Final Flashcards
1
Q
What is meant by a “live” virus?
A
it is capable of replicating
2
Q
Are attenuated vaccines capable of causing infection?
A
yes
3
Q
What is necessary for a virus to cause disease?
A
- must have sufficient virions to cause infection
- the cells targeted must be accessible, susceptible, and permissive
- the local antiviral defense must be absent or ineffective
4
Q
What barriers are present in the respiratory tract to prevent infection
A
- mucus, ciliated cells, mucus-secreting glands, alveolar macrophages
- turbinates to prevent attachment
- tonsilar lymphoid tissues
5
Q
T/F enveloped viruses are less susceptible to drying or inactivation through different environmental factors
A
false
6
Q
If we have a stomach bug, typically it is a (enveloped/nonenveloped) virus
A
non-enveloped
7
Q
What is important about the M cells of the alimentary tract
A
they are constantly sampling whatever’s in the gut and passing it on to the DCs
(the king’s wine taster)
8
Q
what is the series of events that a virus needs to go through to cause disease?
A
- acquisition
- primary replication
- primary viremia
- activation of innate response
- incubation period
- -> asymptomatic or prodrome
- -> spread to secondary site
- replication in target tisse (DISEASE)
- secondary viremia
- immune response
- release (transmission)
- resolution or persistence
9
Q
what are the steps of viral replication for a non-enveloped virus?
A
- recognition: viral attachment proteins (VAPs) identify specific host cells
- Attachment: VAPs bind to cell receptors (proteins or carbs); these attachment sites determine host range and tissue tropism
- Penetration/Entry
- non-enveloped enter by receptor-mediated endocytosis - uncoating: capsid/envelope removed; DNA delivered to nucleus, RNA to cytoplasm
- macromolecular synethesis: synthesis of viral mRNA and proteins
- most DNA viruses use cell RNA POL II
- most RNA viruses encode enzymes for transcription and replication
- all viruses depend on host ribosomes, tRNA, and post-mechanical mechanisms - Assembly: DNA in nucleus, RNA and Pox in cytoplasm
- Release: lysis, exocytosis
10
Q
what are the steps of viral replication for an enveloped virus?
A
- recognition: viral attachment proteins (VAPs) identify specific host cells
- Attachment: VAPs bind to cell receptors (proteins or carbs); these attachment sites determine host range and tissue tropism
- Penetration/Entry
- enveloped enter by fusion of viral and cellular membranes - uncoating: capsid/envelope removed; DNA delivered to nucleus, RNA to cytoplasm
- macromolecular synethesis: synthesis of viral mRNA and proteins
- most DNA viruses use cell RNA POL II
- most RNA viruses encode enzymes for transcription and replication
- all viruses depend on host ribosomes, tRNA, and post-mechanical mechanisms - Assembly: DNA in nucleus, RNA and Pox in cytoplasm
- Budding: viral glycoproteins delivered to cell membranes; capsid interacts with glycoprotein-membrane and surrounds capsid
- budding occurs from plasm membrane, ER, Golgi, or nuclear membrane - Release: lysis, budding, exocytosis
11
Q
replication cycle of (+)RNA Viruses
A
- entry
- translation
- transcription
- assembly
- release
12
Q
replication cycle of (-) RNA viruses
A
- mRNA transcription and replication
- transcription
- assembly
- release
13
Q
What makes retroviruses a bit slower to affect the host
A
it must integrate into the host genome-
14
Q
how do viral mutations/recombinations/reassortments affect the virus
A
- new virus
- quasispecies
- defective genomes
- change the virulence
- affect disease outcome
15
Q
what is a pseudotype virus
A
proteins/capsids from one virus and genome of a different one
allows you to protect against a harmless virus while utilizing the “shell” of a dangerous one that the body can react to immensely
16
Q
T/F mutations occur constantly in viruses
A
true
17
Q
what is reassortment
in which viruses does it occur?
A
- exchange of part of the genome
- occurs in all segmented viruses
18
Q
What is viral pathogenesis outcome determined by?
A
- virus-host interaction
- host’s response to infection
19
Q
what do viruses need to do in order to be effective
A
- break through barriers and invade cells
- evade immune control
- kill cells or trigger destructive immune reponse
20
Q
determinants of disease
A
type of disease
- tissue tropism
- permissiveness of cells for replication
- portal of entry
- access to target tissue
- virus strain
- virulence factors
severity of disease
- virus strain**
- CPE
- immune status
- immunopathology
- inoculum size
- prior exposure
- general health and nutrition
- genetics
- age
21
Q
what is the primary determinant of disease severity
A
virus strain
22
Q
what is the primary determinant of disease type
A
tissue tropism
23
Q
what do virulence genes do?
A
- affect ability of virus to replicate
- modify host defense mechanisms
- facilitate spread in and among hosts
- direct toxicity
24
Q
what are the 3 outcomes of cytopathogenesis
A
- abortive infections
- lytic infections
- persistent infections
25
what are abortive infections
an infection in which the virus fails to replicate
26
what are lytic infections
"virus gets into the permissive cell and will replicate like mad and make the cell explode"
27
what are examples of persistent infections
- chronic: non-lytic, productive
- latent: limited, no virus synethesis
- recurrent: reactivation
- oncogenic: transforming
28
Recall the goals of immune response
- respond (prevent entry and spread, eliminate virus and infected cells)
- return to homeostasis (eliminate virus and infected cells, repair damage)
- remember (develop memory to respond more rapidly to second exposure)
29
why are inapparent or asymptomatic individuals a major source of contagion?
they don't realize that they're infected and spread the virus to susceptible hosts
30
what is the gold standard for Virus ID?
PCR
31
what is the structure of a poxvirus
diseases caused?
dsDNA
linear
envelope
smallpox, Molluscum contagiosum
32
what is the structure of a papillomavirus
diseases caused
dsDNA
circular
naked
warts, epidermodysplasia verruciformis, cancer
33
what is the structure of an adenovirus
diseases caused
dsDNA
linear+ 5'TP
naked
respiratory, conjunctival, GI infection
34
What is the structure of a Herpesvirus
disease caused?
dsDNA
linear
envelope
herpes, chickenpox, zoster, mono, lymphoma, congenital syndrome, roseola, sarcoma
35
T/F poxviruses are the largest viruses
true
36
Where do poxviruses replicate?
what do they encode for?
cytoplasm
encode enzymes for mRNA and DNA synthesis
37
poxvirus tissue tropism
epithelial cells
38
poxvirus tranmission
respiratory, contact
39
T/F poxviruses has a single envelope
false, double envelope
40
incubation period of poxviridae
5-17 days
41
symptoms of smallpox
high fever, fatigue, severe headache, backache, malaise
red spots on tongue and mouth --> papular rash --> pustules --> scabs
42
mortality rate of smallpox
15-62%
43
incubation period of molluscum contagiosum
2-8 wk period
44
transmission of molluscum contagiosum
contact, fomites
45
T/F smallpox and molluscum contagiosum are strict human pathogens, while other poxviruses are asymptomatic
true
46
diagnosis and tx of Poxviruses
- clinical: febrile prodrome, classic lesion, same stage of development
- microscopy: Guarnieri bodies; testing at CDC
tx: post-exp. vaccination; supportive care
47
tissue tropism of papillomaviridae
squamous epithelial tissue
48
transmission of papillomaviridae
direct contact, sexual, and vertical
oncogenic: cervical, anal, vulvar, penile, oral, laryngeal
49
what controls the replication of papillomaviridae
replication controlled by host cell's transcriptional machinery
determined by differentiation of skin or mucosal epithelium
50
where are all of the genes of papillomaviridae located
on the (+) strand, the (-) strand is just a carrier
51
how do genital warts form?
1. HPV invades the skin
2. DNA from virus enter skin cells (makes proteins that induce epidermal growth factor)
3. HPV causes infected skin cells to multiply and form warts
4. Virus sheds, passing on to others
52
How does HPV lead to cancer?
To effectively replicate, the virus will break its own genome and integrate within the host genome, disrupting the cell cycle, thereby losing the brakes on that cell and inducing epidermal growth factor, leading to cancerous growth.
53
what are Koilocytes
enlarged keratinocytes with halos around shrunken nuclei
| - hallmark sign of HPV(?)
54
What causes epidermodysplasia verruciformis
a genetic alteration in certain genes in the host, followed by contraction of HPV leads to a horny growht
55
which HPV strain causes warts
1-4
56
which HPV strain causes papillomas
6 and 11
57
which HPV strain causes Epi. verucciformis
5 and 8 + genetic mutation of EVER1/2
58
genital warts and cancers are caused by which strains of HPV
16, 18, 31, 45
59
diagnosis and tx of HPV
dx: visual, microscopic for hyperkeratosis; PAP smear for dysplasia; PCR for typing
tx: sx, cryotherapy, electrocautery, chemical, salicylic acid removal
Gardasil HPV vx
60
adenovirus tropism
mucepithelial cells, lymhpoid cells
61
adenovirus transmission
fecal-oral, respiratory, contact, fomites
62
what early proteins are required for replication of adenoviruses
- DNA Pol
- TP (rep. primer)
"very simply, virus recognizes receptor, enters cell, replicates, exits cell"
63
what do late proteins do to help adenovirus replication
- suppress immune response
| - provide capsid components
64
general path of adenoviruses
- entry through respiratory mucosa (or other viable areas like eye)
- once in, tends to go to URT, the LRT, or GIT (transports through body via blood or lymph)
65
incubation period of adenovriuses
~4-8 days
66
T/F adenoviruses are easily spread
true
67
those at risk for adenovirus infectoin
- children <14 yo and people in crowded areas
| - children shed virus for months
68
diagnosis and treatment of adenoviruses
dx: ELISA for ID; fluorescent Abs, PCR, ELISA for typing
tx: none; vaccine for type 4 and 7 for military use; CAdV2 for dogs
"you have a virus, go home and drink lots of fluids"
69
alpha-herpesviruses and site of latency
- herpes simplex virus 1 (neurons)
- herpes simplex virus 2 (neurons)
- varicella zoster virus (Chicken pox) (neurons)
70
beta-herpesviruses and site of latency
- cytomegalovirus (monocytes, lymphocytes)
- Human herpesvirus 6 (T cells)
- Human herpesvirus 7 (T cells)
71
gamma-herpesviruses and site of latency
- Epstein-Barr virus (B cells)
| - Kaposi's sarcoma herpesvirus (B cells)
72
what kind of infections do herpesviruses typically cause
- lytic, latent, persistent, or immortalizing infections
73
interesting feature of herpesviruses
they have their viral genome in the center, packaged inside a capsid, and keep what they need for replication (once they get into the cell) in the tegument (space btwn capsid and outer envelope
74
HSV 1 and 2 have:
- multiple glycoproteins
| - bind heparan sulfate and nectin-1 for membrane fusion
75
if HSV1/2 gets into the epithelial cell, what kind of infection occurs
lytic
76
if HSV1/2 gets into the neurons, what kind of infection occurs
latent
77
T/F latent-infection herpesviruses recrudesce in response to stimuli like light, stress, fever, etc.
true
78
HSV1 infections are generally (Above/below) the waist
above
79
HSV2 infections are generally (Above/below) the waist
below
80
HSV1/2 epidemiology
- may be asymptomatic
- once infected, infected for life
- human disease
HSV1: 60-90 of population
HSV2: 20-25% of population (plus sexually active individuals and neonates)
81
HSV1/2 epidemiology
close contact, secretions (vesicle fluid, saliva, vaginal, semen)
82
HSV1/2 Dx and Tx
Dx: serology, PCR, CPE in cell culture
Tx: cell mediated immunity critical to control dz.
- Acyclovir,
83
HSV1 has a predilection for the ___
brain
84
HSV 2 rarely crosses into the ____ but can cause recurrent ______
brain
sacral meningitis
85
where does HSV1/2 establish latency
sensory dorsal root ganglia of the spine
86
what are the 6 childhood exanthems
1. Measles
2. Scarlet fever
3. Rubella
4. Chicken Pox
5. Erythema Infectiosum
6. Roseola infantum
87
paramyxovirus structure and diseases caused
ssRNA
Measles, mumps, RSV, Hendra/Nipah
88
streptococcus pyogenes structure and disease caused
a bacteria
scarlet fever
89
Togavirus structure and diseases caused
rubella (german measles)
90
herpesviruses structure and diseases caused
dsDNA, linear, envelope
fever blisters, genital herpes, chicken pox/zoster, mono, congenital syndrome, roseola, Kaposi Sarcoma
91
parvovirus structure and disease caused
ssDNA +/-, circular, naked
erythema infectiosum (Fifth disease)
92
Varicella Zoster Virvus, aka ___
HHV3 or VZV, chicken pox
93
where does VZV establish latency
in neurons (all dorsal root ganglia along the spine
94
VZV transmission
respiratory
95
typical reccurrence of VZV
only once
96
chickenpox incubation period
15 days
97
symptoms of chickenpox
sometimes mild or asymptomatic
fever, sore throat
* *vesicular rash--> pustules --> scabs in successive crops over 3-5 days
- most severe on trunk than extremities
- primary infection more severe in adults with pneumonia in 20-30%
98
epi of VZV
- may be asymptomatic
- once infected, infected for life
- human disease
chickenpox- mostly children
zoster- older adults who had chickenpox as a child
99
VZV transmission
respiratory, contact with vesicles, saliva
100
dx and tx of VZV
DX: CPE in cell culture, serology, PCR
tx: acyclovir; vaccination; VZIG for IC or older people
101
Cytomegalovirus is a
beta-herpesvirus
| aka CMV or HHV5
102
lytic cytomegalovirus infections target:
epithelial cells and macrophages
103
latent cytomegalovirus infections target:
lymphocytes, bone marrow stromal cells
104
how does CMV spread through host
how is it reactivated
lymphocytes
immunosuppression
105
how is CMV shed?
urine, stool, blood, saliva, breast milk, semen, vaginal secretions, amniotic fluid, transplant organs
106
what is the most common viral cause of congenital defects
CMV
107
epidemiology of CMV
transmission: bodily fluids, transplacental, transfusion, transplanation
108
dx and tx of CMV
Dx: owl's eye intranulcear inclusion, rapid ab test for urine/blood
tx: gancyclovir, foscarnet
109
HHV6 and HHV 7 infection tropisms
lytic: salivary glands, T cells, monocytes, epithelial cells, endothelial cells, neurons
latent: T cells and peripheral blood monocytes
110
Exanthem VI
roseola
111
symptoms/signs
rapid onset high fever (103-105) followed a few days later by a generalized rash lasting 24-48 hours
most common cause of febrile seizures in children 6-24 months
full recovery, no complications
if IC: pneumonitis, encephalitis, hepatitis, fever, organ rejection
112
Epstein-Barr virus infection tropisms
AKA EBV or HHV4
lytic: B cells or nasopharyngela epithelial cells
Latent: B cells
Immortalizing: B cells
Receptor is C3d receptor
113
what does mononucleosis result from
the battle between EBV-infected cells and activaiton/proliferation of protective T cells
114
symptoms of mono
fever, FATIGUE, sore throat, swollen lymph nodes, and spleen
115
Transmission of EBV
saliva
116
Dx and Tx of EBV
Dx: clinical symptoms, atpical lymphocytes, lymphocytosis, viral antigen antibody
tx: none
vx: none
117
Kaposi's Sarcoma (AKA)
infection tropism
KSHV or HHV8
B cells + endothelial cells, monocytes, epithelial cells, sensory nerve cells
118
Kaposi Sarcoma is ____
an opportunistic disease in Advanced AIDS
occurs when endothelial spindle cells proliferate
119
Chilhood Exanthem #5
Erythema infectiosum
120
what causes Erythema infectiosum?
parvovirus B19
121
T/F parvoviruses are the smallest virus
True
122
Parvovirus tropism
erythroid cells
123
parvovirus transmission
respiratory droplets and secretions
124
3 parvoviruses of concern:
- parvovirus B19: Fifth's Disease
- Bocavirus: Resp. disease
- Adeno-associated virus (AAV)
125
Parvovirus tends to prefer which type of RBC?
immature RBCs
126
What are the two stages of B19 infection?
```
Febrile stage (contagious)
- killing of erythroid precursors
```
```
symptomatic stage (Not contagious)
- immune-mediated
```
127
incubation period of EI
5-6 days (?)
128
when does Parvo B19 typically occur?
late winter and spring
129
Parvo B19 transmission
Droplets and secretions
130
Childhood exanthem III
Rubella
131
what does rubella affect
resp tract --> lymph nodes --> viremic spread
132
T/F rubella can cross the placenta
true
133
what does the rubella rash coincide with?
development of antibodies
134
togavirus (rubella) transmission
respiratory
135
rubella incubation period
14-21 days
136
rubella symptoms in children
fever, 3 day rash, swollen glands
137
rubella symptoms in adults
more severe than in children, with arthralgia and arthritis, encephalopathy
138
Why do we vaccinate kids for rubella?
to protect unborn babies
139
is there a tx for rubella?
no
140
childhood exanthem I
rubeola (measles)
141
what kind of virus causes measles
paramyxovirus
142
what kind of tropism do paramyxoviruses have
wide range (resp tract, conjunctiva, urinary tract, small blood vessels, lymphatics, CNS)
143
transmission of paramyxovirus
resp. droplets highly contagious
144
what are the 3 rare outcomes of rubeola
postinfectious encephalitis (immunopathologic etiology)
subacute sclerosing panencephalitis (defective measles virus infection of CNS)
no resolutoin of acute infection caused by defective CMI (frequently fatal outcome)
145
symptoms of rubeola
high fever, Cough, conjunctivitis, coryza, and photophobia
Koplik spots
maculopapular rash
146
what is the cause of most of rubeola's symptoms
cell mediated immunity
147
complications from measles
pneumonia
encephaltis (0.5% of cases, but 15% mortality in those cases)
atypical measles (T cell deficient)
148
T/F clearance of measles results in lifelong immunity
True
149
Measles summary
Rubeola
Has Kolpik spots, rash behind ears
150
Summary of scarlet fever
Caused by strep pyogenes
Only bacterial exanthem
Strawberry tongues
151
Summary of measles/rubella
German measles
Forscheimer’s spot, rash is forehead down
152
Summary of varicella
Chickenpox/zoster
Vesicular rash (will rupture/burst)
153
Summary of erythema infectious
Slapped cheeks appearance
Sudden high fever
154
Summary of rosella infantum
HHV 6 and 7
Lacy body rash
Sudden fever
155
T/F few viral respiratory infections are enveloped
False, they are so they NEED to be wet
156
Viral respiratory barriers
Hairs, nasal turbinates, ciliated cells, alveolar macrophages
Temperature in different sections can determine where viruses can replicate
157
Approx. how many viruses can cause the “common cold”
200
158
Where is the common cold restricted to?
Typically the URT
159
Symptoms of the common cold are mainly due to the:
Immune response;
Virus binds to ICAM-1 and triggers release of inflammatory mediators
160
What is the most common cause of the common cold
Rhinovirus (30-80%)
161
Mumps is caused by a:
Paramyxovirus
162
Mumps pathogens is
Inoculation of resp. Tract —> local replication —> fire is —> systemic infection
- if spread to pancreas: may be associated w/ onset of juvenile diabetes
- can spread to testes, ovaries, peripheral nerves, eyes, inner ear, or CNS (CNS in ~50%)
- can spread to parotid gland: virus multiples in ducal epithelial cells, local inflammation causes marked swelling
163
Mumps epidemiology
- highly contagious P2P contact and droplets
- before vx, 90% of pop. Had it
- virus shed 7 days before symptoms; almost impossible to stop spread
164
Dx and Tx of mumps
Dx: clinical presentation, ELISA, PCR
Tx: supportive; vx in 1967
165
What causes parainfluenza
Paramyoxivirus; 4 stereotypes in humans
166
Clinical signs of parainfluenza
Mild URT dz
Severe LRT dz (2nd to RSV in young children: 25%)
Laryngotracheobronchitis (croup) 2% (subglottal swelling may close airway)
Cell-mediated immune response: cell damage and protective IgA with limited memory
167
Transmission of Parainfluenza
P2P transmission
- usually infants and young children <5yo
- older children and adults: mild infection, pneumonia in elderly
Treatment: nebulizers and supportive care
168
What is the most common cause of fatal acute respiratory tract infection in infants and young children
Respiratory syncytial virus (a paramyxovirus)
169
Clinical signs of RSV
- common cold to pneumonia
- direct invasion of respiratory epithelium —> immune-mediated cell injury
- necrosis of bronchioles-> plugs of mucus, fibrin, and necrotic material in airways
- no viremia or systemic spread
- infection does not prevent reinfection
170
Treatment of RSV
Supportive care
171
Clinical signs of metapneumovirus
- asymptomatic
- mild URT disease + otitis media —> ~ 15% of common colds
- severe bronchial it is and pneumonia (10% of cases)
172
Where do humans often get Hendra Virus from
Fruit Bats
173
Hendra is fatal for which species
Horses and humans
174
Nipah Virus is fatal for which species?
What is the original host
Humans and pigs
Fruit bat
175
Examples of picornavirus
Rhinovirus, enterovirus
176
At what temperature do picornaviruses replicate best at?
33 C
177
Examples of coronaviruses
Severe acute respiratory syndrome (SARS) and Middle East Respiratory Syndrome (MERS)
178
Cold vs. flu
Cold:
- rare headache
- normal temp
- Slight aches and pains
- sneezing
- runny nose
- sore throat
- mild to mod. Hacking cough
Flu
- prominent headache
- sudden onset of temp 102-104 (last 3-4 days)
- severe aches and pains
- extreme fatigue and weakness (lasts 2-3 weeks)
- severe cough
- chest discomfort
179
Where does influenza A replicate?
Nucleus
180
Why does influenza have high mutation rates?
Error-prone RdRP leads to high mutation rates
181
Influenza symptoms
- headache
- fever
- runny/stuffy nose
- sore throat
- aches
- tiredness (muscles)
- coughing
- joint aches
- vomiting
182
Polio is caused by:
A picornavirus
183
What do picornaviruses produce that blocks translation
Proteases that degrade cellular caps to block translation
184
Picornavirus tissue tropism
Broad range: ICAM1, CD55, PVR
185
Transmission of picornaviruses
Fecal-oral, respiratory
186
T/F enteroviruses usually cause enteric disease
False
187
types of picornaviruses
- enteroviruses (poliovirus, Coxsackie A, Coxackie B)
- echovirus (enteric Cytopathic human orphan virus)
- enterovirus 68-71
- heparnavirus —> Hepatitis A
188
Pathogenesis of enteroviruses
- viruses have different secondary target tissues and that determines the type of disease you see (they all enter through primary enteric tissue though, which is why they are ENTERIC viruses)
189
Polio epidemiology
- asymptomatic (90%) —> limited to oropharynx and gut
- abortive poliomyelitis (5%) —> minor illness, fever, headache malaise, sore throat, vomiting
- nonparalytic poliomyelitis or aseptic meningitis (1-2%) —> CNS and meninges; back pain, muscle spasms + other symptoms
190
Paralytic polio facts
- 0.1-2% of pop.
- 3-4 days after abortive subsides
- virus spreads from blood to anterior horn of cord and motor cortex
- spinal or bulbar
- asymmetrical flaccid paralysis with no sensory loss
- Polio type 1 responsible for 85% of cases
- bulbar: more severe (75% fatal)
191
What is postpolio syndrome
20-40% of infected, 30-40 yrs later
Deterioration of muscles
192
Epidemiology of polio
- human dz w/ fecal-oral and resp. Transmission
- asymptomatic shedding (up to 1 month)
- often in poor sanitation and crowded conditions
193
Why is paralytic polio considered a “middle class” dz
Infection in early childhood typically asymptomatic or mild, more severe in adults; so cleaner middle class didn’t get it until later
194
Dx and to of polio
Dx: CSF- lymphocytes, but no neutrophils; serology or RT-PCR
Tx: pleconaril- inhibits picornavirus penetration into cell
- vx: 3 strains, stable, inexpensive, effective
- antibody is a major protective immune response
—> IgA and IgG
—> cell-mediated immunity plays role in pathogenesis
195
T/F Acute Flaccid Myelitis (AFM) is polio
False
It is a polio-like illness, and the CDC and other orgs. Are very careful to differentiate it from polio
196
Norovirus is part of which virus family
It is also known as which two names?
Calicivirus
Norwalk Virus
“Winter vomiting bug”
197
When does clinical dz of norovirus appear
24-48 hrs incubation
Duration: 12-60 hrs
198
Clinical symptoms of norovirus
- acute onset diarrhea, nausea, vomiting, abdominal cramps
No blood
Fever occurs in ~30%
199
What does norovirus do to the intestine
Damage to intestinal brush border which prevents absorption of water and nutrients and watery diarrhea
Gastric emptying may be delayed, causing vomiting
Blunted villi, cytoplasmic vacuolation, mononuclear cell infiltrates
Shedding for 2 was after symptoms stop
200
Epidemiology of norovirus
- outbreaks from a common source
- water, shellfish, salad, food service
- schools, resorts, hospitals, nursing homes, restaurants, cruise ships
- fecal-oral transmission
- 50% of all food borne GI outbreaks caused by noroviruses
201
Dx and tx of norovirus
Dx: RT-PCR, ELISA, Serology
Tx: none; resistant to heat, pH3, detergent, chlorine
- immunity short-lived and not protective
202
Rotavirus facts
- reovirus family
- small RNA viruses
- naked, double shelled capsid
- tissue tropism: epithelial cells
- transmission: fecal-oral
203
Rotavirus epidemiology
- one of the most common causes of serious diarrhea in young children
- 95% of children infected by 3-5 yo
- infect many different mammals and birds
204
Dx and Tx of rotavirus
Dx: detection of virus in stool, EIA
Tx: supportive, electrolyte replacement
- vaccines available (RotaTeq and RotaRix)
205
Hepatitis overview
- infect and damage the liver
- classic symptoms: jaundice (70-80% of adults and 10% of children)
- release of liver enzymes, fever, fatigue, nausea, loss of appetite, abdominal pain, dark urine
206
People at risk for hepatitis
- people who share needles
| - health works who are exposed to infected blood
207
Possible symptoms of hepatitis
- pain in the upper right quadrant of abdomen
- nausea and vomiting
- loss of appetite
- jaundice
- fatigue
- itching
208
Hep A
- Common Name:
- Structure:
- transmission:
- Onset:
- incubation:
- severity:
- mortality:
- chronicity:
- Other dz:
- Lab dx:
- Common Name: infectious
- Structure: picornavirus, capsid + ssRNA
- transmission: fecal-oral
- Onset: abrupt
- incubation: 15-50
- severity: mild
- mortality: <0.5%
- chronicity: no
- Other dz: none
- Lab dx: IgM
209
Hep B
- Common Name:
- Structure:
- transmission:
- Onset:
- incubation:
- severity:
- mortality:
- chronicity:
- Other dz:
- Lab dx:
- Common Name: Serum
- Structure: Hepadnavirus Env. CircDNA
- transmission: parenteral; sexual
- Onset: insidious
- incubation: 45-160
- severity: sometimes severe
- mortality: 1-2%
- chronicity: Yes
- Other dz: carcinoma; cirrhosis
- Lab dx: HBsAg, HBeAG, HB, IgM
210
Hep C
- Common Name:
- Structure:
- transmission:
- Onset:
- incubation:
- severity:
- mortality:
- chronicity:
- Other dz:
- Lab dx:
- Common Name: NonA, NonB, post-transfusion
- Structure: Flavivirus env. +ssRNA
- transmission: parenteral, sexual
- Onset: insidious
- incubation: 14-180
- severity: subclinical; 70% chronic
- mortality: ~4%
- chronicity: yes
- Other dz: carcinoma, cirrhosis
- Lab dx: ELISA
211
Hep D
- Common Name:
- Structure:
- transmission:
- Onset:
- incubation:
- severity:
- mortality:
- chronicity:
- Other dz:
- Lab dx:
- Common Name: Delta Agent
- Structure: viroid env. CircRNA-
- transmission: Parenteral; sexual
- Onset: abrupt
- incubation: 15-64
- severity: Co-HBV; severe
- mortality: high
- chronicity: yes
- Other dz: Cirrhosis; fulminant
- Lab dx: ELISA
212
Hep E
- Common Name:
- Structure:
- transmission:
- Onset:
- incubation:
- severity:
- mortality:
- chronicity:
- Other dz:
- Lab dx:
- Common Name: Enteric NonA, NonB
- Structure: Calicivirus; capsid +ssRNA
- transmission: fecal-oral
- Onset: abrupt
- incubation: 15-50
- severity: mild; preg severe
- mortality: 1-2%; preg 20%
- chronicity: No
- Other dz: None
- Lab dx: -
213
T/F Hep A is not inactivated by chlorine, formalin, UV
False
It is
214
Where do Hep A and Hep E replicate?
When is the virus shed before symptoms show?
T/F it replicates quickly
- hepatocytes and Kupffer cells
- shed 10 days before symptoms
- false, replicates quickly
215
T/F Hep B is unusually resistant for enveloped viruses
True
216
T/F Hep B replicates through an intermediate
True
217
Acute Hep B infections
- may be asymptomatic
- fever, malaise, anorexia, followed by nausea, vomiting, abdominal pain, chills
- classic symptoms: jaundice, dark urine, pale stools
218
Chronic Hep B infections
- 5-10% of infected
- continued destruction of liver with cirrhosis, liver failure
- 9-35 yrs post-infection
- usually fatal
219
What is cirrhosis
Replacement of liver tissue by fibrotic scare tissue and nodules
220
Hep C is the predominant cause of what?
Non A NonB hepatitis
221
Hep C tropism
- hepatocytes and B cells —> tetraspanin receptors coats itself with low density lipoprotein to use LDL receptor for uptake
222
Hep C transmission
Blood and sex (maybe)
223
Where does Hep C assemble and bud?
At the ER
224
T/F you can get rid of Hep C
False
225
Clinical Disease of Hep C
- viremia —> 1-3 wks post exp.
- low inflammatory response
- chronic fatigue
226
What does Hep D need in order to replicate and cause dz in its host?
It needs the host to be actively infected with HBV
- its a coinfection: it needs to have HBV establish an infection before HDV can replicate
- superinfection: more rapid severe progression
227
Hep A and Hep E epidemiology
- 40% caused by hep A
- 90% of infected children and 25-50% of adults have in apparent infection
- virus shed 10-14 days before symptoms
- fecal-oral transmission
- common source outbreaks:
—> sewage contamination, shellfish (clams, oysters, mussels)
- pregnant women have high mortality with HEV (20%)
228
Hep B transmission
- sexual, parenteral, perinatal —> blood transfusion, needle sharing, acupuncture, ear piercing, tattooing, exchange of semen, saliva, vaginal secretions, needle sticks
229
Hep C transmission and epidemiology
Blood-blood and sexually —> IVDU, Tatto recipients, transfusion, organ recipients, hemophiliac
- >90% of HIV+ IVDUs are HCV+
- high Incidence of chronic asymptomatic infections (80-85%) —> 10-30% cirrhosis; 1-3% cirrhosis; 1-3% hepatocellular carcinoma
230
Hep C treatment
PegIFN and ribavirin, liver transplant (50% cure rate); newer drugs, HCV type specific, 8-12 wks
- no vx
231
Hep D epidemiology
Causes 40% of fulminant hepatitis
- acute liver failure
- hepatic necrosis, encephalopathy, coagulopathy within 8 weeks
- >70% mortality
occurs ONLY in HBV+ people -> 5% of HBV chronic carriers
232
HIV is a ?
Lentivirus
