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Viruses > RNA Viruses (-) Sense > Flashcards

RNA Viruses (-) Sense Flashcards

1
Q

List the (-) Sense RNA Viruses (7)

A 
Orthomyxovirus 
Paramyxovirus (a family)
Rhabdovirus
Filovirus
Bunyavirus
Arenavirus 
Reovirus
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2
Q

What is the only RNA virus group that does not replicate in the cytoplasm?

A

Orthomyxovirus - they replicated in nucleus

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3
Q

How many segments does Influenza have? Why is this relevant?

A

8

Segmentation allows very special kinds of mutations to occur.

There are 2 broad categories of mutations:

1) Antigenic Drift - Point mutations in viral genome leading to changes in hemagluttinin (HA) or neuraminadase (NA) molecules.

This is the reason we need a new flu vaccine every year. This also gives rise to epidemics.

Seasonal Flu

2) Antigenic shift - MUCH more serious. Antigenic segments of RNA are shared between different species. The H’s and N’s can combine to form new virus that is a mixture of the surface antigens (reassortment).

This is only possible due to segmentation and causes pandemics.

Ex/ H1N1 - The last pandemic we had. Swine flu bc it was result of antigenic shift between human, avian, and swine influenza viruses.

Both mutation types are types of antigenic variation.

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4
Q

What are the 4 viruses that are segmented?

A

BOAR

B = Bunyavirus
O = Orthomyxovirus
A = Arenavirus
R = Reovirus
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5
Q

Which Influenza viruses have the ability to antigenic shift?

A

Influenza A = shift and drift

Influenza B = drift only

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6
Q

Hemogluttinin (HA)

A

Key glycoprotein on surface of influenza viruses

Binds to sialic acid found on membranes of cells in upper respiratory tract or RBCs. Causes RBCs to clump together in test tubes (hence the name)

H1, H2, H3 are seen in influenza viruses that infect humans. There are many more though. These antigens determine the cell’s tropism (which cells could be infected).

Anti-HA antibodies that we make protect us from the same strain again in the future.

HA on virus binds to Sialic acid on cell membrane. Virus is then endocytosed into cell. Viral uncoating can only be done at the right pH!

M2 helps get the pH right - It’s a proton channel. This is a key drug target*

Target M2 and you prevent replication.

Amantidine and rimantidine do this - inhibit M2, no uncoating. These are no longer recommended due to high resistance in current flu strains.

They only work on influenza A. Influenza B lacks M2.

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7
Q

Amantidine and rimantidine

A

M2 inhibitors

They work to target M2 (a proton channel that helps influenza virus achieve a desirable pH for uncoating) to prevent viral uncoating.

No longer used bc of high resistance in current flu-strains.

Only works on Influenza A bc Influenza B doesn’t even have M2.

Amantidine is also used in parkinson’s to increase Dopamine levels in CNS.

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8
Q

Neuraminidase (NA)

A

The other major virulence factor of influenza virus (+ HA).

Once the virus has already uncoated, it replicates in the nucleus. However, it needs to release its new viruses. New virus is bound to the host cell after replication by the same sialic acid residues that HA was originally attached to.

NA cleaves sialic acid to release newly formed virions from host cell.

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9
Q

Oseltamivir/Anamivir

A

NA inhibitors used in influenza.

Prevents release of new virions. Giving Tamiflu (Oseltamivir) after a 72 hr period will not be effective bc the viruses have already replicated and been released. Give it early!

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10
Q

How is influenza transmitted?

A

Respiratory droplets

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11
Q

What is flu season?

A

Dec - Feb

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12
Q

Influenza vaccine

A

Given around Oct so people can build an adequate immune response prior to exposure.

2 types:

1) Live attenuated nasal spray
2) Killed, injectable - also has 2 forms:
(a) Trivalent (2 A strains, 1 B strain)
(b) Quadrivalent (2 A strains, 2 B strains)

Kids can get vaccine after age 6 months.

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13
Q

What is one possible neurological consequence of influenza infection?

A

Guillain-Barre Syndrome

Ascending paralysis

CSF shows low WBC, high protein - albuminocytologic dissociation

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14
Q

Aspirin in children with flu

A

DONT

Risk of developing Reye’s Syndrome

Life threatening (liver failure, fatty liver, encephalitis)

Kids may also present with fever, rash, vomiting

Aspirin uncouples oxidative phosphorylation in hepatic mitochondria

Avoid aspirin in children and teens who have or are recovering from viral infections.

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15
Q

72 yo woman with myalgias, fever, non-productive cough for 7 days - seemed to get better then started to have productive cough and fever. She looks really sick upon presentation.

A

Pneumonia is a major complication of influenza.

From Staph aureus or Strep pneumo usually

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16
Q

What viruses belong to the paramyxovirus family? (4)

A

Rubeola (Measles), Mumps, Respiratory Synytial virus (RSV), and Parainfluenza

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17
Q

Describe the prodrome of measles infection

A

4 Cs

Cough
Coryza (runny/stuffy nose caused by inflammation of upper airway)
Conjunctivitis
Koplik spots (pathognomonic for measles) - small, bluish white spots on a red background found on buccal mucosa inside cheek near the 2nd molars.

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18
Q

Measles presentation

A

Prodrome with Cough, Coryza, Conjunctivitis, and Koplik spots

Fever that can get pretty high (40C, 104F) that lasts for about 4 days.

About 1-2 days after you see Koplik spots the patient will develop a maculopapular rash

Rash starts near back of ears, spreads to face and neck, and travels down to rest of body (it’s itchy).

Measles is likely to form a confluent rash - rash starts as small dots and then blends together.

Major complications are:

Viral or bacterial pneumonia
Subacute sclerosing panencephalitis - SSPE - inflammation and sclerosing of brain caused by persistent measles infection

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19
Q

Presentation of SSPE

A

Subacute sclerosing panencephalitis is an inflammation and sclerosing of the brain caused by persistent measles infection.

Patient with Hx of measles as a child OR they imply that person was never vaccinated by saying they immigrated to the US. Then 5-15 yrs later the patient develops personality changes, seizures, myoclonus, ataxia, eventually coma/death.

To dx SSPE, you’d find anti-measles antibodies in CSF

No good Tx tho

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20
Q

What virulence factors do members of the paramyxovirus family have?

A

Hemagluttinin
Neuraminidase
Fusion proteins (Multinucleated giant cells - synsytia- In measles they are called Warthrin-Finkeldey cells found in lymphoid tissue. They have many nuclei, are eosinophilic, and have inclusion bodies. Presence of these cells is pathognomonic for measles)

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21
Q

Warthrin-Finkeldey Cells

A

Fusion proteins present in measles

Multinucleated giant cells - many nuclei, eosinophilic, inclusion bodies.

In lymphoid tissue

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22
Q

What reduces measles morbidity and mortality?

A

Vitamin A

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23
Q

What virulence factors does Measles have?

A

HA and FP

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24
Q

What virulence factors does Mumps have?

A

HA, NA, and FP

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25
Q

What virulence factors does RSV have?

A

FP only

26
Q

Where does Mumps replicate?

A

Salivary glands - specifically the parotid glands leading to parotiditis

Can also be found in tests - very bad

27
Q

What are some complications resulting from a Mumps infection?

A

Testes infection - orchitis

Inflammation of epididymis seen when teenage boy or adult man is infected. Usually it is unilateral, but sometimes bilateral. It can cause testicular atrophy or impaired fertility. Sterility is rare, but more common in bilateral manifestation.

Meningitis - Mumps can also replicate in CNS

28
Q

What is the most common cause of pneumonia and bronchiolitis in infants?

A

RSV

29
Q

Who is most at risk of being infected by RSV?

A

infants

30
Q

RSV presentation

A

Infects cells by attaching to respiratory epithelium via G proteins

Causes bronchiolitis, pneumonia, rhinitis, pharyngitis

Infiltrates on CXR

31
Q

RSV Tx

A

Ribavirin - nucleoside analog

Can treat RSV in adults, but not recommended for children or pregnant women

Palivizumab - monoclonal antibody against RSV Fusion Protein. This is used to prevent RSV in kids who are at high risk (premature birth). IgG.

32
Q

What disease is caused by parainfluenza virus?

A

Croup

33
Q

Croup presentation

A

Caused by parainfluenza (member of paramyxovirus family)

Characterized by seal bark cough and inspiratory stridor (whistle).

On XR there is a “Steeple Sign” representing narrowing of the subglottic region

Mainly infects children - adults will just get a bad cold

Croup is also called laryngotracheobronchitis

34
Q

What virulence factors does parainfluenza have?

A

HA, NA, FP

35
Q

What disease is caused by Rhabdovirus?

A

Rabies

36
Q

What does Rhabdovirus look like?

A

Helical nucleocapsid.

The virus capsule is bullet shaped.

37
Q

What animals are most likely to carry Rhabdovirus?

A

In USA, #1 is bats.

Also, squirrels, skunks, foxes, raccoons.

Dogs really only in developing countries

38
Q

Rhabdovirus mechanism/progression

A

Rhabdo has a glycoprotein that binds nicotinic acetyl CoA receptors in post-synaptic membrane of neuromuscular junction/motor end plates. It replicates in motor neurons.

After incubation of weeks-months, symptoms appear. The incubation period depends on how far away from the CNS the original inoculation site was.

Virus travels retrograde via peripheral nerves. It moves about 1-3mm per day until it gets to dorsal root ganglia. As it spreads along nerves it causes tingling/muscle spasms.

Once it gets to salivary glands we get increased salivary production (foaming at the mouth) and very painful muscle spasms of throat/larynx (dysphagia).

Virus continues to travel leading to high fever, encephalitis, neuronal death and is usually fatal.

There are not many survivors of rabies who did not receive immediate early treatment.

39
Q

Rabies dx

A

Clinical focusing on exposure Hx

Confirmed via biopsy by finding negri bodies in neurons

these are eosinophilic cytoplasmic inclusions that can be found in soma of Perkinje cells within cerebellum or in pyramidal cells of hippocampus.

40
Q

Rabies Tx

A

Antidote needs to be given before symptoms onset. ASAP after exposure.

Tx is passive immunity with human rabies immunoglobulin - given to those who have been bitten by animals suspected to be infected with rabies.

Pt should also be actively immunized with killed viral particles after being bitten.

Patient should be vaccinated even if they just woke up in a room with a bat and have no trace of being bitten since bite marks may be small and go unnoticed.

41
Q

What does filovirus look like?

A

Helical capsid

42
Q

What are the main filovirus infections?

A

Ebola

Marburg

43
Q

Filovirus symptoms

A

Fever
Sweating
Petechial rash (not always)
Hemorrhagic fever

Symptoms can start days or weeks after contracting virus

Progresses to hemorrhagic fever and end-organ failure.

Most of the filovirus infections are fatal due to severe blood loss leading to hypovolemic shock (within days of symptoms)

44
Q

Who is most at risk from filovirus?

A

People in direct contact with animals infected with the virus (monkeys or fruit bats).

People in contact with these animals in endemic areas (Africa)

In USA, the most at risk are healthcare workers taking care of the sick individuals

Once people get it, it can spread fast through contact with bodily fluids - especially after the death of an infected individual.

45
Q

How does Bunyavirus obtain its envelope?

A

From Golgi complexes of host cells

46
Q

How many segments does Bunyavirus have?

A

One of the segmented viruses (BOAR)

3 segments. Circular segments.

47
Q

Which Bunyaviruses are arboviruses?

A

Most are. The two we should know are Rift Valley Fever and California Encephalitis

Spread by mosquito (Aedes)
Most cases not fatal
Causes neuro problems (Seizure, encephalitis, fever, myalgias)

48
Q

Which bunyavirus is not an arbovirus?

A

Hantavirus - spread through contact with rodents or their poop

49
Q

Hantavirus presentation

A

Caused by Bunyavirus - “Sin Nombre Virus”

Causes Hantavirus Cardiopulmonary Syndrome (HCPS)

Reservoir = deer mouse (A robovirus - rodent borne)

Transmitted via rodent urine/feces

Causes pulmonary edema via capillary leak and prerenal azotemia (due to all the capillary leak and loss of fluids)

Can also cause hemorrhagic fever.

50
Q

Arenavirus replication

A

Classified as (-) sense, but it is actually ambisense

It can encode both (+) and (-)

51
Q

What does arenavirus look like?

A

Helical nucleocapsid (like Filo, Rhabdo)

Characteristic sandy look on EM - outer capsid looks granular

52
Q

How many segments does Arenavirus have?

A

One of the BOAR segmented viruses

2 segments.

53
Q

Arenavirus presentation

A

Associated with rodent transmitted diseases in humans

Lymphocytic choriomeningitis virus (LCV):

Leads to febrile aspetic meningeoencephalitis

Fever

54
Q

How is arenavirus inactivated?

A

Heating
Low pH
Irradiation
Detergents

An example of an arenavirus is LCV

55
Q

Reovirus genetic profile

A

It is the only double stranded RNA virus

It is ambisense - but this doesn’t apply since it is double stranded.

56
Q

How many segments does reovirus have?

A

One of the BOAR segmented viruses

11 segments on avg (can be 9-12)

57
Q

Reovirus transmission

A

fecal-oral

58
Q

What are 2 examples of Reoviruses?

A

Rotavirus

Colorado Tick Virus

59
Q

Rotavirus presentation

A

Type of reovirus

Causes a toxin-mediated secretory diarrhea (fairly explosive, watery - a lot like norovirus)

The toxin is NSP4 - a viral enterotoxin that increases Cl- permeability leading to secretory diarrhea

Seasonal - Winter is common

Children are at high risk.
Classic patient is infant or young child especially in daycare

60
Q

What is the #1 cause of severe diarrhea in infants and children?

A

Rotavirus (a reovirus)

61
Q

Colorado Tick Virus presentation

A

fever, vomiting, myalgia

NO RASH

62
Q

Treatment for a reovirus infection

A

supportive care - oral rehydration is enough for Rotavirus

Prophylaxis: Live, attenuated oral vaccine is part of the standard vaccination schedule - 1st dose is before 3 months old

Vaccine may increase risk of intussusception due to stimulation and enlargement of Peyer’s Patches

Viruses (3 decks)

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