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BMS 622 Exam 3 > Lecture 16: Paramyxovirus, Orthomyxovirus, (Rhabo,Filo,Borna) Chap 48, 49, 50s > Flashcards

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
Q

What disease is most commonly associated with Rhabdoviruses?

A

Rabies

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26
Q

Describe the Rabies virus lifecycle in the host.

A

1) Entry via animal bite, 2) Replication near entry site, 3) Ascends nerves to CNS, 4) Spreads to salivary glands

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27
Q

What are hallmark symptoms of Rabies?

A

Hydrophobia, agitation, paralysis, and coma

28
Q

How is Rabies virus transmitted?

A

Through saliva, typically via animal bites

29
Q

What is the incubation period for Rabies, and what factors influence it?

A

Weeks to months; depends on bite location and viral load

30
Q

How is Rabies diagnosed?

A

Skin biopsy, saliva PCR, and direct fluorescent antibody tests

31
Q

What treatments are available for Rabies post-exposure?

A

Wound cleaning, rabies immunoglobulin (HRIG), and vaccination

32
Q

What vaccines are available for Paramyxovirus diseases?

A

MMR vaccine for measles, mumps, rubella; RSV immunoprophylaxis for high-risk infants

33
Q

How is Rabies controlled in animal populations?

A

Vaccination of pets, bait vaccines for wildlife

34
Q

What is the function of the HA and NA proteins in Influenza?

A

HA: entry by binding sialic acid; NA: facilitates exit by cleaving sialic acid

35
Q

What complications can arise from Measles infection?

A

Pneumonia, encephalitis, and subacute sclerosing panencephalitis (SSPE)

36
Q

Question

A

Answer

37
Q

What is the structure of the Paramyxoviridae genome?

A

Single-stranded, negative-sense RNA.

38
Q

Which proteins mediate viral attachment in Paramyxoviridae?

A

HN (hemagglutinin-neuraminidase) for parainfluenza, H for measles, and G (glycoprotein) for RSV.

39
Q

How do Paramyxoviruses typically enter and exit host cells?

A

Enter via fusion with the plasma membrane; exit by budding.

40
Q

What is a defining cytopathic effect of Paramyxoviridae?

A

Formation of syncytia (multinucleated giant cells).

41
Q

How is the measles virus primarily transmitted?

A

Respiratory droplets.

42
Q

What receptors does the measles virus bind to on host cells?

A

CD46, CD150 (SLAM), and nectin-4.

43
Q

What are common symptoms of measles?

A

High fever, cough, conjunctivitis, and maculopapular rash.

44
Q

What characteristic sign is found in the mouth during measles?

A

Koplik spots.

45
Q

How does measles affect immunity?

A

Causes immunosuppression and weakens host defenses.

46
Q

How is mumps virus transmitted?

A

Large-droplet aerosols.

47
Q

What is a hallmark symptom of mumps?

A

Swelling of the parotid and salivary glands.

48
Q

What are common complications of mumps?

A

Orchitis, oophoritis, and meningitis.

49
Q

How is mumps diagnosed in the lab?

A

By RT-PCR, ELISA, or detection of giant cells in cell culture.

50
Q

What is the primary disease caused by Respiratory Syncytial Virus (RSV) in infants?

A

Bronchiolitis and pneumonia.

51
Q

How does RSV differ from measles in its spread within the body?

A

RSV causes localized respiratory infections without viremia.

52
Q

What treatment options exist for severe RSV infections?

A

Ribavirin aerosol and monoclonal antibodies (e.g., palivizumab).

53
Q

Describe the genome structure of Orthomyxoviruses (e.g., influenza).

A

Segmented, single-stranded, negative-sense RNA.

54
Q

How do Hemagglutinin (HA) and Neuraminidase (NA) proteins function in influenza?

A

HA facilitates entry; NA assists in viral exit.

55
Q

What are two mechanisms of genetic variation in influenza?

A

Antigenic drift (mutation) and antigenic shift (reassortment).

56
Q

How is influenza primarily transmitted?

A

Through inhalation of small aerosol droplets.

57
Q

What is the primary cell receptor used by rabies virus for neural infection?

A

Nicotinic acetylcholine receptor (AChR).

58
Q

Describe the progression of rabies after a bite.

A

Local replication, entry into neurons, CNS travel, and brain infection.

59
Q

What are characteristic symptoms of rabies?

A

Hydrophobia, hallucinations, and excessive salivation.

60
Q

What is a unique feature of Rhabdoviridae (e.g., rabies)?

A

Bullet-shaped virions.

61
Q

What are key zoonotic reservoirs for rabies?

A

Wild animals like bats, raccoons, and foxes.

62
Q

What is the primary treatment for rabies exposure?

A

Immediate wound cleaning, HRIG, and post-exposure vaccination.

63
Q

What is the structure of Filoviruses (e.g., Ebola)?

A

Filamentous, single-stranded, negative-sense RNA.

64
Q

How does Ebola cause tissue damage and shock?

A

By infecting multiple cell types, causing cytokine storms and vascular leakage.

65
Q

What are the main transmission routes for Ebola?

A

Contact with bodily fluids, contaminated needles, and funeral practices.

66
Q

What treatments are available for Ebola?

A

Antiviral antibodies (e.g., Inmazeb, Ebanga) and the Ervebo vaccine.

BMS 622 Exam 3 (12 decks)

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