Semester 2 - Enveloped RNA viruses Flashcards

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1
Q

What are some features of enveloped RNA viruses?

A

Generally less stable than non-enveloped viruses in the environment
Generally smaller than DNA viruses
Cause a wide variety of human infections
Require an RNA-dependent RNA polymerase (exception?)

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2
Q

What are some characteristics of orthomyxoviruses?

A

(-) ssRNA segmented genome

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3
Q

What are the different types of Influenzas and what are the differences between them?

A

Influenza A- most pathogenic, widest host range. Highly mutagenic, susceptible to antigenic drift and shift.
Influenza B - Relatively less pathogenic, narrow host range, relatively less mutagenic (1 serotype)
Influenza C - mild disease, narrow host range, relatively less mutagenic (1 serotype)

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4
Q

How are the Influenza A serotypes named?

A

Based on surface proteins hemagglutinin (H1-17) and neuraminidase (N1-9). Hemagglutinin binds sialic acid cellular receptor. Neuraminidase cleaves sialic acid upon egress

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5
Q

How does influenza A replicate?

A
  1. binding involves HA:SA
  2. endosome acidification (M2 proton pump)
  3. Gene expression and replication within the nuclear compartment (splicing, capping)
  4. Assembly (reassortment)
  5. Egress (NA)
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6
Q

Where does replication of influenza A occur?

A

In the nucleus. Gene splicing occurs in the nucleus (increases genetic diversity, conserves genetic space). 5’ mRNA cap is added in the nucleus (provides RNA stability, increases recognition by ribosomes)

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7
Q

How does having a segmented genome benefit the influenza virus?

A

Reassortment of segmented genomes introduces genetic variability

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8
Q

How does antigenic drift occur?

A

By random mutation. New serotypes occur when mutations to H or N sufficientyly escape antibody cross reactivity

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9
Q

How does antigenic shift occur?

A

By reassortment. Segments from multiple strains/serotypes are assembled into a single virion. Results in new combinations of serotypes (H1N1 + H5N3 = H5N1)

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10
Q

What is sialic acid?

A

A family of derivatives of neuraminic acid. Involved in cell surface expression.

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11
Q

What are the functions of sialic acid?

A

Cation transport across membranes
Recognition site within cellular receptors for endogenous molecules (hormones, cytokines)
Protection from erythrocyte degradation
Modification and regulation of function of a wide variety of molecules

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12
Q

What is 2,3-sialic acid?

A

sialic acid linked to galactose sugar by 2nd carbon residue of SA and 3rd carbon residue of Gal

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13
Q

What is 2,6-sialic acid?

A

sialic acid linked to 6th carbon residue of galactose

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14
Q

What animal is a reservoir for influenza in humans?

A

Pigs

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15
Q

What are the clinical features of an influenza infection?

A

chills, fever, sore throat, coughing, nasal congestion, muscle ache, fatigue, Pneumonia; primary (viral) or secondary (often bacterial)

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16
Q

How is influenza virus transmitted?

A

mucosal (respiratory droplets), seasonal pattern of infection. Possibly zoonotic?

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17
Q

What factors affect severity of infection?

A

age and immune status
strain/serotype
level of pre-existing immunity

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18
Q

How is influenza treated?

A

Seasonal vaccine 2 A strains H1N1 H3N2, 1 B strain
Antiviral drugs M2 proton pump inhibitors, neuraminidase inhibitors
Treat symptoms in milder cases

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19
Q

What are some characteristics of paramyzoviruses?

A

(-) ssRNA virus, enveloped

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20
Q

What are the human pathogens of paramyzoviruses?

A

respiratory syncytial viruses
parainfluenzavirus
Measles virus
Mumps virus

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21
Q

What is the Respiratory syncytial virus (RSV)?

A

Causes syncytia formation in infected cells
Lower respiratory tract infection
typically affects young children, seasonal pattern of infection (most common LRT infection in young children)

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22
Q

When are individuals most commonly infected with RSV?

A

Most individuals infected by 2-3 years of age

Prematurity a risk for severity

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23
Q

What are the two subtypes of RSV?

A

A and B, occurrence varies over the course of a season

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24
Q

What are the clinical features of an RSV infection?

A

Runny nose, sore throat, cough
Otitis media
Croup
Bronchiolitis, pneumonia, dyspnea, wheezing

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25
Q

How is RSV transmitted?

A

Direct contact

Transmission rates very high (survives hours/days on inanimate surfaces)

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26
Q

How is RSV treated?

A

Largely supportive
No vaccine
Prophylactic antibodies for high risk infants
Monitoring complications important for infants/toddlers

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27
Q

What is the second most common cause of respiratory tract infections in young children?

A

Parainfluenzavirus

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28
Q

How many serotypes of parainfluenzavirus are there?

A

4 hPIV 1-4

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29
Q

What are the clinical features of a parainfluenzavirus infection?

A

Lower respiratory tract
Croup
Bronchitis, pneumonia
Fever, malaise, fatigue

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30
Q

How is parainfluenzavirus treated?

A

Ribavarin (purine analog)

Severe cases require corticosteroid treatment to relieve RT inflammation

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31
Q

How many serotypes of the measles virus are there?

A

8 clades (A-H), 23 serotypes

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32
Q

What are the clinical features of a measles infection?

A

fever, cough, anorexia, rash
Early - white spots (koplik’s spots) in the mouth/throat
Later - generalized maculopapular, erythematous rash: itchy, ‘staining’
Subacute sclerosing panencephalitis (SSPE) rare

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33
Q

What is the treatment for measles?

A

vaccine-preventable (live attenuated)

Interferon and ribavarin (nucleotide analog)

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34
Q

How is measles transmitted?

A

contact, respiratory droplets

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35
Q

How many genotypes of the mumps virus is there?

A

Rubulavirus subfamily, several genotypes A-H

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36
Q

What are the clinical features of a mumps infection?

A

Feaver, headache, malaise, painful inflammation of the parotid gland. Also associated with inflammation of the testicles, prostate. Associated with sterility in post-pubescent adolescents.
CNS invasion rare - aseptic meningitis/encephalitis

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37
Q

How is mumps treated?

A

Vaccine preventable

Treatment is supportive

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38
Q

How is mumps transmitted?

A

mucosal (respiratory droplets)

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39
Q

What are some characteristics of the rubella virus?

A

+ ssRNA Rubivirus subfamily

aka the german measles

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40
Q

How is the rubella virus gene expressed?

A

+ RNA genome is used directly to translate viral non-structural proteins (genome serves as mRNA for NS proteins). Structural proteins are transcribed from the antigenome (-) into mRNA (+) before translation

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41
Q

What are the clinical features of a rubella virus infection?

A

Fever, lymphadenopathy. Rash on face which progresses to limbs. Joint pain, arthritis symptoms very common in females

42
Q

How is rubella virus treated?

A

Vaccine preventable

Supportive

43
Q

How is rubella virus transmitted?

A

mucosal, respiratory droplets

44
Q

What are some characteristics of the coronavirus (SARS CoV)

A

(+) ssRNA, corona = crown

Severe Acute Respiratory Syndrome (SARS-CoV) most well characterized

45
Q

What are the reservoirs of SARS

A

Civet cat, chinese bat

46
Q

What are the clinical features of a SARS infection?

A

Fever, chill, non-productive cough, body ache, fatigue, myalgia
Primary or secondary pneumonia
Mortality >50% for persons over 65. Severe symptoms in immune competent individuals

47
Q

How is SARS treated?

A

Supportive, IFN

48
Q

How is SARS transmitted?

A

mucosal, respiratory droplets

49
Q

What is the ‘novel coronavirus’ MERS?

A

Very similar to SARS but with lower transmissibility (close contact). Current public health risk is low, contained within middle eastern countries. 50% mortality rate. Bats, camels have been identified as hosts

50
Q

What are some characteristics of the flavivirus?

A

(+) ssRNA virus

Most are arboviruses (arthropod born viruses)

51
Q

How is flavivirus gene expressed?

A

Genomic RNA serves as mRNA template for polyprotein production and subsequent proteolytic cleavage

52
Q

What are the human pathogens of Flaviviruses?

A
Yellow fever virus
West nile virus
Japanese encephalitis
Dengue virus
Hep C
53
Q

Where is the yellow fever virus endemic to?

A

Africa and south america (tropical climate)

54
Q

How is yellow fever virus transmitted?

A

Vector borne (Aedes aegypti mosquito)

55
Q

What are the clinical features of a yellow fever infection?

A

Fever, chills, muscle ache, nausea, jaundice (hepatotrophic virus). Viral hemorrhagic fever - septic shock, DIC, increased vascular permeability, multiple organ failure

56
Q

How is yellow fever treated?

A

Vaccine available for travellers

Treatment supportive

57
Q

Where is the dengue virus endemic to?

A

Africa, South america, south east asia (tropical climate)

58
Q

How is dengue virus transmitted?

A

Aedes aegypti mosquito

59
Q

How many serotypes of dengue fever are there?

A

4 DENV1-4

60
Q

What are the clinical features of Dengue Fever?

A

mild febrile illness, rash, joint muscle or bone pain

61
Q

What are the clinical features of Dengue Hemorrhagic fever?

A

increased severity, high fever, hemorrhagic manifestations, progresses to multi-organ bleeding and failure - ascites, pleural effusion

62
Q

What happens with subsequent dengue infections?

A

subsequent infections increase severity of symptoms = antibody mediated enhancement

63
Q

What is the treatment for dengue virus?

A

no vaccine or treatment - DEET preventative, supportive therapy. NSAIDs are CI’d as they may increase bleeding

64
Q

What is the vector for the west nile virus?

A

Spread by the Culex sp. mosquito, humans are incidental hosts

65
Q

What are the clinical features of the West Nile Virus?

A
Asymptomatic in most patients
West nile fever
West nile meningitis
West nile encephalitis
Acute flaccid paralysis (aka WNV poliomyelitis)
66
Q

What are the symptoms of West Nile Fever?

A

Fever, headache, body aches, mild rash, lymphadenopathy

Severe cases experience CNS invasion

67
Q

What distinguishes West Nile Meningitis and West Nile Encephalitis from other forms of Meningitis and encephalitis?

A

Clinically indistinguishable

68
Q

What are the clinical features of Acute Flaccid Paralysis?

A

Infection of the spine leading to partial paralysis
Damage to anterior horn cells, respiratory distress, similar to poliomyelitis symptoms
Paralysis may occur in the absence of prodromal phase of fever

69
Q

How is West Nile Virus treated?

A

Treatment is supportive, preventable
Pain relievers may be used as supportive treatment
WNV vaccine has been developed for horses, birds. Prevention transmission to humans

70
Q

What are some characteristics of the Hantavirus?

A

Bunyavirus family
(-) ssRNA, enveloped
Sin Nombre virus endemic to N. America

71
Q

How is the Hantavirus transmitted?

A

Mice

Contact with rodent urine/feces, airborne transmission, ingestion, bites

72
Q

What are the clinical features of the Hantavirus pulmonary syndrome (HPS)?

A

Sin Nombre Hantavirus
Early (1-2 weeks): fever, fatigue, muscle aches, chills, dizziness, abdominal pain
Late: dyspnea, tachypnea, SOB, circulatory shock - hypoxia, hypotension, tachycardia

73
Q

What are the clinical features of Hemorrhagic fever with renal syndrome (HFRS)

A

Hantaan virus, Dobrava virus, Saaremaa virus, Seoul virus, Puumala virus
Fever, intense headache, chills, blurred vision, rash, back or abdominal pain
Hemorrhagic fever: hypotension, vascular leakage, multi-organ hemorrhage
Renal syndrome: renal hemorrhage and dysfunction, proteinuria, polyuria

74
Q

How is the hantavirus treated?

A

No vaccine or antiviral treatment. Supportive treatment

Ribavarin antiviral effective early

75
Q

What are some characteristics of the Filoviruses?

A

(-) ssRNA, enveloped, filamentous-shaped
Genes expressed via linear attenuation of transcription
Highly infectious outbreaks

76
Q

What are the Filoviruses hemorrhagic fevers?

A

Ebola virus

Marburg Virus

77
Q

How is the Ebola virus transmitted?

A

Body fluids, contact, potentially airborne

78
Q

Where are the outbreaks of the Ebola virus?

A

First recorded: Ebola river, Congo

Congo, Zaire, Sudan, Uganda, Cote d’lvoire

79
Q

What are the clinical features of the Ebola Virus?

A

Sudden fever, malaise, nausea, respiratory tract involvement. GI involvement, cutaneous presentation (maculopapular rash, hematoma), Coagulopathy, disseminated intravascular coagulation, shock, multi-organ failure
Hemorrhagic symptoms appear 1 week after onset of fever

80
Q

What is the fatality rate of the Ebola virus?

A

40-70%

81
Q

What is the treatment of the Ebola virus?

A

No vaccine or antiviral treatment

Supportive

82
Q

How is the Marburg virus transmitted?

A

Body fluids, contact, potentially airborne

83
Q

Where are the outbreaks of the Marburg Virus?

A

1st: Marburg, Germany.

Congo, Angola, Uganda

84
Q

What are the clinical features of the Marburg Virus?

A

Clinically similar to Ebola virus: Viral hemorrhagic fever. Onset of hemorrhagic symptoms occur about 10 days after onset of fever

85
Q

What is the fatality rate of the Marburg virus?

A

30-90%

86
Q

What is the incubation period of the Ebola virus and the Marburg virus respectively?

A

2-21 days

5-10 days

87
Q

What are some characteristics of the arenavirus?

A

(-)ssRNA, enveloped, 2 segmented genome (S and L segments)
Acquires cellular ribosomes into virus particle following infection. Gene expression is complex - genes are encoded in both the forward and reverse direction (ambisense RNA)

88
Q

What are the Arenaviruses that cause viral hemorrhagic fever?

A

Lymphocytic choriomenigitis virus
Lassa virus
Bolivian hemorrhagic fever virus

89
Q

How is the lymphocytic choriomeningitis virus transmitted?

A

House mice - contact with urine, feces, saliva etc

90
Q

What are the clinical features of lymphocytic choriomeningitis virus?

A

Aseptic meningitis, encephalitis
Low mortality rate
Some neurological complications reported (rare) - nerve deafness, arthritis
Important teratogen: may lead to hydrocephalus, mental retardation (irreversible)

91
Q

Where is lymphocytic choriomeningitis virus found?

A

Worldwide distribution

92
Q

Where is the lassa virus endemic to?

A

West Africa (Sierra Leone, Nigeria, LIberia)

93
Q

How is the Lassa virus transmitted?

A

wild rats

94
Q

What are the clinical features of the Lassa virus?

A

80% cases mild, but severe cases have high mortality (50%)
Gradual onset of fever, fatigue, vomiting, diarrhea, myalgia. Hemorrhagic fever: shock, hypotension, pleural effusion, pleural effusion,multi-organ hemorrhage including cerebral

95
Q

What may distinguish Lassa virus hemorrhagic fever from other hemorrhagic fever?

A

White tonsilar patches

96
Q

Where is the Machupo virus endemic to?

A

Bolivia

97
Q

How is the Machupo Virus transmitted?

A

Wild vesper mouse (airborne, contact)

98
Q

What are the clinical features of the Bolivian Hemorrhagic Fever?

A

Fever, headache, fatigue, myalgia, arthralgia
Hemorrhagic symptoms: bleeding, multi-organ hemorrhage. Neurological invovlement (encephalitis, seizure, loss of muscle control.
Symptoms last 1 week

99
Q

What is the fatality rate of the Machupo Virus?

A

approximately 50%

100
Q

What is the treatment for the Machupo Virus?

A

Supportive, ribavarin