(+) Strand RNA Viruses Flashcards

1
Q

Describe at least 5 common features of (+) Strand RNA Viruses.

A
  1. replicate in cytoplasm
  2. Genomic RNA serves as message and is DIRECTLY translated
  3. Genomic RNA is infectious
  4. Virions LACK enzymes
  5. Viral proteins are translated as Polyproteins.
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2
Q

List the 2 non-enveloped, viral families of (+) strand RNA viruses.

A
  1. Picornaviridae (enteroviruses and rhinoviruses)

2. Caliciviridae

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3
Q

Briefly describe the features of the 2 major types of Picornaviridae.

A
  1. Enteroviruses grow at 37 C in the GI and are acid stable. Transmitted by fecal-oral contamination.
  2. Rhinoviruses grow at 33 C in the nose and are acid labile. Can be transmitted through fomites and enters host cells via ICAM-1
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4
Q

List the 3 enveloped, (+) RNA strand virus families.

A
  1. Togaviruses (icosahedral)
  2. Flaviviruses (icosahedral)
  3. Coronaviruses (helical)
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5
Q

Describe 2 special features of the viral (+) strand genome RNA.

A
  1. PolyA sequence at 3’ end

2. vPg bound to 5’ end of viral RNA

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6
Q

Define the purpose of the internal ribosomal entry site in 5’ UTR of viral genome.

A

Since there is no 5’ cap, ribosomes recognize viral IRES to start translating the message. Polio uses a cap-independent process.

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7
Q

Describe how the virus shuts off protein synthesis of the infected cell.

A

Viral proteases cleave a critical protein in initiation complex that would scan AUG codon. This disables synthesis of cellular proteins, but allows viral protein synthesis (because it is cap-independent)

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8
Q

Explain the significance of RNA-dependent RNA Polymerase in polio virus.

A

This early enzymatic RDRP enables the virus to make more RNA, since mammalian cells only make RNA from DNA. This makes an “anti-sense” (-) strand to serve as a template for (+) strand RNA.

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9
Q

Explain the significance of anti-sense RNA strand.

A

This is made from the template (+) sense RNA strand. (+) strands are made in XS over (-) strands.

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10
Q

Describe the polio paradox.

A

The worst polio outbreaks started 200 years ago in more developed parts of the world. Although, virus is highly infectious most newborns (before the hygiene advent) had maternal ABs for protection. This resulted in more severe diseases and epidemics (before the Salk vaccine).

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11
Q

Explain how the MOA of poliovirus manifests clinically.

A

Poliovirus is an enterovirus that is asymptomatic in the GI tract. Once it enters the blood it can travel to the spinal cord or lungs to result in respiratory paralysis or club foot.

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12
Q

What is the significance of paralytic polio?

A

Only 1% of polio-virus infections result in aseptic meningitis or paralytic polio (respiratory paralysis or muscle weakness)

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13
Q

Explain how the Sabin vaccine is more advantageous to the original Salk vaccine.

A

Oral Sabin vaccine had better coverage and spurred an effective IgG response in kids. The problem arose from recombination between wild-type and vaccine strain to cause activated polio in recipients.

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14
Q

List 4 common features of enveloped (+) strand RNA viruses.

A

Flaviviruses and Togaviruses are…

  1. non-segmented (+) strand genome
  2. Enveloped
  3. Most are “arthropod-borne”
  4. Bud off from internal organelles
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15
Q

Explain what is meant by “accidental” or “dead-end hosts” as it relates to alphaviruses.

A

Dead-end hosts have blood levels of viral particles that aren’t high enough for mosquito vectors to transfer the virus to another organism.

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16
Q

Define some features of the Chikungunya virus.

A
  1. Humans and primates are hosts, mosquitoes are vectors
  2. Outbreaks occur in Africa, Asia and Europe (only recently did they come to the US, Florida)
  3. Presents as arthritis-related ailments (joint pain, headaches and rashes).
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17
Q

These types of alpha-viruses feature humans and horses as accidental hosts. Which is more severe?

A

Eastern-Equine Encephalitis virus (wild bird-mosquito tsm; 50% fatality); Western-Equine Encephalitis Virus (less severe and more frequent); Venezuelan Equine Encephalitis (Rodent-mosquito tsm)

18
Q

Define the mode of transmission, symptoms and vaccine for the Rubivirus.

A

Rubella is spread by respiratory tsm; symptoms include fever, sore throat and runny nose; Congenital rubella syndrome (CRS) is SEVERE for fetuses; MMR is the successful live attenuated vaccine

19
Q

For what 3 types of Flaviviruses are humans the accidental hosts?

A

Japanese Encephalitis Virus, Saint Louis Encephalitis Virus and West Nile Virus

20
Q

This type of Flavivirus is transmitted between pigs, aquatic birds. Humans are the accidental host. Severe disease presents with an altered mental status, seizures and is 20-30% fatal. In inactivated vaccine exists.

A

Japanese Encephalitis virus

21
Q

This type of flavivirus appears in the elderly, in which 20% of those infected are symptomatic (fever, headaches, muscle weakness (GBS)); 10% fatality rate.

A

West Nile Virus

22
Q

This type of flavivirus presents as an abrupt onset of fever, dizziness and nausea; 90% of elderly develop severe CNS disease; with a 15% fatality rate

A

Saint Louis Encephalitis Virus

23
Q

Compare and contrast Classic Dengue Fever from Dengue Hemorrhagic Fever and Shock Syndrome.

A

Classic dengue = breakbone fever where terrible joint/bone pain lasts months after recovery with little mortality;
Dengue Hemorrhagic Fever = 10% fatal with shock and bleeding at GI and in skin.

24
Q

Describe the MOA for Dengue Hemorrhagic fever and Shock Syndrome.

A

4 serotypes result in a neutralizing AB that’s not cross reactive. Ag-AB complexes form > activates complement > cytokines are released > HUGE immunological reaction ensues. Vasopermeability from complement. Shock from infection of macrophages.

25
Q

Compare and contrast the 2 types of Yellow Fever and how they spread.

A
  1. Jungle yellow fever is spread from monkey to monkey via Haemagogus mosquitoes.
  2. Urban yellow fever is spread from human to human via Aedes mosquitoes.
26
Q

Briefly describe the transmission and symptoms of someone infected by Zika virus.

A

Flavivirus transmitted by Aedes mosquito; asymptomatic/ mild fever, rash, arthralgia in person; microcephaly of child from pregnant mother

27
Q

Briefly describe the replication strategy, serology, symptoms and treatment of Hepatitis C.

A

Replication strategy similar to Flaviruses; > 6 serotypes that are constantly changing the hyper-variable region on glycoprotein envelope; transmitted by blood (IV use, sex or transplacentally); Can present as acute hepatitis in 25% of cases or hepatocellular carcinoma years later; Treatment with Acyclovir

28
Q

Explain how the onset of Hepatitic C can put someone at risk of developing liver cancer.

A

Viral killing of hepatocytes and immune response causes the liver cells to regenerate. Chronic infection can lead to enhanced hepatocellular carcinoma in the future. Cirrhosis and alcoholism can put people at risk of developing this too.

29
Q

Describe some features of the Corona-viruses.

A
  1. Glycoprotein spikes appear as a crown
  2. Helical nucleocapsid
  3. Respiratory tsm and the presentation of common cold
30
Q

Briefly describe 2 examples of corona-viruses.

A
  1. SARS = presents as pneumonia, spread quickly by respiratory aerosols, 10% fatality
  2. MERS-CoV = Severe acute respiratory illness; spread by close contact, 40% fatality; recently introduced to USA.
31
Q

Describe the transmission, clinical features and prophylactic treatment of: Rubivirus (Rubella)

A

Tsm: Respiratory droplets (not an arbovirus);
Cx: fever, headache, sore throat, lymph nodes, rash;
Prophylaxis: MMR live attenuated vaccine

32
Q

What are the TORCHeS infections?

A
Toxoplasma gondii,
Rubella,
CMV,
HIV/HSV,
Syphillis
33
Q

Name at least 3 symptoms that can be experienced with Congenital rubella syndrome (CRS).

A
  1. Patent ductus arteriosus
  2. Cataracts
  3. Sensory-neural deafness
  4. Jaundice, Blue-berry muffin rash
34
Q

Describe the transmission, clinical features, diagnosis and treatment for: Coronavirus

A

Tsm: respiratory;
Cx: common cold, SARS, MERS-CoV (40% fatality!);
Dx: PCR without antibodies;
Tx: Corticosteroids, Ribavirin

35
Q

How do Flaviviruses and Togaviruses differ?

A

Transcriptional pattern;

Transmission: Flaviviruses via mosquitoes; Togaviruses via mosquito (except Rubella virus via respiratory route)

36
Q

What accounts for the repeated outbreaks of Norovirus (Norwalk) on cruise ships?

A

Stability of virus within the environment and relative resistance to disinfection. It causes explosive watery diarrhea. Those at risk are children, raw shellfish eaters, and cruise ship attendants.

37
Q

Describe at least 4 features of Picornaviruses.

A
  1. Small
  2. Icosahedral
  3. Naked (non-enveloped)
  4. Transmitted via digestive tract or respiratory tract
38
Q

What type of virus is Coxsackievirus? Name a few symptoms.

A

Enterovirus within the Picornavirus family. Results in Meningitis, Hand-foot-and-mouth Disease, pleurodynia and dilated cardiomyopathy.

39
Q

Define the 2 major types of Togaviruses.

A
  1. Arbovirus - Eastern, Western and Venezuelan Equine viruses (spread by mosquitoes)
  2. Rubella - Rubivirus (spread by respiratory transmission)
40
Q

How does Polio virus genome differ from typical mammalian mRNA? What is the significance of this feature?

A

Has a small protein (IRES) covalently bound to the 5’ (UTR) end of the mRNA. This allows polio viruses to translate viral message in a cap-independent manner.

41
Q

What type of Flavivirus is transmitted by Aedes Egyptian mosquito and manifests as “Breakbone fever”?

A

Classic Dengue Virus - Dengue fever (terrible joint and bone pain, even after recovery); Hemorrhagic fever -> thrombocytopenia

42
Q

What type of Flavivirus is associated with a lot of dead birds (reservoir) in which humans are the dead end host? List the symptoms.

A

West Nile Virus - 20% symptomatic for fever, headaches, muscle weakness; <1% encephalitis/paralysis