Ch23 Flashcards
(184 cards)
1
Q
Which has a higher mutation rate: RNA or DNA?
A
RNA — about 100 times higher than DNA.
2
Q
Why do RNA viruses evolve rapidly and develop drug resistance easily?
A
Because they have high mutation rates and lack proofreading mechanisms.
3
Q
What is deamination?
A
It’s the spontaneous conversion of cytosine into uracil.
4
Q
Why is cytosine-to-uracil conversion a bigger problem in DNA?
A
Because uracil is not normally found in DNA, so it’s recognized as a mutation.
5
Q
Why is the cytosine-to-uracil change often missed in RNA?
A
Because uracil is a normal base in RNA, so the change goes unnoticed.
6
Q
What’s the key difference in replication between RNA and DNA?
A
DNA has proofreading during replication, but RNA does not.
7
Q
What are the key structural features of picornaviruses?
A
Small (30 nm), non-enveloped, icosahedral capsid, with 12 pentamers and proteins VP1–VP4.
8
Q
What is the role of VP4 protein in picornaviruses?
A
Stabilizes the capsid and is released during cell entry.
9
Q
What type of genome do picornaviruses have?
A
Positive-sense single-stranded RNA (+ssRNA) genome (~7.2–8.4 kb), with a VPg protein and poly-A tail.
10
Q
What is IRES and its function in picornaviruses?
A
Internal Ribosome Entry Site — allows translation to begin without a 5’ cap.
11
Q
Why do picornaviruses cause diverse diseases?
A
Due to differences in:
• Receptor targeting
• Tissue susceptibility
• Virulence
• Transmission methods
12
Q
What environmental conditions can picornaviruses tolerate?
A
They are resistant to heat, detergents, and sewage.
13
Q
How does picornavirus attach to host cells?
A
It binds to specific receptors (e.g., ICAM-1 for rhinovirus, CD155 for poliovirus).
14
Q
How does picornavirus enter the host cell?
A
VP1 forms a pore in the cell membrane, and the genome is injected into the cytoplasm.
15
Q
How does picornavirus initiate protein translation?
A
Using IRES (Internal Ribosome Entry Site) for cap-independent ribosome binding.
16
Q
What is the function of VPg in picornavirus?
A
It primes RNA synthesis and helps in RNA packaging.
17
Q
What does the viral polyprotein encode?
A
It includes:
• Structural proteins: VP1–VP4
• Non-structural proteins: Proteases and RNA-dependent RNA polymerase
18
Q
What is the role of viral proteases in picornaviruses?
A
They cleave the polyprotein into functional proteins.
19
Q
How is RNA replicated in picornaviruses?
A
The viral RNA-dependent RNA polymerase makes a –ssRNA template to generate new +ssRNA genomes.
20
Q
What happens during assembly of picornavirus particles?
A
A procapsid is formed, then VP0 is cleaved into VP2 + VP4 during maturation.
21
Q
How are picornaviruses released from the host cell?
A
Mostly through cell lysis, releasing up to 100,000 virions per cell (except for Poliovirus and HAV, which use non-lytic release).
22
Q
Why are enteroviruses suited for fecal-oral transmission?
A
Because they are stable in acidic environments, such as the stomach.
23
Q
What are the main types of enteroviruses?
A
• Polioviruses
• Coxsackieviruses A & B
• Echoviruses
• Numbered Enteroviruses (e.g., EV71)
24
Q
What is the typical entry point for enterovirus infection?
A
Through the oropharynx or intestine.
25
Where does initial replication of enteroviruses occur?
In lymphoid tissues such as:
• Tonsils
• Peyer’s patches (in the intestine)
26
What happens after initial replication of enteroviruses?
Viremia (virus in blood) spreads the virus to target organs.
27
What are common target organs (tissue tropism) of enteroviruses?
• Central nervous system (CNS)
• Heart
• Skin
• Muscle
• Liver
28
What innate immune receptors recognize picornaviruses?
TLRs and RIG-I-like receptors
29
What cytokines are induced after viral recognition?
IFN-α/β and pro-inflammatory cytokines
30
What is the role of NK cells during picornavirus infection?
They are activated and exert cytotoxicity to kill infected cells.
31
How do some picornavirus strains evade the immune system?
By blocking interferon (IFN) signaling pathways.
32
Why is humoral immunity critical in picornavirus defense?
Because neutralizing antibodies:
• Prevent viremia
• Block CNS invasion
• Provide long-term, type-specific protection
33
What roles do CD4+ and CD8+ T cells play?
• CD4+ T cells: Help in antibody production
• CD8+ T cells: May clear infected cells via cytotoxicity
34
What are the main specimens used to diagnose picornavirus infections?
Stool, CSF, oropharyngeal secretions (first 3–5 days), spinal cord/brain (at autopsy).
35
How is the virus directly demonstrated in stool?
By electron microscopy or immune electron microscopy.
36
Which cell lines are used for virus isolation?
Primary monkey kidney cells and HeLa cells.
37
What cytopathic effect (CPE) is observed during virus isolation?
Rounding of cells, usually seen within 36 hours.
38
How is picornavirus serotyped?
By neutralization of CPE using standard antisera pools, then specific antisera.
39
What serologic methods are used to detect antibody response?
• ELISA
• Immunofluorescent assay (IFA)
• Neutralization test
• Complement fixation test (CFT)
40
What is the significance of a “four-fold rise” in antibody titre?
It indicates recent infection or active immune response.
41
What molecular technique is used for detecting viral RNA?
RT-PCR
42
What is the primary mode of transmission for enteroviruses?
Fecal-oral route
43
What is a less common mode of transmission for enteroviruses?
Respiratory droplets
44
What is the only known reservoir for enteroviruses?
Humans only
45
What environmental factors increase the spread of enteroviruses?
Poor sanitation and crowding
46
Where are enteroviruses distributed globally?
They have a worldwide distribution
47
When is the peak incidence of enterovirus infections?
In summer and early fall
48
Which age group is most affected by enteroviruses?
Children under 15 years
49
Are asymptomatic infections with enteroviruses common?
Yes, they are very common
50
How many types of poliovirus are there?
Three types: Type 1, Type 2, Type 3
51
Which poliovirus type is responsible for most paralytic polio cases?
Type 1 — causes about 85% of paralytic polio
52
What is the risk associated with the Type 2 vaccine strain?
It may revert to virulence, causing vaccine-associated paralytic polio (VAPP)
53
Why is wild-type poliovirus now rare?
Because of successful vaccination programs
54
What type of tissue do polioviruses have a strong affinity for?
Nervous tissue
55
What is the most common course of poliovirus infection?
Asymptomatic infection, occurring in about 90% of cases
56
Where does the virus remain during asymptomatic poliovirus infection?
In the oropharynx and gut
57
Are there any symptoms in asymptomatic poliovirus infection?
No — there are no clinical signs or symptoms
58
What is Abortive Poliomyelitis?
A minor illness occurring in about 5% of poliovirus infections
59
What are the symptoms of Abortive Poliomyelitis?
Fever, headache, malaise, sore throat, vomiting
60
When do symptoms of Abortive Poliomyelitis typically appear?
3–4 days after exposure
61
What is Nonparalytic Poliomyelitis also known as?
Aseptic Meningitis
62
How common is Nonparalytic Poliomyelitis?
Occurs in 1–2% of poliovirus infections
63
Where does the virus spread in Nonparalytic Poliomyelitis?
To the central nervous system (CNS) and meninges
64
What are the main symptoms of Nonparalytic Poliomyelitis?
• Fever
• Headache
• Back pain
• Muscle spasms
65
Is there paralysis in Nonparalytic Poliomyelitis?
No, there is no paralysis
66
What is the most severe form of poliovirus infection?
Paralytic Poliomyelitis
67
How often does Paralytic Poliomyelitis occur?
In about 0.1–2.0% of infections
68
What is meant by “biphasic illness” in Paralytic Poliomyelitis?
1. Starts with minor illness
2. Followed by paralysis
69
What parts of the nervous system does poliovirus invade in Paralytic Poliomyelitis?
• Anterior horn cells of the spinal cord
• Motor cortex of the brain
70
What type of paralysis is seen in Paralytic Poliomyelitis?
Asymmetric flaccid paralysis without sensory loss
71
What parts of the body can paralysis from poliovirus affect?
A single limb or multiple extremities
72
How does poliovirus-related paralysis progress?
It develops gradually over several days
73
What are the possible outcomes of paralytic poliomyelitis?
• Full recovery
• Residual (permanent) paralysis
• Death (in severe cases)
74
How long can recovery from poliovirus paralysis take?
Between 6 months and 2 years
75
What is Bulbar Poliomyelitis?
A severe form of polio that affects:
• Pharynx
• Vocal cords
• Respiratory muscles
76
What is the mortality rate of Bulbar Poliomyelitis?
Up to 75%
77
What device was used in the 1950s to help patients with Bulbar Polio breathe?
The Iron Lung
78
When was Bulbar Poliomyelitis most commonly seen?
Before widespread vaccination
79
What is Post-Polio Syndrome (PPS)?
A late complication that occurs in some individuals who had poliomyelitis.
80
How common is Post-Polio Syndrome?
Affects about 29% of former polio patients.
81
When does Post-Polio Syndrome usually occur?
30–40 years after the initial poliovirus infection.
82
What are the main symptoms of Post-Polio Syndrome?
• Progressive muscle weakness
• Fatigue
• Muscle pain
83
Is active poliovirus present in Post-Polio Syndrome?
No, there is no active virus.
84
What causes Post-Polio Syndrome symptoms?
Due to loss of neurons in muscles that were previously affected by polio.
85
Into how many groups are Coxsackieviruses divided?
Two groups: Group A and Group B
86
What are the effects of Group A Coxsackieviruses?
• Diffuse myositis
• Acute inflammation
• Necrosis of voluntary muscle fibers
87
What are the effects of Group B Coxsackieviruses?
• Focal degeneration in the brain
• Necrosis in skeletal muscles
• Inflammation in:
• Dorsal fat pads
• Pancreas
• Occasionally the myocardium (heart muscle)
88
What type of lesions are associated with Coxsackievirus A infections?
Vesicular lesions
89
What are the two major illnesses caused by Coxsackievirus A?
• Herpangina
• Hand-Foot-and-Mouth Disease
90
What are the symptoms of Herpangina?
• Fever, sore throat, vomiting, anorexia
• Pain on swallowing
• Vesicular ulcerated lesions on soft palate and uvula
91
What causes Herpangina?
Mainly Coxsackievirus A
92
What is the treatment for Herpangina?
It is self-limiting; only supportive care is needed.
93
What causes Hand-Foot-and-Mouth Disease?
Mainly Coxsackievirus A16
94
What are the symptoms of Hand-Foot-and-Mouth Disease?
• Mild fever
• Vesicular lesions on hands, feet, mouth, and tongue
95
How long does Hand-Foot-and-Mouth Disease last?
Usually resolves in a few days
96
What are the three major syndromes caused by Coxsackievirus B?
• Pleurodynia (Bornholm Disease)
• Myocarditis & Pericarditis
• Aseptic Meningitis
97
What are the symptoms of Pleurodynia (Bornholm Disease)?
• Sudden fever
• Pleuritic chest pain, unilateral thoracic pain
• Abdominal pain, vomiting
• May relapse
• Self-limiting (usually ~4 days)
98
Who is most severely affected by Coxsackievirus B myocarditis?
Neonates — may have fatal febrile illness with:
• Heart failure
• Cyanosis
• Hepatomegaly
• Multiorgan involvement
99
How does myocarditis present in adults with Coxsackie B infection?
As acute benign pericarditis that may mimic myocardial infarction (MI)
100
What are the symptoms of Coxsackie B-related aseptic meningitis?
• Fever
• Headache
• Neck stiffness
• Sometimes petechial or vesicular rash
101
Which virus is a common cause of summer aseptic meningitis outbreaks?
Echovirus 11
102
When is aseptic meningitis more severe?
In infants <1 year or if associated with encephalitis
103
Which enteroviruses can cause common cold-like symptoms?
• Coxsackie A21, A24
• Echoviruses 11, 20
104
What type of rash may be seen with some enterovirus infections?
Maculopapular or petechial rash
105
What serious condition must be ruled out when a petechial rash is present?
Meningococcemia (life-threatening bacterial infection)
106
What causes Acute Hemorrhagic Conjunctivitis?
• Enterovirus 70
• Coxsackievirus A24 variant
107
What are the features of Acute Hemorrhagic Conjunctivitis?
• Highly contagious eye infection
• Rapid onset (within 24 hours)
• Recovery in 1–2 weeks
108
Which viruses can cause severe neonatal disease?
• Parechoviruses (HPeV1, HPeV2) → sepsis-like illness
• Echoviruses, Coxsackie B → disseminated infection
109
Can these viruses be transmitted across the placenta?
Yes — transplacental transmission is possible
110
What is the risk level of severe neonatal enterovirus infection?
High risk of mortality
111
What are Rhinoviruses known for causing?
They are the most common cause of the common cold.
112
What is the main habitat of Rhinoviruses in the human body?
The nose and throat (not the intestine)
113
Why can’t Rhinoviruses infect the gastrointestinal tract (GIT)?
Because they are acid-labile (destroyed by stomach acid)
114
At what temperature do Rhinoviruses grow best?
33°C, which matches the temperature of the nasal cavity
115
How many antigenic types of Rhinoviruses are there?
113 types
116
What is the primary transmission route of Hepatitis A Virus (HAV)?
Fecal-oral route
117
What are common sources of HAV infection?
• Contaminated water
• Shellfish
• Food
118
What type of genome does HAV have?
Single-stranded, positive-sense RNA (~7470 nucleotides)
119
How stable is HAV in the environment?
It is extremely stable
120
How many serotypes and genotypes does HAV have?
One serotype, but multiple genotypes
121
What receptor does HAV bind to on hepatocytes and T cells?
HAVCR-1 / TIM-1 receptor
122
How is HAV released from infected cells?
Through exocytosis (not cytolytic)
123
Are clinical isolates of HAV easy to culture?
No, they are difficult to culture
124
In which cells do adapted HAV strains grow?
In monkey kidney cells
125
How does HAV enter the bloodstream?
Through the oropharynx or intestine
126
What cells in the liver are targeted by HAV?
Hepatocytes and Kupffer cells
127
How and when is HAV excreted from the body?
Shed in bile, and excreted in feces ~10 days before symptoms
128
Does HAV cause liver damage directly?
No, liver damage is immune-mediated via:
• CD8+ T cells
• NK cells
129
Does HAV cause chronic infection or cancer?
No, HAV infection is self-limiting
130
What percentage of acute hepatitis cases are caused by HAV?
About 40%
131
Are asymptomatic HAV infections common?
Yes, especially in children
132
What is the primary mode of HAV transmission?
Fecal-oral route: via food, water, or contaminated hands
133
What environmental conditions is HAV resistant to?
Acid, heat, and detergents
134
What are major sources of HAV outbreaks?
• Day-care centers
• Unsanitary conditions
135
What is the incubation period of HAV?
15–50 days
136
What are the early symptoms of HAV infection?
• Fever
• Fatigue
• Nausea, vomiting
• Anorexia
• Abdominal pain
137
What are the signs of the icteric phase in HAV?
• Jaundice
• Dark urine
• Pale stool
138
How does HAV infection differ in children under 6 years?
Usually asymptomatic
139
How does HAV infection present in adults?
More symptomatic — 70–80% develop jaundice
140
How long does HAV illness typically last?
2–8 weeks; recovery is usually complete
141
When is HAV shed in the stool?
Before symptoms appear
142
Which antibody appears during the symptomatic phase of HAV?
IgM
143
Q: Which antibody provides lifelong immunity to HAV?
IgG
144
What serologic test is used to diagnose acute HAV infection?
ELISA to detect anti-HAV IgM
145
What molecular test detects HAV RNA in blood or stool?
RT-PCR or real-time PCR
146
Is liver biopsy commonly used in HAV diagnosis?
No, it is rarely performed
147
Is viral culture practical for HAV diagnosis?
No, it is not practical
148
Is there a specific antiviral treatment for HAV?
No, only supportive therapy
149
What are key preventive measures against HAV?
• Good hygiene
• Safe food/water practices
• Chlorination of water
150
What post-exposure prophylaxis is used within 2 weeks?
What post-exposure prophylaxis is used within 2 weeks?
151
What is the standard HAV vaccine regimen?
Killed vaccine, 2 doses given 6 months apart
152
What is the genome type of Orthomyxoviruses?
Segmented, enveloped, negative-sense RNA viruses
153
What are the key types of influenza viruses?
• Influenza A
• Influenza B
• Influenza C
• Influenza D
154
What are characteristics of Influenza A?
• Zoonotic (infects birds, pigs, humans)
• Causes pandemics via antigenic shift
• Causes seasonal epidemics via antigenic drift
155
What are characteristics of Influenza B?
• Infects humans only
• Causes seasonal epidemics
156
What is Influenza C known for?
Causes mild illness
157
What is Influenza D associated with?
Infects cattle, not humans
158
What are Thogotoviruses?
Tick-borne viruses
159
What is Isavirus and who does it infect?
A virus that infects fish, not humans
160
What is the morphology of influenza viruses?
Pleomorphic — can be spherical or tubular
161
How many RNA segments are in influenza viruses?
How many RNA segments are in influenza viruses?
A:
• 8 RNA segments for Influenza A & B
• 7 segments for Influenza C
162
What is the role of HA (Hemagglutinin) protein?
• Binds to sialic acid on host cells
• Mediates viral entry
• Has 18 subtypes
163
What is the function of NA (Neuraminidase) protein?
• Cleaves sialic acid
• Facilitates viral release from infected cells
• Has 11 subtypes
164
What is the M2 Proton Channel and what drugs target it?
• Regulates pH inside the virus (important for uncoating)
• Targeted by amantadine and rimantadine
• Present in Influenza A only
165
What is the role of Matrix protein (M1)?
Provides structural stability to the virus
166
What is HEF and where is it found?
• Hemagglutinin-esterase-fusion protein
• Found in Influenza C and D
• Combines functions of HA and NA
167
What is the main site of influenza virus infection?
Respiratory epithelium, especially ciliated cells (which are destroyed)
168
How does influenza virus evade the immune system?
Via the NS1 protein, which inhibits interferon response
169
What are common complications of influenza virus infection?
• Secondary bacterial pneumonia (e.g., S. aureus, S. pneumoniae)
• Systemic symptoms like fever and myalgia (due to cytokines)
170
What provides protection against influenza virus?
• Neutralizing antibodies against HA and NA
• T cells targeting NP (nucleoprotein) and M1 (matrix protein)
171
What happens during the attachment stage of influenza virus replication?
HA binds to sialic acid receptors on host cells
172
What happens during the entry stage of influenza replication?
What happens during the entry stage of influenza replication?
A:
• Virus enters by endocytosis
• Fusion occurs via HA at low pH
173
Where does influenza virus replication and transcription occur?
In the nucleus of the host cell
174
What happens during the assembly stage of influenza replication?
Viral proteins are transported to the cell surface
175
How is the influenza virus released from the host cell?
• NA cleaves sialic acid receptors
• Virus buds from the apical membrane
176
How is influenza virus transmitted?
Through aerosols and fomites (contaminated surfaces)
177
Who are considered high-risk groups for severe influenza?
• Elderly
• Children
• Immunocompromised individuals
• Pregnant women
178
What is antigenic drift in influenza?
Minor mutations in HA/NA, causing annual epidemics
179
What is antigenic shift in influenza?
Reassortment of RNA segments from different strains, causing pandemics
180
What are the classic symptoms of influenza?
• Fever
• Cough
• Myalgia (muscle pain)
• Malaise (general discomfort/fatigue)
181
What are possible complications in severe influenza cases?
• Pneumonia
• ARDS (Acute Respiratory Distress Syndrome)
• Reye syndrome (especially in children taking aspirin)
182
What are common pediatric complications of influenza?
• Croup
• Otitis media (middle ear infection)
• Bronchiolitis
183
What is a common rapid diagnostic method for influenza?
Antigen detection using nasal swabs
184
What lab technique is used with culture to detect influenza virus?
Hemadsorption — binding of red blood cells to infected cells
