respiratory syndrome (MERS)
caued by?
mortality?
from?

A

caused by corona too
30-40 mortality
zoonoitc

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5
Q

corona virus life cyle

A
  1. adsorbed- spike pro bind receptor
  2. virus uncoated/ + RNA undergoes 1st translation= polyproteins formed and proteolysis occurs to form non-structural proteins and an RNA dependent RNA polymerase
  3. replicate transcriptase complex forms
  4. transcription and RNA replication occur
  5. products assemble to form nucleocapsid
  6. acquire membrane from budding at ER
  7. follow exocytosis path
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6
Q

clincal presentation of SARS Cov-2 infection

different severity?

A

asymptomatic

mild: sore throat, cough
moderate: some lower respiratory disease, lower O2
severe: SpO2 under 94%, PaO2/FiO2 under 300mmHg, respiratory freq under 30 breaths a minute/ lung infiltrates over 50%
critical: respiratory failure, spetic shock, organ dysfunction

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7
Q

entry of SARS-Cov 2 into cell

A

Spike protein will bind ACE2

spike then cleaved by TMPRSS2

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8
Q

effects of SARS CoV 2 entry

A

direct cytotoxic effect

dysregulation of RAAS due to downregulated ACE2: decreased cleavage of angiotensin I

endothelial cell damage and thromboinflammation

dysregulated immune response: virus can inhibit interferon signaling, t cell lyphodepletion, and production of inflammatory cytokines

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9
Q

COVID only effect pulmonary?

A

no, multiple systemic effects

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10
Q

Picornaviruses
DNA/RNA
envelope?

A

+ stranded RNA

no envelope

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11
Q

Picornaviruses classes

A
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12
Q

enteroviruses
habitat
includes what viruses?

A

habitat = gastrointestinal tract
include: poliovirus and coxsackievirus
also echoviruses - enteric cytopathic human orphan viruses

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13
Q

rhinoviruses habitat

A

respiratory epithelium

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14
Q

why would enteroviruses be in GI tract?

A

very stable in food and water

also stable at pH 3 (stomach)

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15
Q

why are rhinoviruses confined to the respiratory tract?

A

Sensitive to acidic pH

Replicate poorly above 33 C

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16
Q

enterovirus replication occurs where?

organ involvement

A

in oropharynx/intestines then to lymphoid tissues, can progress to viremia
organ involvement only occurs if viremia persists

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17
Q

where do rhino viruses replicate

A

upper respiratory tract

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18
Q

poliovirus, types?
genome
symmetry

A

3 antigenic types: PV1, PV2, PV3= Capsid differences between types
plus strand RNA genome 7500 nt in length
Icosahedral capsid

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19
Q

Poliovirus replication/life cyclce

A
  1. adherence via virus binds CD155 receptor, penetrance
  2. +RNA in the cell
  3. translation occurs= viral proteins made, includes a RNA dependent RNA poly
  4. replication of RNA occurs, + and - strands made (- used to make more positive strands)
  5. proteins and RNA packaged into nucleocapsid and released, cell destroyed via lysis NO ENVELOPE FORMED
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20
Q

danger of polivirus RNA alone

A

alone even this can cause infection

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21
Q

polio as a lytic virus

A

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

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22
Q

transmission polio virus

A

fecal oral

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23
Q

Poliovirus IRES

difference in start site due to this?

A

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

Because of IRES, translation starts far from the 5’ end of
poliovirus RNA (normal mRNA translation starts near 5’ end)
24
Q

pathogenesis of polio diagram

A
25
Q

clinical manifestations of polio
at CNS?
most severe from?
factors increasing severity?

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

26
Q

Poliovirus vaccines:

A

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

27
Q

immune result of the live oral vax

A

elevated serum IgG
increased nasal IgA
increased duodenal IgA
inital increased IgM

28
Q

immune result to the killed parenteral vax

A

elevated serum IgG

initial increased IgM

29
Q

nonpolio enteroviruses (EVD-68) are associated with what new disease?

A

acute flaccid myelitis

30
Q

Coxsackieviruses groups

A

a and B

31
Q

group A coxsackieviruses cause what?

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

32
Q

group B coxsackieviruses targets/diseases?

A

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

33
Q

Rhinoviruses
# serotypes
responsible for how much of the common cold
bind to what cells/how
replication similar to what other virus?
sensitive to? optimal temp?
tissue destruction?

A

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

34
Q

complications with rhinovirus infections

A

sometimes infection has complications: secondary infections with bacteria
sinusitis, otitis media
worsening of asthma (assoc. with 50% of attacks)

35
Q

vax prospects of rhinovirus

A

poor, too many serotypes

36
Q

Arboviruses
transmitted by?
multiply where?
humans are what kind of host?

A

viruses transmitted by arthropods
multiply in tissues of vector, often without producing disease

For many arboviruses humans are “dead-end” hosts:
viremia of short duration and virus levels in blood are low

37
Q

togavirus
disease caused
vector
geogrpahic distribution

A

encephalitis
mosquito
eastern and western US

38
Q

flavivirus
disease caused
vector
geogrpahic distribution

A

encephalitis
mosquito
North america

39
Q

dengue
disease caused
vector
geogrpahic distribution

A

fevers/hemmorhages
mosquitos
tropics

40
Q

yellow fever
disease caused
vector
geogrpahic distribution

A

hemorrhagic fever
mosquito
africa, central and south America

41
Q

west nile
disease caused
vector
geogrpahic distribution

A

encephalitis
mosquito
worldwide

42
Q

zika
disease caused
vector
geogrpahic distribution

A

encephalitis, birth defects
mosquito
africa; recently to americas

43
Q

Togaviruses
genome
envelope?

A

plus stranded RNA (single linear molecule)

enveloped

44
Q

Togavirus replication

A

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

  • like coronavirus
    1. bind receptors/ internalized
    2. nucleocapsid released into cyto
    3. ribo bind + RNA
    4. translate poly proteins, cleaved
    5. cleavage includes a polymerase to transcribe the genome into a negative-sense RNA template.
    6. The template is used to produce a full-length 42S positive-sense mRNA genome and a late 26S mRNA for the structural proteins.
    7. viral assembly
    8. budding from membrane to acquire capsule
45
Q

Rubella virus
member of what family?
arthopod borne?

A

Member of Togavirus family
Rubivirus genus
but not arthropod-borne

46
Q

rubella causes?

A

Rubella = German measles
one of the 5 childhood exanthems
(along with measles, roseola, chickenpox,
and fifth disease)

47
Q 
rubella entry and spread
where it enters? 
spreads to?
what can block viral transfer/ viremia? 
immunologically def pregnancies?
A

Rubella enters and infects the nasopharynx and lung and then spreads to the lymph nodes and monocytemacrophage system.

The resulting viremia spreads the virus to other tissues and the skin.

Circulating antibody can block the transfer of virus and prevent primary and secondary viremia (prevent involvement of skin/placenta)

In an immunologically deficient pregnant woman, the virus can infect the placenta and spread to the fetus.

48
Q

Flaviviruses
genome?
envelope?

A

plus stranded RNA (single linear molecule)

enveloped

49
Q

flavivirus life cycle/replication

A
  1. virus adherence/ penetrance
  2. disassembly in endosome- RNA released
  3. polyproteins translated> RNA dependent RNA poly
  4. RNA replicated
  5. viral assembly and budding into ER- ACQUIRES MEM HERE
  6. exocytosis cycle and release of virus
50
Q

Disease syndromes of togaviruses and flaviviruses

immune protection?

A

Primary viremia may be associated with mild systemic disease, Most infections are limited to this.

If sufficient virus is produced during the secondary viremia to escape immune protection and to reach critical target tissues, severe systemic disease or encephalitis may result.

For dengue virus, rechallenge with another strain can result in severe dengue hemorrhagic fever (DHF), which can cause dengue shock syndrome (DSS) because of the loss of fluids from the vasculature.

51
Q

zika virus is what kind of virus

A

flavivirus

52
Q

Zika virus causes?

transmitted by?

A

(a Flavivirus)
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), possibly sexual
Aedes aegypti mosquito

53
Q 
Dengue fever
caused by? 
prevalence?
mortality?
transmission?
A

caused by a Flavivirus
most prevalent disease caused by arboviruses, does not cause significant mortality

generally not a zoonosis: transmitted by mosquitos from person to person

54
Q

dengue fever when partial immunity exists due to prior infection
virus will form? effect of this?
memory t cells role?
result?

A

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

55
Q

Yellow Fever
caused by?
historical?
spread routes?

A 
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

clinical manifestations of yellow fever (severe cases)

A
  • jaundice

* lesions and hemorrhaging of infected organs

57
Q

yellow fever vax

A

attenuated live vaccine and insect control measures

microbiology (42 decks)

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