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Major RNA viruses Flashcards

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1
Q

Classification of medically important RNA viruses

A

1. +ssRNA

  • Enveloped
    • Icosahedral (President FTR)
      • Flavi-viridae
      • Toga-viridae
      • Retro-viridae
    • Helical (The rona)
      • Corona-viridae
  • Non-enveloped
    • Icosahedral (Please Call Home)
      • Pico-RNA-viridae
      • Herpe-viridae

2. -ssRNA

  • Enveloped
    • Helical (before anyone recommend food, please offer)
      • Bunya-viridae
      • Arena-viridae (-ssRNA and ambisense)
      • Rhabdo-viridae
      • Filo-viridae
      • Paramyx-viridae
      • Orthomyxo-viridae

3. dsRNA

  • Nonenveoped
    • Icosahedral
      • Reo-viridae
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2
Q

General info on medically important RNA viruses

A
  1. All nonenveloped viruses are icosahedral
  2. All RNA viruses replicate in the cytoplasm except Orthomyxoviridae (influenza virus) & Retroviridae
  3. All RNA viruses are single stranded except Reoviridae
  4. All RNA viruses are enveloped except Picornaviridae, Caliciviviridae, Hepeviridae, Reoviridae
  5. +ssRNA – viral genome acts as a mRNA; translated as polyprotein
  6. -ssRNA – viral genome is the template for viral mRNA; RdRp= core enzyme
    • All -ssRNA viruses are enveloped & helical
  7. Ambisense
    • -ssRNA viruses, but they have a segment whose complementary strand acts as the template for mRNA
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3
Q

List the groups of naked/icosahedral viruses

A
  1. +ssRNA
  • nonenveloped
    • Icosahedral (please call home)
      • Pico-RNA-viridae
      • Calici-viridae
      • Hepe-viridae
  1. dsRNA
  • nonenveloped
    • Icosahedral
      • Reo-viridae
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4
Q

Reoviridae (general info)

source and Transmission

timeline of infection within the infected host

dz associations

Dx, management, prevention*

A
  1. REO – Respiratory Enteric Orphan viruses
    * Virus isolated from respiratory & GI tracts but associated disease unknown
  2. Segmented, dsRNA genome; naked, icosahedral capsid
    * Segmented genomes allows for reassortment (mixing of gene segments between different variants of virus)
  3. Double or triple protein-layered capsid
    * Makes it very resistant to environmental conditions
  4. Human pathogens
  • Rotavirus – gastroenteritis in infants & young children
  • Coltivirus – Colorado tick fever (fever, headache, myalgia)
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5
Q

Rotavirus (general info)

A
  1. Buds into the ER, but loses the lipid bilayer
  2. Outer shell proteins: VP7 (G) & VP4 (P)
  • Induces neutralizing antibody
  • defines serotypes (Group A = most common cause of human infections
  • Important vaccine components
  1. NSP4 (nonstructural protein 4)
  • Acts like an enterotoxin
  • Promotes calcium influx into enterocytes, which disrupts cytoskeleton & cell/cell junction fluid loss & watery diarrhea
  1. Virus released during cell lysis
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6
Q

Rotavirus:

  • source and Transmission
  • timeline of infection within the infected host
  • dz associations
  • Dx, management, prevention*
A

1. Source: Ubiquitous; fecal oral route

  • outbreaks in day care

2. Transmission: Fecal/Oral

3. Clinical disease:

  • Gastroenteritis in infants
    • Watery diarrhea; vomiting
      • NSP4 enterotoxin activity
      • Loss of infected enterocytes cells in intestinal villi loss of absorptive cells
      • Dehydration possible, especially in infants
  • Milder diarrhea in older children and adults:
    • Most ppl exposed by 3-5 years of age
    • Prior exposure results in some protective antibody

4. Diagnosis:

  • Clinically, resembles that of other viral gastroenteritis
    • Self resolves; identification of virus often not necessary
  • Detect viral antigen in stool (ELISA, latex agglutination)
  • PCR – identify serotype

5. Management

  • Manage dehydration & electrolyte imbalance

6. Prevention – 2 live virus vaccines; administered at 2, 4, 6 months of age

  • RotaTeq (RV5)
    • human-bovine reassortant vaccine
    • 5 reassortant rotaviruses expressing the most common human G & P proteins
  • Rotarix (RV1)
    • Monovalent, human attenuated vaccine
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7
Q

Coltivirus

A

Colorado Tick Fever

1. Transmission: Dermacentor tick vector

  • Found in western US

2. Animal reservoir:

  • small rodents
    • squirrels,
    • chipmunks
    • mice
  • Larger animals can be infected but likely to be “dead end hosts”
    • Viral titer in blood is too low to be transmitted back to the tick vector
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8
Q

Colivirus–Colorado Tick Fever

A
  1. Infects erythrocyte precursors & remains in mature RBCs
  2. Causes a viremia; weeks or months
  3. Infection of vascular endothelial cells & vascular smooth muscle cells ==> leaky blood vessels; rash
  4. Fever (biphasic), chills, headache, lethargy, myalgia
    • Aseptic meningitis in severe cases
  5. Leukopenia (involving both neutrophils & lymphocytes)
  6. Diagnosis – immunofluorescence for viral antigens; PCR for viral sequences; serology for past exposure
  7. Management – self resolves; supportive care; antivirals; no vaccine
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9
Q

Pico-RNA-viridae

genus and subtypes

A

Pico-rna-virus: little RNA virus ==> naked/Icosahedral; +ssRNA

see image for genus and subtypes

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10
Q

Classification of pico-rna-viruses & examples of clinical diseases

A

1. Family: Pico-rna-viridae

2. Genus:

  • Enterovirus
    • subtypes
      • Poliovirus 1 – 3
      • Coxsackie A 1 – 24
      • Coxsackie B 1 – 6
      • Enterovirus 68 – 71
      • Echo 1 – 34
      • Ex: “Polio”
  • Rhinovirus
    • ​subtype
      • Human Rhinovirus 1 – 115
      • Ex: “common cold”
  • Hepatovirus
    • subtype
      • Ex: “Viral Hepatitis”
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11
Q

Enteroviruses

(Recall genus of the pico-rna-viruses)

A

1. Stable at acidic pH

  1. Replicates in oropharynx & GI tract
    * Transmitted via respiratory route & fecal/orally
  2. Disseminated via blood
  3. Associated with a variety of clinical illnesses, depending on viral tropism
  • Hand-foot-mouth disease – Coxsackie A16
  • Myocarditis, pericarditis – Coxsackie B
  • Meningitis, encephalitis & acute flaccid paralysis/myelitis – polio, Coxsackie & Echo viruses

Image:

Pathogenesis of enterovirus infection. The target tissue infected by the enterovirus determines the predominant disease caused by the virus . Coxsackie, Coxsackievirus; echo, echovirus; HAV, hepatitis A virus; polio, poliovirus.

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12
Q

Enteroviruses serotypes associated with CNS disease

A
  1. Poliovirus
  2. Enterovirus 71 – most virulent next to poliovirus
  • Hand-foot-mouth disease
  • Poliomyelitis-like paralytic disease, meningitis, meningoencephalomyelitis
  • Has caused outbreaks in Asia, Russia, eastern Europe
  1. Enterovirus D68 – associated with cases of acute flaccid myelitis
  2. Coxsackie B1 virus
    * myocarditis, aseptic meningitis, meningoencephalitis, neonatal systemic illness (encephalomyocarditis syndrome)
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13
Q

Poliovirus

(recall: subtype of Enterovirus genus of Pico-rna-virus family)

A

1. Replication following respiratory or fecal/oral transmission

  • Oropharynx; tonsils; lymph nodes of the neck; small intestine; Peyer patches

2. Dissemination

  • Causes a viremia & crosses the blood/brain barrier
  • Infects via the axons of peripheral nerves
    • Infects motor neurons of the anterior horn of the spinal cord
    • Can occasionally spread to medulla, cerebellum and motor cortex
  • Spreads to the CNS in ~1% of cases

3. Range of illness

  • Asymptomatic, especially in young children to flaccid paralysis

4. clinical disease:

  • 90 – 95% of the cases remain subclinical ==> asymptomatic
  • 5 – 8% of the cases may be associated with flu-like symptoms, sore throat, etc.
    • No dissemination to the CNS
  • 1 – 2% of the cases are associated with CNS disease
    • Aseptic meningitis or paralytic poliomyelitis
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14
Q

Polio–CNS disease

A

1. Nonparalytic poliomyelitis (aseptic meningitis)

  • fever, malaise, drowsiness, headache, nausea, vomiting, constipation, sore throat
  • stiffness & pain in the back & neck
  • 2-10 days duration with complete recovery

2. Paralytic poliomyelitis

  • Loss of reflexes; flaccid paralysis (reduced muscle tone)
  • Severe muscle aches or weakness
  • Spinal poliomyelitis
    • Most common form of polio
    • Virus damages anterior horn cells of the spinal cord, causing limb paralysis
  • Range of severity
    • paralysis remaining after 6 months is permanent
    • I_nvolvement of the medulla may result in paralysis of the diaphragm ==> death_
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15
Q

Pic of polio children paralyzed in iron lungs

A
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16
Q

Vaccination and elimination of polio

A

1. Vaccination & surveillance efforts have almost eradicated polio

  • Wild poliovirus type 1 reported in two countries – Afghanistan & Pakistan
  • Wild poliovirus type 2 – certified eradicated in 2015
  • Wild poliovirus type 3 – not detected since 2012

2. Outbreaks of vaccine-associated paralytic poliomyelitis (VAPP)

  • Associated with the use of a live, attenuated polio vaccine
  • Virus will replicate & can be shed in feces
  • Potential to up mutations that restore neurovirulence

3. Salk vaccine

  • trivalent, formalin inactivated polio vaccine (IPV)
  • Used in US
    • no risk of VAPP; can be administered to immunocompromised individuals

4. Sabin vaccine

  • oral polio vaccine (OPV); live attenuated vaccine
  • replicates in the gut and shed in stool
    • potential to cause VAPP (risk = ~1 per 2.6 x 106 doses given)
    • Can induce “herd immunity”
  • April 2016 – trivalent replaced with bivalent
    • PV type 2 was removed – no longer circulating & it was the most common cause of vaccine-derived polio virus
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17
Q

Rhinoviruses

(recall: genus of pico-rna-virus family)

“Think, common cold”

A
  1. Acid labile (will not survive in the GI tract)
    * Exception to the rule that naked icosahedral viruses are acid stable
  2. Optimal temperature for growth is 33-35 degrees C
    * Replicates better in upper & larger airways – cooler
  3. Most frequent cause of the common cold (“rhino” refers to nose)
    * >100 serotypes; would be difficult to generate a vaccine against the common cold
  4. Usually associated with upper respiratory tract infections but can cause bronchiolitis & wheezing illness in infants and young children
  5. Major trigger of asthma exacerbations
  6. May play a role in the development of childhood asthma
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18
Q

Hepatovirus

(recall: genus of the pico-rna-virus family)

“viral hepatitis”

A
  1. “Hepato” = hepatitis A virus
  2. Transmission:
  • Outbreaks due to contaminated food
  • Fecal oral transmission in daycares or among close contacts
  • IV drug use
  1. Acute hepatitis:
  • Asymptomatic or acute illness
  • 2-8 week incubation period
  • Jaundice, abnormal liver enzymes, fever, fatigue, nausea, abdominal discomfort
  • Self resolving; no chronic hepatitis
  1. Vaccine – inactivated virus
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19
Q

Calciviridae

(recall: +ssRNA => naked/nonenveloped => “please call home” (pico-rna, calic = cruise ship, hepe)

A
  1. Naked, icosahedral virus; +ssRNA
  2. Resistant to heat & detergents
  3. Fecal oral transmission
  4. Most important human pathogen – norovirus
  • 1st isolated in Norwalk, OH ==> called Norwalk agent; then identified as a Calicivirus
  • Leading cause of viral gastroenteritis (watery diarrhea & vomiting)
  • Outbreaks associated with ingestion of contaminated food
    • Picnics; cruise ships
    • Virus shed for several days after resolution of infections ==> food preparer who is no longer symptomatic can still transmit virus
  • Low infectious dose
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20
Q

Hepeviridae

(recall: +ssRNA => naked/nonenveloped => “please call home” (pico-rna, calic = cruise ship, hep-e)

A
  1. Hep e virus = hepatitis E virus
  2. Naked, icosahedral virus; +ssRNA
  3. Used to be classified as a Caliciviridae; now given its own family
  4. Hepatitis E:
    * uncommon in US; most common in developing countries (Asia, the Middle East, Africa & Central America)
  5. Transmission
  • Fecal/oral; typically spread via drinking water contaminated with feces (developing countries)
  • Outbreaks in developed countries have been associated with undercooked pork or deer meat
    • Foodborne outbreaks have not occurred in the US
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21
Q

What are the enveloped +ssRNA supergroups of RNA viruses

A
  1. +ssRNA
  • Enveloped Icosahedral (President FTR)
    • Flavi-viridae
    • Toga-viridae
    • Retro-viridae
  • Helical (The rona)
    • Corona-viridae
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22
Q

Flavi-viridae

(Recall: +ssRNA > enveloped > Icosahedral > “president FTR” (Flavi, Toga, Retro)

A
  • Enveloped, icosahedral, +ssRNA
  • Most are arboviruses (arthropod-borne viruses)
    • Exception = hepatitis C virus
  • Flavivirus arboviruses are antigenically related
    • Antibodies for the different arboviruses can cross react
    • May provide some protection against infection by a different arbovirus
  • Primary targets: cells of the monocyte/macrophage lineage; includes dendritic cells
  • Viruses may infect endothelial cells of capillaries

Image: Cross section of flavivirus. The envelope protein surrounds the membrane envelope, which encloses an icosahedralnucleocapsid. RNA, Ribonucleic acid.

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23
Q

What are some medically significant Flavi-viruses and their distribution, disease manifestations, that are arboviruses = arthropod-borne viruses)

think mostly mosquitoes (Aedes, Culex), Ixodes Ticks

A
24
Q

Describe the transmission of arboviruses:

A
  1. _Female mosquitos acquire virus from the blood of a viremic vertebrate hos_t
  • Encephalitis viruses: animal reservoirs are usually birds or small mammals
    • Humans are often considered an “accidental host” because titers in blood are not high enough to be transmitted from people to mosquitoes
  • Zika, yellow fever, dengue viruses: primates are animal reservoirs
    • Sylvatic cycle – primate – mosquito – human
    • Urban cycle – human – mosquito – human
  1. Virus infects the midgut of the mosquito; disseminates to the salivary glands
  2. Virus replicates in the salivary glands & is released into saliva
  3. Mosquito bites a host & virus in saliva is released into host’s skin & bloodstream

NOTE: In some cases, these viruses can be spread by exposure to contaminated blood

25
Q

Arboviruse–Clinical disease (general info)

A
  • Viremia & induction of interferons & cytokines ==> systemic, flu-like symptoms
    • Fever, chills, headaches, possibly arthralgias
  • Majority of infections do not progress beyond this mild systemic disease
  • If virus is not cleared after primary viremia, secondary viremia can produce enough virus to infect other organs
    • Vasculature, liver, skin, brain ==> hemorrhagic fever, shock or encephalitis
    • Encephalitis following infection of endothelial cells lining small blood vessels of the brain or the choroid plexus
    • Hemorrhagic fever & shock resulting from viral-induced cytolysis of infected vascular endothelial cells & virus-induced interferon & other cytokine production (cytokine storm)
26
Q

Arbovirus (Dengue)

A
  1. Antibody can prevent viremia
  2. Dengue:
  • Infection is enhanced when non-neutralizing antibody coats the virus; promotes uptake of virus by cells via Fc receptors
  • 4 subtypes of dengue virus
  • A 2nd infection with a different subtype increases the risk of more severe illnessdent enhance
  • Antibody-dependent enhancement

Image: DHF: dengue hemorrhagic fever; DSS: dengue shock syndrome

27
Q

Yellow fever and Dengue viruses

A
  1. Envelope (E) glycoprotein
  • Mediates attachment
  • Induces neutralizing antibody
  1. prM or preM protein
    * proteolytic processing during release forms the M protein in the mature viral particle

NOTE: antibody response to E & prM is involved in antibody-dependent enhancement of dengue infection

28
Q

Yellow fever clinical disease

A
  • 3-6 day incubation period
  • 3 stages: infection, remission & intoxication
  • Infection stage:
    • Nonspecific febrile illness (fever, chills, headache, myalgias, fatigue, nausea, vomiting)
    • Flushed skin; red conjunctiva; may have hepatomegaly
    • Patients will be viremic
  • Remission stage
    • Clinical improvement; most patients fully recover at this point
    • 15 to 20% progress to the intoxication stage where symptoms recur after 24-28 hours
29
Q

Severe yellow fever illness

A
  1. Intoxication
  • High fevers
  • Coagulopathy; hemorrhagic manifestations – bleeding from gums, hematuria, petechiae & bruising, blood in vomitus & stool
  • Severe hepatic dysfunction & jaundice
  • Renal failure; cardiovascular dysfunction
  • Shock
  • Viremia has usually resolved
  1. Outcome = convalescence or death
  2. Case-fatality rates – 20 to 60% in patients having severe disease
30
Q

Yellow fever management & prevention

A
  1. Supportive care
    * Control fluid loss; electrolyte imbalance; bleeding
  2. No specific antiviral therapy available
    * Hyperimmune globulin or monoclonal antibody – requires further investigation
  3. Vaccination _for preventio_n of yellow fever
  • A live-attenuated vaccine developed in 1936; YFV vaccine strain called “17D”
  • WHO maintains an emergency stockpile for use during outbreaks
  • Approved for individuals ≥ 9 months of age (increased risk of severe adverse events, including vaccine-associated encephalitis, in younger children)
  • Recommended for individuals living in endemic areas & travelers to endemic areas
    • Parts of Africa & South America
31
Q

Dengue–Clinical disease

A

image

32
Q

Dengue “Breakbone fever” and Dengue “hemorrhagic fever”

A
  1. Dengue fever (4-7 days)
  • Fever, chills, malaise
  • Headache & retro-orbital pain
  • Myalgia, arthralgia
  • Nausea, vomiting
  • Rash

Recovery or develop severe disease

  1. Dengue hemorrhagic fever
  • Thrombocytopenia
  • Hypovolemic shock from plasma leakage
  • Multiple organ failure
  • Severe hemorrhage
  • Encephalopathy
33
Q

Antibody-dependent enhancement (relating to dengue)

A
  • 4 subtypes of dengue virus
  • A 2nd infection with a different subtype increases the risk of more severe illness
  • 1st infection generated antibodies to the infecting subtype
  • These antibodies can cross react with other dengue subtypes but are unable to neutralize the 2nd subtype
  • Following exposure to a 2nd subtype, antibodies bind to the virus & enhance uptake by cells that express Fc receptors
    • Monocytes/macrophages, B lymphocytes, natural killer cells, neutrophils, mast cells
34
Q

Zika–Clinical disease

A
  1. Illness is usually mild; symptoms self resolve within 2-7 days
    * Low-grade fever; maculopapular rash (face, trunk, extremities, palms & soles); arthralgia (typically in the small joints of the hands and feet); conjunctivitis; headache; myalgia
  2. Congenital Zika Syndrome:
    * Microcephaly, intracranial calcifications, hearing & visual defects, limb deformities, club feet
  3. Encephalitis, meningoencephalitis, encephalomyelitis
  4. Guillain-Barré syndrome (demyelinating syndrome)
  5. Chronic inflammatory demyelinating polyneuropathy
  • Progressive weakness and impaired sensory function in the legs & arms caused by damage to the myelin sheath of the peripheral nerves
  • Considered the chronic counterpart of Guillain-Barré syndrome

Note:

Inflammation of the meninges, the membranes that surround the brain and spinal cord, is called meningitis; inflammation of the brain itself is called encephalitis. Myelitis refers to inflammation of the spinal cord. When both the brain and the spinal cord are involved, the condition is called encephalomyelitis.

35
Q

Encephalitis Viruses (WNV, SLE, POW)

A
  1. Most infections are asymptomatic
  2. Non-neuroinvasive disease is usually mild or flu-like
  • fever, headache, fatigue
  • nausea, vomiting can occur
  1. Neuroinvasive disease
  • Range of severity depending on the virus & host
  • Includes meningitis, acute flaccid paralysis, encephalitis
  • Symptoms can involve coma, seizures & paralysis
  • Neurological sequelae can occur (convulsions, paralysis, cognitive deficits & behavioral abnormalities)
36
Q

Hepatitis C virus (HCV)

general info

A
  1. Flavivirus but not an arbovirus
  2. Transmission – iv drug use; exposure to contaminated blood; sexual transmission
  3. Replication complex forms within a network of ER-derived membranes
  4. Encapsulation of the genome by core proteins is done in association with lipid droplets
  5. Assembly & release of HCV is intertwined with the maturation & release of very low density lipoprotein (VLDL) particles
  • Association of HCV with VLDL forms a lipo-viral particle (LVP)
  • Viral antigens within LVPs are shielded from the immune response

Note: VLDL carry Triglycerides

37
Q

HCV clinical disease

A

HCV hepatitis – 6 week to 6 month incubation period

Acute HCV is often asymptomatic or a mild clinical illness

Chronic infection

  • Most people with HCV viremia are chronically infected

Chronic HV can progress to cirrhosis & hepatocellular carcinoma or end stage liver disease

Note:

Following initial infection with HCV, approximately 75 to 85% of persons develop chronic infection. Among those with chronic infection, approximately 20 to 30% will eventually develop cirrhosis. Patients who have HCV-related cirrhosis have a 2 to 7% per year risk of developing either end-stage liver disease or hepatocellular carcinoma. Abbreviations: ESLD = end stage liver disease HCC = hepatocellular carcinoma

38
Q

Togaviridae

recall:

+ssRNA

  • Enveloped Icosahedral (President FTR)
    • Flavi-viridae
    • Toga-viridae
    • Retro-viridae
A

Alphavirus morphology. (A) Morphology of the alphavirus virion obtained from cryoelectron microscopy and image processing of the micrographs to show that the envelope is held tightly and conforms to the icosahedral shape and symmetry of the capsid. (B) Cross section of alpha-togavirus. The envelope is tightly associated with the capsid. (C) Cross section of flavivirus. The envelope protein surrounds the membrane envelope, which encloses an icosahedral nucleocapsid. RNA, Ribonucleic acid.

39
Q

Medically significant alphaviruses (recall, a type of Togavirus)

A
40
Q

Rubella Dz (image)

A

Spread of rubella virus within the host. Rubella enters and infects the nasopharynx and lung and then spreads to the lymph nodes and monocyte-macrophage system. The resulting viremia spreads the virus to other tissues and the skin. Circulating antibody can block the transfer of virus at the indicated points (X) . In an immunologically deficient pregnant woman, the virus can infect the placenta and spread to the fetus.

Time course of rubella disease. Rubella production in the pharynx precedes the appearance of symptoms and continues throughout the course of the disease. The onset of lymphadenopathy coincides with the viremia. Fever and rash occur later. The person is infectious as long as the virus is produced in the pharynx.

41
Q

Rubella Disease

A
  1. May be mild or asymptomatic
    * 30-60% of infections result in clinical disease
  2. Maculopapular rash
  • begins on the face & spreads to trunk, extremities
  • Fades away in few days
  1. Fever maybe mild or not present
  2. Lymphadenopathy
42
Q

Congenital Rubella

A
  1. Virus can cross the placenta
  2. The severity of the symptoms depends on fetal age at time of maternal viremia
    * Fetus is at major risk until 20th week of pregnancy
  3. Most common manifestations:
  • Cataracts,
  • mental retardation,
  • cardiac abnormalities,
  • deafness
  1. Rubella & CRS have been eliminated in the Americas
  • The last endemic cases of rubella and CRS were reported in the Americas in 2009.
  • Currently, rubella cases are due to infections acquired when traveling outside of the US
43
Q

Prevention of Rubella

A
  1. MMR vaccine – measles, mumps, rubella
  • Live, attenuated virus
  • 2 doses: 12 – 15 months of age & 4 – 6 years of age
  1. MMRV vaccine – measles, mumps, rubella, and varicella
    * MMR with live, attenuated VZV virus
44
Q

Corona-viridae

Recall:

+ssRNA

  • Enveloped Icosahedral (President FTR)
    • Flavi-viridae
    • Toga-viridae
    • Retro-viridae
  • Helical (The rona lol)
    • Corona-viridae
A
45
Q

SARS-CoV2

A

1. Viral structural proteins:

  • S (spike) – attachment & entry
  • M – assembly
  • E – helps with assembly & release
  • N – protects RNA

2. Spike:

  • Binds to angiotensin converting enzyme 2 (ACE2)
  • Contains a fusion domain that mediates viral/cell fusion
  • Antibodies to spike provide immunity
    • Vaccine induces antibodies to spike
46
Q

Overview of SARS-2 replication

A
  1. Entry – plasma membrane or endosome
  2. Formation of the replicase-transcriptase complex
    * Translation of the genomic RNA
  3. Additional viral proteins
  • Translated from subgenomic RNA
  • Envelope glycoproteins translated on ER
  1. New viral particle buds into the ERGIC
  2. Viral particle is released via exocytosis
47
Q

Where did coronaviruses come from?

A
48
Q

Severe acute respiratory syndrome (SARS) & Middle East respiratory syndrome (MERS)

A

SARS outbreak in 2002-2003

  1. Centered around China & Hong Kong but spread to Canada through international travel
  2. Total of 8098 cases with 774 (9.5%) deaths; no longer circulating
  3. Containment involved home quarantine, isolation, closures of hospitals & schools, travel advisories

MERS 1st reported in 2012; ongoing sporadic outbreaks; ~2600 cases

  1. Saudi Arabia & the United Arab Emirates – largest outbreaks
  2. Infection ranges from mild to severe pneumonia
  3. ~ 34% fatality rate (may be off since mild cases may not be reported)
  4. Person to person transmission is limited (close contacts)
  • No sustained transmission within the community
49
Q

SARS-CoV vs SARS-CoV-2

A
  1. SARS-CoV & SARS-CoV-2 are closely related
  • 82% homologous; nucleotide level
  • Both use angiotensin-converting enzyme 2 (ACE-2) as a receptor
  1. SARS-CoV is more pathogenic than SARS-CoV-2
50
Q

COVID-19 Clinical illness

A
  • Ranges from mild to severe (pneumonia & ARDS)
    • More severe in elderly & patients with co-morbidities
  • Initial symptoms:
    • Onset of symptoms 2-11 days after exposure; mean = 5 days
    • Cough, low grade fever, myalgias
    • Loss of smell
  • Progression (8-9 days post onset of symptoms)
    • Dyspnea, pneumonia, acute respiratory distress syndrome (ARDS)
  • Viral titers peak ~ 4 days after onset of symptoms
    • Viral RNA can be detected for several weeks after resolution of symptoms
      • May not necessarily mean infectious viral particles are present
  • Multisystem inflammatory syndrome :
    • Can occur in adults but more common in children
    • Persistent fever, abdominal pain, vomiting, diarrhea, skin rash, mucocutaneous lesions
    • Severe cases – hypotension and shock
    • Elevated laboratory markers of inflammation (e.g., CRP, ESR)
    • May develop myocarditis, cardiac dysfunction, and acute kidney injury
  • Post-acute sequelae of SARS-CoV-2 infection (also known as Long COVID)
    • Can occur in individuals who had mild acute infection;
    • Symptoms for >4 weeks after initial infection
    • Fatigue, muscle weakness, shortness of breath, trouble sleeping, “brain fog”
      • Cognitive dysfunction or memory loss that affects everyday living
    • Additional symptoms: headache, myalgia, chest pain, diarrhea, vomiting, anxiety, depression
51
Q

SARS-CoV-2 Variants

A
  • Variability – why it occurs
    • RNA polymerases make a lot of mistakes when copying RNA
    • Recombination is common among related strains of CoV
  • Potential consequences of variability
    • May change pathogenicity or infectivity
    • Easier to escape the immune response
  • Selection of immune escape mutants in the presence of an immune response
  • Increase in infectivity makes it easier to spread among susceptible hosts
52
Q

COVID-19 Management

A
  1. Remdesivir is the only FDA-approved drug for the treatment of COVID-19
  • Adenosine analog; binds to the viral RNA-dependent RNA polymerase & inhibits viral replication through premature termination of RNA transcription
  • Active against the most common SARS-CoV-2 variants
  1. Molnupiravir – new antiviral developed by Merck
  • Shown to be effective in clinical trials
  • Seeking Emergency Use Authorization (EUA) by the FDA
  • Ribonucleoside analog
  1. Anti-SARS-CoV-2 Monoclonal Antibodies
    * Can be used in non-hospitalized patients with mild to moderate COVID-19
53
Q

COVID-19 Vaccines

A
  1. Pfizer-BioNTech & Moderna
    * mRNA vaccine that encodes S protein
  2. Johnson & Johnson’s Janssen
    * Adenovirus vector expressing S protein
  3. Very affective protecting against severe illness; also protects against transmission
  4. Protects against variants, though reduced effectiveness
  5. Potential side effects
  • Fever,
  • fatigue,
  • headache,
  • redness & pain at injection site;
  • severe allergic reaction
  • Myocarditis & pericarditis (Pfizer; Moderna)
  • Blood clots with low platelets (J&J); rate – 7/106 vaccinations; women 18-49 years of age
54
Q

Enveloped, helical, -ssRNA viruses

A

-ssRNA

  • Enveloped
    • Helical (before anyone recommend food, please offer)
      • Bunya-viridae
      • Arena-viridae (-ssRNA and ambisense)
      • Rhabdo-viridae
      • Filo-viridae
      • Paramyx-viridae
      • Orthomyxo-viridae
55
Q

Orthomyxo-viridae

A
  • Helical, enveloped virus; segmented -ss RNA
  • Influenza – 3 subgroups
    • Influenza A – multiple subtypes; human, avian & swine strains
    • Influenza B – human strains
    • Influenza C – human strains but rare
  • Most cases of flu are due to influenza A & B
  • Influenza A subtypes are based on the antigenicity of hemagglutinin (HA) & neuraminidase (NA) proteins
    • Circulating strains – H3N2, H1N1pdm09

NOTE: segmented genome allows reassortment – swapping of genes between influenza viruses

56
Q

Influenza A–Viral Proteins

A

Image

57
Q
A

microbiology (6 decks)

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