Corona-picorna-arbo viruses Flashcards
corona RNA/DNA? strand? envelope? agent of
+ strand RNA viruses
enveloped
SARS-CoV-2 is agent of COVID-19
what causes up to 30% common colds
corona virus
• SARS-CoV is agent of:
severe acute respiratory syndrome (SARS)= atypical pneumonia
middle east respiratory syndrome (MERS)
caued by?
mortality?
from?
caused by corona too
30-40 mortality
zoonoitc
corona virus life cyle
- adsorbed- spike pro bind receptor
- virus uncoated/ + RNA undergoes 1st translation= polyproteins formed and proteolysis occurs to form non-structural proteins and an RNA dependent RNA polymerase
- replicate transcriptase complex forms
- transcription and RNA replication occur
- products assemble to form nucleocapsid
- acquire membrane from budding at ER
- follow exocytosis path
clincal presentation of SARS Cov-2 infection
different severity?
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
entry of SARS-Cov 2 into cell
Spike protein will bind ACE2
spike then cleaved by TMPRSS2
effects of SARS CoV 2 entry
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
COVID only effect pulmonary?
no, multiple systemic effects
Picornaviruses
DNA/RNA
envelope?
+ stranded RNA
no envelope
Picornaviruses classes
enteroviruses
habitat
includes what viruses?
habitat = gastrointestinal tract
include: poliovirus and coxsackievirus
also echoviruses - enteric cytopathic human orphan viruses
rhinoviruses habitat
respiratory epithelium
why would enteroviruses be in GI tract?
very stable in food and water
also stable at pH 3 (stomach)
why are rhinoviruses confined to the respiratory tract?
Sensitive to acidic pH
Replicate poorly above 33 C
enterovirus replication occurs where?
organ involvement
in oropharynx/intestines then to lymphoid tissues, can progress to viremia
organ involvement only occurs if viremia persists
where do rhino viruses replicate
upper respiratory tract
poliovirus, types?
genome
symmetry
3 antigenic types: PV1, PV2, PV3= Capsid differences between types
plus strand RNA genome 7500 nt in length
Icosahedral capsid
Poliovirus replication/life cyclce
- adherence via virus binds CD155 receptor, penetrance
- +RNA in the cell
- translation occurs= viral proteins made, includes a RNA dependent RNA poly
- replication of RNA occurs, + and - strands made (- used to make more positive strands)
- proteins and RNA packaged into nucleocapsid and released, cell destroyed via lysis NO ENVELOPE FORMED
danger of polivirus RNA alone
alone even this can cause infection
polio as a lytic virus
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
transmission polio virus
fecal oral
Poliovirus IRES
difference in start site due to this?
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)
pathogenesis of polio diagram
clinical manifestations of polio
at CNS?
most severe from?
factors increasing severity?
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
Poliovirus vaccines:
Live oral vaccine (Sabin) mimics the normal infection process of poliovirus
Killed parenteral vaccine (Salk) only generates serum antibodies
immune result of the live oral vax
elevated serum IgG
increased nasal IgA
increased duodenal IgA
inital increased IgM
immune result to the killed parenteral vax
elevated serum IgG
initial increased IgM
nonpolio enteroviruses (EVD-68) are associated with what new disease?
acute flaccid myelitis
Coxsackieviruses groups
a and B
group A coxsackieviruses cause what?
type A16?
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
group B coxsackieviruses targets/diseases?
heart (myocarditis)
respiratory tract (pleurodynia)
mucous membranes of eye (hemorrhagic conjunctivitis)
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?
~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
complications with rhinovirus infections
sometimes infection has complications: secondary infections with bacteria
sinusitis, otitis media
worsening of asthma (assoc. with 50% of attacks)
vax prospects of rhinovirus
poor, too many serotypes
Arboviruses
transmitted by?
multiply where?
humans are what kind of host?
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
togavirus
disease caused
vector
geogrpahic distribution
encephalitis
mosquito
eastern and western US
flavivirus
disease caused
vector
geogrpahic distribution
encephalitis
mosquito
North america
dengue
disease caused
vector
geogrpahic distribution
fevers/hemmorhages
mosquitos
tropics
yellow fever
disease caused
vector
geogrpahic distribution
hemorrhagic fever
mosquito
africa, central and south America
west nile
disease caused
vector
geogrpahic distribution
encephalitis
mosquito
worldwide
zika
disease caused
vector
geogrpahic distribution
encephalitis, birth defects
mosquito
africa; recently to americas
Togaviruses
genome
envelope?
plus stranded RNA (single linear molecule)
enveloped
Togavirus replication
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
Rubella virus
member of what family?
arthopod borne?
Member of Togavirus family
Rubivirus genus
but not arthropod-borne
rubella causes?
Rubella = German measles
one of the 5 childhood exanthems
(along with measles, roseola, chickenpox,
and fifth disease)
rubella entry and spread where it enters? spreads to? what can block viral transfer/ viremia? immunologically def pregnancies?
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.
Flaviviruses
genome?
envelope?
plus stranded RNA (single linear molecule)
enveloped
flavivirus life cycle/replication
- virus adherence/ penetrance
- disassembly in endosome- RNA released
- polyproteins translated> RNA dependent RNA poly
- RNA replicated
- viral assembly and budding into ER- ACQUIRES MEM HERE
- exocytosis cycle and release of virus
Disease syndromes of togaviruses and flaviviruses
immune protection?
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.
zika virus is what kind of virus
flavivirus
Zika virus causes?
transmitted by?
(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
Dengue fever caused by? prevalence? mortality? transmission?
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
dengue fever when partial immunity exists due to prior infection
virus will form? effect of this?
memory t cells role?
result?
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
Yellow Fever
caused by?
historical?
spread routes?
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
clinical manifestations of yellow fever (severe cases)
- jaundice
* lesions and hemorrhaging of infected organs
yellow fever vax
attenuated live vaccine and insect control measures
