Ch 26 Flashcards
(194 cards)
1
Q
What type of genome does Reoviridae have?
A
Double-stranded RNA (dsRNA), segmented (10–12 segments)
2
Q
Is Reoviridae enveloped or nonenveloped?
A
Nonenveloped
3
Q
What is the symmetry and size of Reoviridae virions?
A
Icosahedral symmetry, 60–80 nm in diameter
4
Q
Where does replication of Reoviridae occur in the host cell?
A
In the cytoplasm
5
Q
How stable is Reoviridae in the environment?
A
Stable in detergents and across wide pH and temperature ranges
6
Q
Name the main genera included in the Reoviridae family.
A
Orthoreoviruses, Rotaviruses, Orbiviruses, Coltiviruses
7
Q
Which Reoviridae genera are classified as arboviruses?
A
Orbiviruses and Coltiviruses
8
Q
Are Reoviruses generally symptomatic or asymptomatic in humans?
A
Generally asymptomatic
9
Q
What is the capsid structure of Rotavirus?
A
It has a triple-layered icosahedral capsid.
10
Q
How many genome segments does Rotavirus have?
A
11 segments (compared to 10 in Reovirus).
11
Q
What are the structural proteins of Rotavirus?
A
VP1 to VP7 and non-structural proteins (NSPs).
12
Q
What is the role of VP4 in Rotavirus?
A
Attachment to host cells and membrane fusion; it is cleaved into VP5 and VP8.
13
Q
Which proteins act as spike proteins in Reovirus and Rotavirus?
A
σ1 in Reovirus and VP4 in Rotavirus.
14
Q
What are the three structural layers of the Rotavirus capsid?
A
• VP2: inner core
• VP6: intermediate layer
• VP4 and VP7: outer layer
15
Q
What does Rotavirus look like under electron microscopy?
A
It has a “wheel-like” appearance.
16
Q
What enzymes are present in Rotavirus?
A
Enzymes for RNA synthesis.
17
Q
What is the major clinical significance of Rotavirus?
A
It is a leading cause of infantile gastroenteritis.
18
Q
What percentage of childhood diarrhea hospitalizations did Rotavirus cause before vaccines?
A
Around 50%.
19
Q
Where is Rotavirus-associated mortality highest?
A
In underdeveloped countries.
20
Q
What has been the impact of vaccines on Rotavirus?
A
Vaccines significantly reduced the global disease burden.
21
Q
What activates Rotavirus after ingestion?
A
Proteolytic activation by trypsin in the gut.
22
Q
What is the ISVP and when is it formed?
A
ISVP (Intermediate Subviral Particle) is formed after trypsin activation to prepare the virus for cell entry.
23
Q
Which viral protein is responsible for attachment to host cell receptors?
A
VP4 in Rotavirus (or σ1 in Reovirus).
24
Q
How does Rotavirus enter the host cell?
A
Through direct penetration or endocytosis.
25
Where is the viral core released after entry?
Into the cytoplasm of the host cell
26
What happens in the cytoplasm during replication?
Core enzymes transcribe (+) mRNAs from the dsRNA genome.
27
Where do viral proteins and RNA assemble?
In viroplasms, specialized compartments in the cytoplasm.
28
How are new virions released from the cell?
By cell lysis.
29
What is reassortment in Rotavirus?
Exchange of genome segments between different strains, due to the segmented genome.
30
Why is reassortment important?
It contributes to vaccine development and strain variability, similar to influenza.
31
Which cells does Rotavirus infect?
Columnar epithelial cells in the small intestine.
32
What is the function of NSP4 protein?
It acts as an enterotoxin, causing Ca²⁺ influx and cytoskeletal disruption, leading to watery diarrhea and ion imbalance.
33
Which type of antibody is crucial for mucosal protection against Rotavirus?
Local IgA.
34
Which viral proteins trigger neutralizing antibodies?
VP4 and VP7.
35
What is the effect of maternal antibodies on Rotavirus infection?
They reduce disease severity but do not prevent reinfection.
36
By what age are most children infected with Rotavirus?
95% of children are infected by age 3–5.
37
How is Rotavirus transmitted?
Via the fecal-oral route.
38
Where can Rotavirus survive outside the host?
On fomites, hands, and in the environment.
39
Where do Rotavirus outbreaks commonly occur?
In daycares, hospitals, and developing countries.
40
What are the main symptoms of Rotavirus infection?
Vomiting, watery diarrhea, fever, and dehydration.
41
Are blood or leukocytes present in stool during Rotavirus infection?
No, stool is typically free of blood and leukocytes.
42
What is the typical course of Rotavirus illness?
It is self-limited, and complete recovery is expected.
43
What tests are commonly used to detect Rotavirus antigens?
ELISA and latex agglutination.
44
What microscopy techniques are used to visualize Rotavirus?
Electron microscopy and immunoelectron microscopy.
45
What molecular method is used for genotyping Rotavirus?
RT-PCR (Reverse Transcriptase Polymerase Chain Reaction).
46
Is cell culture commonly used for Rotavirus diagnosis?
No, it is not commonly used in clinical settings.
47
Is there a specific antiviral treatment for Rotavirus?
No, there is no antiviral treatment available.
48
What is the main treatment for Rotavirus infection?
Oral rehydration therapy to prevent or correct dehydration.
49
What preventive measure is recommended in hospitals?
Isolation of infected patients to prevent spread.
50
51
What virus family do Norovirus and Sapovirus belong to?
Caliciviridae
52
Are Norovirus and Sapovirus enveloped or non-enveloped?
Non-enveloped
53
What type of genome do they have?
Single-stranded positive-sense RNA (ss [+] RNA)
54
How many capsid proteins do these viruses contain?
One single capsid protein
55
Are Norovirus and Sapovirus resistant to environmental conditions?
Yes, they are resistant to detergents, drying, and acid.
56
How are Norovirus and Sapovirus transmitted?
Via the fecal-oral route, through contaminated water or food.
57
What disease do these viruses commonly cause?
Outbreaks of gastroenteritis
58
How long does the illness typically last?
It resolves in about 48 hours and usually has no serious consequences.
59
How many human serotypes of Astrovirus exist?
HuAstV 1–8
60
What type of genome does Astrovirus have?
Single-stranded RNA (ssRNA), non-enveloped
61
How does Astrovirus appear under electron microscopy (EM)?
Shows a 5- or 6-pointed star within a smooth edge
62
Which age groups are most commonly affected by Astrovirus?
Mainly infants and children <7 years, also elderly and immunocompromised
63
What is the incubation period of Astrovirus?
1–4 days
64
What are the gastrointestinal symptoms of Astrovirus?
Nausea, vomiting, abdominal cramping, and watery diarrhea
65
What constitutional (general) symptoms can occur?
Fever, malaise, and headache
66
How is Astrovirus transmitted?
Person-to-person via the fecal-oral route
67
What causes Astrovirus outbreaks?
Fecal contamination of seafood or water
68
Are coronaviruses enveloped or non-enveloped viruses?
They are enveloped viruses.
69
What type of genome do coronaviruses have?
They have the longest positive-sense single-stranded RNA genome (27–30 kb).
70
What gives coronaviruses their crown-like appearance under electron microscopy?
Club-shaped glycoprotein projections (E1 and E2).
71
Why are coronaviruses called “corona” viruses?
Because of their crown-like appearance under the electron microscope.
72
What is the second most common viral cause of the common cold?
Coronaviruses (after rhinoviruses).
73
Which major diseases are caused by coronaviruses?
SARS, MERS, and COVID-19.
74
Are coronaviruses resistant to detergents?
Yes, unusually resistant for enveloped viruses.
75
Where does coronavirus replication occur in the host cell?
In the cytoplasm.
76
How is the coronavirus genome initially translated?
Into a polyprotein that is cleaved into functional proteins.
77
What enzyme is responsible for RNA synthesis in coronaviruses?
RNA-dependent RNA polymerase (L protein).
78
What does the RNA-dependent RNA polymerase synthesize?
• A (-) sense RNA template
• New genomic RNAs
• Subgenomic mRNAs (5–7)
79
What is the function of the E2 protein?
Attachment and membrane fusion; it is also the target of neutralizing antibodies.
80
What is the role of the E1 protein in coronaviruses?
It is a transmembrane matrix protein.
81
What does the N protein do in coronaviruses?
It forms the nucleocapsid.
82
What additional protein may be present in some coronavirus strains and what is its function ?
E3 protein (hemagglutinin-neuraminidase), involved in binding and cleavage of sialic acids.
83
Where are common human coronaviruses typically restricted in the body?
To the upper respiratory tract (optimal replication at 33–35°C).
84
What makes SARS-CoV and MERS-CoV different from common human coronaviruses in terms of replication temperature?
They replicate at 37°C and cause systemic disease.
85
What type of infection do coronaviruses typically cause at the cellular level?
Cytolytic infections that disrupt the ciliated epithelium.
86
What are the main routes of coronavirus transmission?
Aerosols, direct contact, fecal-oral route, and contaminated water.
87
During which seasons are coronavirus outbreaks most common?
Winter and spring.
88
What type of symptoms do common human coronaviruses usually cause?
Common cold-like symptoms with mild upper respiratory tract (URT) infection.
89
Which coronavirus strains are associated with severe disease?
SARS-CoV and MERS-CoV.
90
What are common symptoms of severe coronavirus infections (e.g., SARS, MERS)?
High fever, chills, cough, and acute respiratory distress syndrome (ARDS).
91
Besides respiratory symptoms, what other symptom may occur in SARS or MERS cases?
Diarrhea in some cases.
92
What is the approximate mortality rate for SARS?
Around 10%.
93
What is the approximate mortality rate for MERS?
Around 50%.
94
What diagnostic method is used for SARS and MERS?
RT-PCR on respiratory or stool samples.
95
Is there a vaccine for SARS-CoV-2?
Yes, vaccines have been developed for SARS-CoV-2.
96
Are there specific antiviral treatments for coronaviruses?
No, only supportive care is available.
97
Name two important genera in the Rhabdoviridae family.
Lyssavirus (e.g., Rabies virus) and Vesiculovirus (e.g., Vesicular stomatitis virus).
98
What is the shape and size of Rhabdovirus virions?
Bullet-shaped, enveloped
99
What do the glycoprotein (G) spikes on Rhabdoviruses do?
They help with attachment and entry into host cells and are targets for neutralizing antibodies.
100
What does the nucleocapsid of Rhabdoviruses contain?
Helical negative-sense RNA + proteins N, L, and NS (RNA polymerase).
101
Why is rabies considered medically significant?
Because it is fatal if post-exposure prophylaxis is not given in time.
102
What viral protein mediates attachment in Rhabdoviruses, and to which receptors does it bind in rabies?
The G-protein; it binds to AChR and NCAM receptors.
103
What enzyme is responsible for transcription and replication of the viral genome?
RNA-dependent RNA polymerase.
104
How does the Rhabdovirus enter the host cell?
Through endocytosis followed by fusion in the endosome.
105
Where is the nucleocapsid of Rhabdoviruses assembled?
In the cytoplasm of the host cell.
106
What does the RNA polymerase produce during replication?
mRNAs and new genomic RNA.
107
What role does the M protein play in virus assembly?
It helps condense and shape the virus structure.
108
In rabies, from which part of the body are virions typically released?
From the salivary glands.
109
How is rabies virus typically transmitted to humans?
Through the bite of a rabid animal; virus in saliva enters through the wound.
110
After entry, how does the rabies virus spread inside the body?
By retrograde axonal transport along peripheral nerves to the CNS.
111
Which areas of the brain are commonly affected by rabies?
The hippocampus and brainstem.
112
After reaching the brain, where does the virus spread next?
To the salivary glands, skin, and other tissues.
113
How does rabies virus evade the immune system?
It causes minimal inflammation and hides inside neurons.
114
What are Negri bodies and where are they found?
They are viral aggregates found in neurons, characteristic of rabies infection.
115
What are the symptoms during the prodromal phase of rabies?
Fever, malaise, and itching at the bite site.
116
Name some symptoms of the neurologic phase of rabies.
Hydrophobia (20–50% of cases), seizures, paralysis, aggression, and hallucinations.
117
What is the typical outcome of rabies without treatment?
Coma followed by death, usually due to respiratory failure.
118
What test is used to detect rabies antigens in samples like saliva or skin?
Direct fluorescent antibody (DFA) test.
119
Which molecular method is used to detect the rabies genome?
RT-PCR.
120
What serologic test is used to detect late-stage rabies antibodies?
ELISA on cerebrospinal fluid (CSF) or serum.
121
What are public health strategies for preventing rabies?
Dog vaccination and controlling stray animals.
122
How is rabies prevented in wild animals?
By distributing oral vaccines, such as vaccinia-rabies G-protein recombinant.
123
What are prions?
Proteinaceous infectious particles that cause neurodegenerative diseases without having a genome.
124
What makes prions unique compared to viruses and bacteria?
They have no genome, elicit no immune response, and are extremely resistant to inactivation.
125
What is the incubation period for prion diseases?
It can be very long—up to 30 years.
126
Name three types of human prion diseases based on origin.
Sporadic, Genetic, and Acquired.
127
Give examples of sporadic prion diseases.
Sporadic Creutzfeldt–Jakob disease (CJD), Fatal familial insomnia (FFI)
128
What are some genetic prion diseases?
Genetic CJD, Gerstmann–Sträussler–Scheinker syndrome (GSS), and Fatal familial insomnia (FFI).
129
List acquired prion diseases.
Kuru, Variant CJD (vCJD), and iatrogenic CJD.
130
Name animal prion diseases.
Scrapie (sheep), Bovine Spongiform Encephalopathy (BSE), Chronic Wasting Disease (deer/elk), and Transmissible Mink Encephalopathy.
131
What disease is also called “mad cow disease”?
Bovine Spongiform Encephalopathy (BSE).
132
How are prion diseases generally classified?
By mode of transmission: Sporadic, Genetic, Acquired, and Animal-related.
133
What is the infectious form of the prion protein called?
PrPSc (scrapie prion protein).
134
What is the normal form of the prion protein?
PrPC (cellular prion protein).
135
How does PrPC differ in protease sensitivity from PrPSc?
PrPC is sensitive, while PrPSc is resistant.
136
What is the structural difference between PrPC and PrPSc?
PrPC is α-helical, while PrPSc is β-sheet.
137
Which form of the prion protein is soluble?
PrPC is soluble; PrPSc aggregates.
138
Where is PrPC normally located in the cell?
It is GPI-anchored to the membrane.
139
Where does PrPSc accumulate in the body?
It accumulates in the central nervous system (CNS).
140
What is the basic mechanism of prion disease pathogenesis?
Template-mediated protein refolding.
141
How does PrPSc propagate in the brain?
It binds to PrPC and converts it into more PrPSc.
142
What kind of cycle is formed by prion propagation?
A self-perpetuating cycle.
143
What does prion accumulation lead to in the brain?
Amyloid fibril formation and neurodegeneration.
144
In what ways can different PrPSc strains vary?
In structure, incubation time, and clinical features.
145
Which major neurodegenerative diseases may involve prion-like protein misfolding?
Alzheimer’s disease, Huntington’s disease, and Parkinson’s disease.
146
What is the proposed mechanism linking prion-like proteins to other diseases?
Misfolding and accumulation of proteins similar to prions.
147
What are the possible routes of prion entry into the body?
Ingestion, cuts in the skin, and neurosurgical contamination.
148
After entry, where do prions initially accumulate?
In lymphoid tissues.
149
How do prions spread to the central nervous system (CNS)?
They travel via nerves to the CNS.
150
What are the hallmark neuropathological changes in prion diseases?
Spongiform changes with vacuolated neurons.
151
Do prion diseases involve inflammation in the brain?
No, there is no inflammation.
152
What type of glial cell is hypertrophied in prion diseases?
Astrocytes (Astrocyte hypertrophy).
153
What accumulates in the brain tissue in prion diseases?
Amyloid plaques, fibrils, and high concentrations of PrPSc.
154
What are common symptoms of prion diseases?
Dementia, Myoclonus, Ataxia, Tremors, and death within a year.
155
Which prion diseases are inherited?
Fatal Familial Insomnia (FFI) and Gerstmann–Sträussler–Scheinker (GSS).
156
What is Kuru, and what is its cause?
A prion disease linked to cannibalism in the Fore tribe of New Guinea.
157
What is the definitive method for diagnosing prion diseases?
Brain biopsy or autopsy.
158
Is there a direct detection method for prion diseases?
No, there is no direct detection.
159
What type of genetic material do retroviruses have?
Positive-strand RNA.
160
What is the size and structure of retroviral virions?
80–120 nm, enveloped with glycoprotein spikes (e.g., HIV gp120/gp41).
161
How do retroviruses replicate?
Via reverse transcriptase, which creates a DNA intermediate.
162
What are the main components of the retroviral genome?
Two RNA copies with:
• gag (structural proteins)
• pol (enzymes like RT)
• env (envelope proteins)
163
What do LTRs (Long Terminal Repeats) do in retroviruses?
Regulate transcription of viral genes.
164
What are the three subfamilies of retroviruses?
• Oncovirinae (e.g., HTLV-1/2): cause leukemia/lymphoma
• Lentivirinae (e.g., HIV-1/2): cause chronic infections like AIDS
• Spumavirinae: not pathogenic in humans
165
How are retroviruses classified morphologically?
By core structure: Types A, B, C, and D.
166
What is the first step in retroviral infection?
Entry – The virus binds to CD4 and a co-receptor (CCR5 or CXCR4 for HIV).
167
What happens during reverse transcription?
Viral RNA is converted to DNA by reverse transcriptase, which is error-prone.
168
What enzyme integrates viral DNA into the host genome?
Integrase.
169
What happens after integration in the host cell?
Transcription and translation produce viral mRNA and polyproteins
170
How are the polyproteins processed?
They are cleaved by protease into functional viral proteins.
171
What happens during assembly and budding?
New immature virions are assembled and released, then mature outside the cell.
172
What cells does HIV primarily target?
CD4+ T cells and macrophages.
173
Which co-receptors are used by HIV for cell entry?
CCR5 (early infection) and CXCR4 (late infection).
174
What are the stages of HIV clinical progression?
Acute infection → Asymptomatic phase → AIDS (when CD4 < 200/μL).
175
What are the modes of HIV transmission?
Sexual contact, blood exposure, and vertical (mother to child).
176
What are common opportunistic infections in AIDS patients?
Pneumocystis pneumonia, candidiasis, and CMV retinitis.
177
What fungal infection commonly affects the mouth or vagina in AIDS
Candidiasis.
178
What viral eye infection can lead to blindness in AIDS?
CMV retinitis.
179
What are common malignancies seen in AIDS?
Kaposi sarcoma (caused by HHV-8) and lymphomas.
180
What is Kaposi sarcoma and what causes it?
A cancer causing purple skin lesions, linked to HHV-8.
181
What neurologic conditions are associated with AIDS?
AIDS dementia and peripheral neuropathy.
182
What is AIDS dementia?
Cognitive decline caused by HIV’s effect on the brain.
183
What is wasting syndrome in AIDS?
Severe weight loss and chronic diarrhea, common in late-stage HIV.
184
What test is used to measure viral load in HIV patients?
PCR to quantify HIV RNA in the blood.
185
What immunologic test helps determine AIDS progression?
CD4+ T cell count – if <200/μL, it indicates AIDS.
186
What does PrEP stand for?
Pre-Exposure Prophylaxis – taken before potential HIV exposure.
187
What does PEP stand for?
Post-Exposure Prophylaxis – taken after potential HIV exposure.
188
What type of cells does HTLV-1 infect?
CD4+ T cells.
189
What viral protein in HTLV-1 activates oncogenes?
Tax protein.
190
What type of cancer is associated with HTLV-1?
Adult T-cell Leukemia/Lymphoma (ATLL).
191
What neurological condition is linked to HTLV-1?
HTLV-associated myelopathy (HAM).
192
What is the role of the HERV-derived protein Syncytin?
It facilitates placental function during pregnancy.
193
HERVs have been linked to which diseases?
Cancers and autoimmune diseases (e.g., Multiple Sclerosis).
194
What proteins regulate and suppress HERV replication?
APOBEC proteins.
