Lecture 16: Paramyxovirus, Orthomyxovirus, (Rhabo,Filo,Borna) Chap 48, 49, 50s Flashcards

1
Q

What type of genome do Paramyxoviruses have?

A

Single-stranded, negative-sense RNA

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2
Q

Describe the structure of Paramyxoviruses.

A

Helical nucleocapsid with an envelope; includes F, HN, H, or G proteins depending on the virus

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3
Q

Which protein is responsible for syncytia formation in Paramyxoviruses?

A

Fusion (F) protein

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4
Q

How do Paramyxoviruses typically evade immune detection?

A

Forming syncytia for cell-to-cell spread, avoiding antibody detection

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5
Q

What diseases are caused by Paramyxoviruses?

A

Measles, mumps, respiratory syncytial virus (RSV) infections, and parainfluenza

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6
Q

What is the primary transmission route for Measles?

A

Respiratory droplets

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7
Q

Describe the life cycle of Paramyxoviruses.

A

1) Attachment via surface proteins, 2) Fusion at plasma membrane, 3) Replication in cytoplasm, 4) Budding from host cell

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8
Q

What are the hallmark symptoms of Measles?

A

High fever, cough, conjunctivitis, coryza, and maculopapular rash

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9
Q

Which receptors does Measles virus bind to on host cells?

A

CD46, nectin-4, and CD150 (SLAM)

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10
Q

How is RSV different from other Paramyxoviruses in disease mechanism?

A

RSV causes localized respiratory infections without systemic spread

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11
Q

What immune response primarily controls Paramyxovirus infections?

A

Cell-mediated immunity

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12
Q

What type of genome do Orthomyxoviruses have?

A

Segmented, negative-sense RNA

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13
Q

Describe the structure of Orthomyxoviruses.

A

Enveloped with 8 RNA segments and surface proteins hemagglutinin (HA) and neuraminidase (NA)

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14
Q

Where does Orthomyxovirus replication take place, and why is it unique?

A

In the nucleus, which is rare for RNA viruses

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15
Q

Explain antigenic drift and shift in Orthomyxoviruses.

A

Drift: minor mutations; Shift: major genome reassortment, both enhancing immune evasion

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16
Q

What is the main disease caused by Orthomyxoviruses?

A

Influenza (flu)

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17
Q

Describe the symptoms and complications of Influenza.

A

Fever, cough, body aches; complications include pneumonia and secondary bacterial infections

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18
Q

Which protein facilitates Influenza virus entry into host cells?

A

Hemagglutinin (HA) binds to sialic acid receptors

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19
Q

How does neuraminidase (NA) aid in Influenza virus spread?

A

Cleaves sialic acid to release new virions from infected cells

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20
Q

What seasonal pattern does Influenza follow, and why?

A

Winter seasonality due to cooler, less humid conditions that stabilize the virus

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21
Q

What diagnostic tests are used for Influenza?

A

PCR, antigen tests, and viral culture from respiratory samples

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22
Q

How is Influenza typically treated?

A

Antivirals (e.g., oseltamivir), supportive care, and annual vaccination

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23
Q

What type of genome do Rhabdoviruses have?

A

Single-stranded, negative-sense RNA

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24
Q

Describe the shape and structure of Rhabdoviruses.

A

Bullet-shaped with an envelope; helical nucleocapsid

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25
What disease is most commonly associated with Rhabdoviruses?
Rabies
26
Describe the Rabies virus lifecycle in the host.
1) Entry via animal bite, 2) Replication near entry site, 3) Ascends nerves to CNS, 4) Spreads to salivary glands
27
What are hallmark symptoms of Rabies?
Hydrophobia, agitation, paralysis, and coma
28
How is Rabies virus transmitted?
Through saliva, typically via animal bites
29
What is the incubation period for Rabies, and what factors influence it?
Weeks to months; depends on bite location and viral load
30
How is Rabies diagnosed?
Skin biopsy, saliva PCR, and direct fluorescent antibody tests
31
What treatments are available for Rabies post-exposure?
Wound cleaning, rabies immunoglobulin (HRIG), and vaccination
32
What vaccines are available for Paramyxovirus diseases?
MMR vaccine for measles, mumps, rubella; RSV immunoprophylaxis for high-risk infants
33
How is Rabies controlled in animal populations?
Vaccination of pets, bait vaccines for wildlife
34
What is the function of the HA and NA proteins in Influenza?
HA: entry by binding sialic acid; NA: facilitates exit by cleaving sialic acid
35
What complications can arise from Measles infection?
Pneumonia, encephalitis, and subacute sclerosing panencephalitis (SSPE)
36
Question
Answer
37
What is the structure of the Paramyxoviridae genome?
Single-stranded, negative-sense RNA.
38
Which proteins mediate viral attachment in Paramyxoviridae?
HN (hemagglutinin-neuraminidase) for parainfluenza, H for measles, and G (glycoprotein) for RSV.
39
How do Paramyxoviruses typically enter and exit host cells?
Enter via fusion with the plasma membrane; exit by budding.
40
What is a defining cytopathic effect of Paramyxoviridae?
Formation of syncytia (multinucleated giant cells).
41
How is the measles virus primarily transmitted?
Respiratory droplets.
42
What receptors does the measles virus bind to on host cells?
CD46, CD150 (SLAM), and nectin-4.
43
What are common symptoms of measles?
High fever, cough, conjunctivitis, and maculopapular rash.
44
What characteristic sign is found in the mouth during measles?
Koplik spots.
45
How does measles affect immunity?
Causes immunosuppression and weakens host defenses.
46
How is mumps virus transmitted?
Large-droplet aerosols.
47
What is a hallmark symptom of mumps?
Swelling of the parotid and salivary glands.
48
What are common complications of mumps?
Orchitis, oophoritis, and meningitis.
49
How is mumps diagnosed in the lab?
By RT-PCR, ELISA, or detection of giant cells in cell culture.
50
What is the primary disease caused by Respiratory Syncytial Virus (RSV) in infants?
Bronchiolitis and pneumonia.
51
How does RSV differ from measles in its spread within the body?
RSV causes localized respiratory infections without viremia.
52
What treatment options exist for severe RSV infections?
Ribavirin aerosol and monoclonal antibodies (e.g., palivizumab).
53
Describe the genome structure of Orthomyxoviruses (e.g., influenza).
Segmented, single-stranded, negative-sense RNA.
54
How do Hemagglutinin (HA) and Neuraminidase (NA) proteins function in influenza?
HA facilitates entry; NA assists in viral exit.
55
What are two mechanisms of genetic variation in influenza?
Antigenic drift (mutation) and antigenic shift (reassortment).
56
How is influenza primarily transmitted?
Through inhalation of small aerosol droplets.
57
What is the primary cell receptor used by rabies virus for neural infection?
Nicotinic acetylcholine receptor (AChR).
58
Describe the progression of rabies after a bite.
Local replication, entry into neurons, CNS travel, and brain infection.
59
What are characteristic symptoms of rabies?
Hydrophobia, hallucinations, and excessive salivation.
60
What is a unique feature of Rhabdoviridae (e.g., rabies)?
Bullet-shaped virions.
61
What are key zoonotic reservoirs for rabies?
Wild animals like bats, raccoons, and foxes.
62
What is the primary treatment for rabies exposure?
Immediate wound cleaning, HRIG, and post-exposure vaccination.
63
What is the structure of Filoviruses (e.g., Ebola)?
Filamentous, single-stranded, negative-sense RNA.
64
How does Ebola cause tissue damage and shock?
By infecting multiple cell types, causing cytokine storms and vascular leakage.
65
What are the main transmission routes for Ebola?
Contact with bodily fluids, contaminated needles, and funeral practices.
66
What treatments are available for Ebola?
Antiviral antibodies (e.g., Inmazeb, Ebanga) and the Ervebo vaccine.