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MICROBIOLOGY > LECTURE 15 (Virology) > Flashcards

LECTURE 15 (Virology) Flashcards

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1
Q

How are viruses different from other microorganisms?

A
  • Viruses are not cells
  • Not capable of independent replication (cannot synthesise their own energy or their own proteins)
  • Too small to be seen in a light microscope
  • Particles composed of an internal core containing either DNA or RNA (not both) covered by a protective protein coat (CAPSID)
  • ONLY VIRUSES have genetic material composed of single-stranded DNA or of single-stranded or double-stranded RNA
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2
Q

Describe the virus structure

A
  • Nucleic acid genome (DNA or RNA) surrounded by protein shell “CAPSID”
  • Some human viruses packaged into a LIPID MEMBRANE/ENVELOPE (usually acquired from cytoplasmic membrane of infected during release from cell)
  • Genomes of enveloped viruses form protein complex “NUCLEOCAPSID” + surrounded by MATRIX which serves as bridge between nucleocapsid and inside of viral membrane
  • “SPIKES” protrude from surface of virus + involved in initial contact with host receptors
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3
Q

What is the function of the Capsid/Envelope?

A
  • To protect nucleic acid genome from damage
  • To aid in process of entry into cell
  • To package enzymes for early steps of infection process
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4
Q

What are some examples of Enveloped and Non-enveloped viruses?

A

Enveloped virus = HIV, HSV, HBV & Influenza virus

Non-enveloped virus = Norovirus, Parvovirus, HAV, HEV

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5
Q

Describe the envelope structure

A
  • Outer lipid bilayer membrane called “ENVELOPE”
  • Viral envelope contains “spikes”, “peplomers” or “viral envelope proteins” -> bind to host receptors + antigens for immune response
  • “MATRIX PROTEIN” serves as a bridge between nucleocapsid and inner membrane of envelope
  • MORE SENSITIVE to detergents (solvents, ethanol, ether, heat) compared to non-enveloped viruses
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6
Q

What are capsids/nucleocapsids?

A

Capsids/Nucleocapsids = virus-encoded specific proteins that protect the genome and confer shapes to viruses

PROPERTIES:
- composed of many copies of one/different kinds of protein subunits
- presence of many identical protein subunits in viral capsids + existence of identical spikes in envelope membrane -> important in adsorption, haemagglutination + recognition of viruses by neutralising antibodies

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7
Q

Describe the genome structure

A
  • Either DNA or RNA
  • Either single-stranded DNA/RNA or double-stranded RNA
  • Either POSITIVE SENSE (polarity of mRNA) or NEGATIVE SENSE (complementary to/antisense of mRNA) or AMBISENSE (++ –)
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8
Q

What are the steps of Virus replication?

A

1) ADSORPTION of the virus specific to receptors on the cell surface
2) PENETRATION by the virus + intracellular release of nucleic acid
[cell engulfs virus by endocytosis]
3) PROLIFERATION of viral components
[virus-coded synthesis of capsid and non-capsid proteins + replication of nucleic acid by viral and cellular enzymes]
4) ASSEMBLY of replicated nucleic acid + new capsid protein
5) RELEASE of virus from cell into ECF

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9
Q

What are the different virus replication effects that can happen?

A
  • Non-productive response = when some viruses enter a host cell but no new virus is produced -> the cell survives and divides and the viral genetic material persists indefinitely in a latent-state
  • Persistent infection = A “chronic infection” where a low level of virus is produced with little or no damage to target tissue
  • Abortive infection = early viral proteins that cause cell death
  • Lytic/Virulent viruses = Viruses that enter only into a productive relationship
  • Temperate viruses = viruses that establish either a productive/non-productive relationship with host cell
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10
Q

What are the possible consequences of viral infection for the host cell?

A
  • CYTOCIDAL INFECTION (NECROSIS) = cell destruction
  • APOPTOSIS = cell suicide -> interrupts viral replication cycle
  • NONCYTOCIDAL INFECTION = does not destroy host cell (but may be destroyed by secondary immunological reactions)
  • LATENT INFECTION = neither replicates or destroys
  • TUMOUR TRANSFORMATION = viral infection transforms into a cancer cell
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11
Q

What is the pathogenesis of viruses?

A

1) Transmission of virus + entry into the host
2) Replication of virus + damage to cells
3) Spread of virus to other cells + organs
4) Immune response
5) Persistence of virus in some instances

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12
Q

Describe how viruses are transmitted + portal of entry

A
  • Main portals are respiratory, GI and genital tracts, skin, across placenta, blood
  • Transmission from mother to offspring is “VERTICAL TRANSMISSION” + all other transmissions (faecal-oral, respiratory aerosol, insect bite) are “HORIZONTAL TRANSMISSION”
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13
Q

What are symptoms of viral disease usually caused by?

A

Death of infected cells and a consequent loss of function

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14
Q

What is Immunopathogenesis?

A

The process by which the symptoms of viral disease are caused by the immune system rather than the killing of cells by the virus

TYPES:
- Killing of virus-infected cell by cytotoxic T cells
- Formation of virus-antibody complexes deposited in the tissues

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15
Q

Describe the Innate immune response

A
  • Largely mediated by IFNs
    [induce expression of enzymes that block viral replication -> antiviral state]
  • Able to recognise viruses as “foreign”
  • Presence of cytokines is one of the earliest indications of viral infection
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16
Q

Describe the adaptive immune response

A
  • Second-line of defence if innate defences are overwhelmed
  • Comprised of antibodies + immune cells (B cells and T cells)
  • Key feature: MEMORY
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17
Q

What are the several ways of immune evasion?

A
  • Some viruses encode the receptors for various mediators of immunity (e.g IL-1 and TNF) -> when released from virus-infected cells, proteins bind to immune mediators + block their functions -> “CYTOKINE DECOYS”
  • Reduce the expression of MHC class I proteins -> reducing ability of cytotoxic T cells to kill virus-infected cells
  • Synthesis of RNAs that block phosphorylation of an initiation factor (eIF-2) -> reduces ability of interferon to block viral replication
  • Have multiple antigenic types (serotypes)
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18
Q

How do viruses affect the immune system?

A
  • CYTOTOXIC T CELLS = reduces MHC class I proteins -> decreases killing by cytotoxic T cells
  • HELPTER T CELLS (Th-1) = Block IL-12 which reduces formation of Th-1 cells -> decreases cell-mediated immunity
  • INTERFERON = blocks synthesis of IF by virus-infected cells + blocks synthesis of kinase that phosphorylates initiation factor-2
  • INTERLEUKINS = encode receptors for immune mediators (secreted by infected cells) -> bind mediators + inactivate them
  • CHEMOKINES = encode chemokine-binding protein -> inhibits migration of inflammatory cells to sites of infection
  • COMPLEMENT = encodes protein that binds to C3b -> blocks opsonisation + ability to participate in forming the membrane attack complex
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19
Q

What are the different states that viruses can persist in the host?

A
  • Carrier state = people who produce virus for long periods of time + serve as a source of infection for others
    (e.g hepatitis C)
  • Latent infections = do not produce virus at present time but can be reactivated at a subsequent time
    (e.g herpes)
  • Slow virus infections = diseases with a long incubation period
20
Q

What are the direct and indirect methods in which viruses can be diagnosed?

A

DIRECT METHODS
- virus isolation
- genome detection
- NS1 detection

INDIRECT METHODS
- serology IgM
- serology IgG

21
Q

What are the different lab procedures that can detect viruses?

A
  • Identification in Cell culture
    [“cytopathic effect” (CPE) in cell culture + antibody-based test e.g fluorescent antibody, complement fixation, ELISA]
  • Microscopic identification
    [Inclusion bodies seen in nucleus/cytoplasm of infected cells + Multinucleated giant cells + Electron microscopy]
  • Serologic procedures
    [presence of IgM = diagnose current infection, presence of IgG = not used to diagnose current infection]
  • Detection of viral antigens & nucleic acids
22
Q

What is Selective toxicity?

A

The ability of a drug to inhibit viral replication without significantly damaging the host cell

ADDITIONAL INFO:
difficult to achieve a high degree of selective toxicity with antiviral drugs since virus can only replicate within cells + uses many cellular functions

23
Q

What are the different types of Antiviral drugs and their MOA?

A
  • Nucleoside/Nucleotide analogs
  • Reverse transcriptase inhibitors
  • Protease inhibitors
    [inhibit viral protease required at late stage of replicative cycle to cleave the viral polypeptide]
  • Integrase inhibitors
    [lock activity of “viral integrase” -> without integration of virally encoded DNA into host chromosome, life cycle cannot continue]
  • Fusion inhibitors = disrupt fusion of viral envelope with cell membrane
24
Q

What are the two classes and the different types of vaccines?

A

CLASSES:
- those that contain live virus whose pathogenicity has been attenuated
- those that contain killed virus

DIFFERENT TYPES:
- live attenuated vaccine
- chimeric live attenuated vaccine
- inactivated vaccine
- subunit vaccine
- nucleic acid-based vaccine

EXPLANATION: the purpose of viral vaccines is to use the adaptive immune response of the host to prevent viral disease

25
Q

Why are live viral vaccines preferable to killed vaccines?

A
  • Induce a higher titer of antibody -> longer-lasting protection
  • Induce a broader range of antibody (both IgA and IgG, not just IgG)
  • Activate cytotoxic T cells -> kill virus-infected cells
26
Q

What is the disadvantage of live-viral vaccines?

A
  • Reversion to virulence -> should not be given to immunocompromised individuals or to pregnant women
  • Vaccines grown in chick embryos should not be given to those with an anaphylactic reaction to eggs
27
Q

Describe the structure of a bacteriophage

A
  • Capsid head
  • Nucleic acid (DNA)
  • Tail (composed of collar + sheath)
  • Baseplate
  • Spikes/Tail fiber
28
Q

Which viruses are Orthomyxoviruses and Paramyxoviruses?

A

ORTHOMYXOVIRUSES
- influenza virus

PARAMYXOVIRUSES
- parainfluenza viruses
- measles virus
- mumps virus

29
Q

What are the different types of Influenza?

A
  • Influenza A
    [causes worldwide epidemics (pandemics) of influenza + main host are humans, swine, avians, equines, marine animals, bats]
  • Influenza B
    [causes major outbreaks of influenza + main host are humans and seals]
  • Influenza C
    [causes mild respiratory tract infections but does not cause outbreaks of influenza]

EXPLANATION: Pandemics occur when a variant of influenza A virus that contains a new haemagglutinin against which people do not have pre-existing antibodies is introduced into the human population

30
Q

Describe the structure of Influenza

A
  • Composed of a segmented single-stranded RNA genome + a helical nucleocapsid + an outer lipoprotein envelope
  • Contains an RNA-dependent RNA polymerase -> transcribes the NEGATIVE-POLARITY genome into mRNA
  • Envelope covered with spikes [HEMAGGLUTININ + NEURAMINIDASE]
31
Q

What is the function of Hemagglutinin and Neuraminidase?

A

Hemagglutinin = binds to cell surface receptor to initiate infection of cell

Neuraminidase = cleaves neuraminic acid (sialic acid) to release progeny virus from infected cell

32
Q

Influenza viruses show changes in antigenicity of their hemagglutinin and neuraminidase proteins, what are the two types of antigenic changes?

A
  • Antigenic shift = major change based on reassortment of segments of the genome RNA
    [appear infrequently]
  • Antigenic drift = minor change based on mutations in the genome RNA
    [appear virtually every year]
33
Q

What is a Non-structural protein called “NS-1”?

A

An important determinant of the virulence of the virus encoded by the genome

FUNCTION:
Inhibits the production of Interferon mRNA -> innate defences are reduced + viral virulence is correspondingly enhanced

34
Q

Describe the antigenic drift/shift in influenza A and B

A
  • Influenza A animal viruses are the SOURCE OF RNA SEGMENTS that encode the antigenic shift variants that cause epidemics among humans
  • Influenza B has no animal source of new RNA segments -> does NOT undergo antigenic shifts -> but undergoes enough antigenic drift that current strain must be included in new influenza vaccine each year
35
Q

What is Influenza?

A

An infectious disease that is caused by influenza viruses

TRANSMISSION & EPIDEMIOLOGY:
- Transmitted by airborne respiratory droplets
- Occurs in winter months in northern hemisphere but year-round in tropics
- Bacterial pneumonia secondary to influenza cause a significant number of deaths (especially in elderly)

PATHOGENESIS:
- After virus in inhaled, NEURAMINIDASE degrades the protective mucous layer, allowing virus to gain access to cells of upper + lower respiratory tract

SYMPTOMS:
- Fever
- Myalgia
- Headache
- Sore throat
- Cough

COMPLICATIONS:
- Pneumonia caused by Staphylococcus aureus
- Reye’s syndrome
[encephalopathy + liver degeneration -> life-threatening complication in children after influenza B exposure]

LAB DIAGNOSIS:
- FLU OIA and QuickVue tests -> detect viral antigen using monoclonal antibodies
- ZSTATFLU tests -> detect viral neuraminidase

PREVENTION:
- immunisation

36
Q

What do Parainfluenza viruses cause?

A
  • “Croup” (acute laryngotracheobronchitis), laryngitis, bronchiolitis and pneumonia is CHILDREN
  • A disease resembling the common cold in ADULTS
37
Q

Describe the structure of Paramyxoviruses

A
  • Composed of one piece of single-stranded RNA, a helical nucleocapsid and an outer lipoprotein envelope
  • Contains RNA dependent RNA Polymerase -> transcribes NEGATIVE-POLARITY genome into mRNA
  • Contain a hemagglutinin + neuraminidase on the same spike
38
Q

What are the different types of Parainfluenzas?

A
  • Parainfluenza 1 = major cause of “acute croup” (laryngotracheitis) in infants/young children + URI, pharyngitis and tracheobronchitis in all ages + outbreaks occur in fall months
  • Parainfluenza 2 = associated with croup, mild URI and acute lower respiratory disease in children + outbreaks occur in fall months
  • Parainfluenza 3 = major cause of severe lower respiratory disease in infants and young children + URI or tracheobronchitis in adults + happens in all seasons
  • Parainfluenza 4 = least common + associated with mild upper respiratory illness only
39
Q

What is the progression of Parainfluenza viruses?

A

Onset begins as a mild upper respiratory infection with variable progression over 1-3 days to involvement of middle or lower respiratory tract

Duration varies from 4-21 days but is usually 7-10 days

40
Q

What is Respiratory Syncytial Virus?

A

The most important cause of pneumonia and bronchiolitis in infants and causes otitis media in children and pneumonia in elderly + chronic cardiopulmonary patients

PATHOGENESIS:
infects the bronchi, bronchioles and alveoli of lung -> acute phase of cough, wheezing and respiratory distress lasts 1-3 weeks

TRANSMISSION & EPIDEMIOLOGY:
- Occurs via respiratory droplets + direct contact of contaminated hands with nose or mouth
- Causes outbreaks of respiratory infections every winter + in hospitalised infants

SYMPTOMS:
- Fever
- Dry or wet cough + difficulty breathing/wheezing
- Sneezing + runny nose
- Loss of appetite/refuse breastfeed

DIAGNOSIS:
- Virus isolation (usually in monkey kidney cell cultures)
- PCR
- Serology
- Immunofluorescence or immunoenzyme assays

TREATMENT:
- Adequate oxygenation + ventilatory support
- Close observation for bacterial super-infection and right-sided heart failure
- Ribavirin aerosol

PREVENTION:
- Monoclonal antibody + immune globulin for prophylaxis
- No vaccine
- Breastfeeding (to increase immunity naturally)
- Avoid crowded areas

41
Q

Describe the Respiratory Syncytial Virus (RSV)

A
  • Causes syncytium formation in cell cultures
  • Enveloped RNA virus has a linear (unsegmented) genome
  • Two glycoproteins (G and F) mediate attachment and syncytium formation
  • Most important respiratory virus that causes severe infection in infants
42
Q

What are the common epidemiological and clinical characteristics of Measles and Mumps?

A
  • Worldwide distribution with a high incidence of infection in non-immune individuals
  • Humans are sole reservoir
  • Person-to-person spread by respiratory (aerosol) route
43
Q

What is Measles?

A

A highly contagious virus caused by measles virus that is characterised by a maculopapular rash. It’s a Paramxyovirus (Morbillivirus), envelope, single-stranded RNA.

Incubation period is 10-14 days + duration is 3-5 days

TRANSMISSION:
- via respiratory droplets produced by coughing + sneezing (during prodromal period + few days after rash appears)

PATHOGENESIS:
Inoculation of respiratory tract + local replication in respiratory tract -> Lymphatic spread + Viremia -> Wide dissemination (conjunctivae, respiratory tract, urinary tract, small blood vessels, lymphatic system, CNS) -> Virus-infected endothelial cells + immune T cells -> Rash -> Recovery (have life-long immunity)

COMPLICATIONS:
- Post-infectious encephalitis
- Subacute sclerosing panencephalitis (defective measles virus infection of CNS)
- No resolution of acute infection due to defective CMI

SYMPTOMS:
- Fever
- Cough
- Conjunctivitis
- Koplik spots
[bright red lesions with a white , central dot located on buccal mucosa]

DIAGNOSIS:
- Usually diagnosed with symptoms
- Cell culture
- PCR

TREATMENT:
- No antiviral therapy

PREVENTION:
- Live, attenuated vaccine given at 15 months
[vaccine should not be given before 15 months since maternal antibody in child can neutralise the virus + reduce immune response]

44
Q

What is Mumps?

A

A disease characterised by parotid gland swelling that occurs primarily in childhood and is caused by the Mumps virus.

Incubation period of 18-21 days and duration is 1 week

TRANSMISSION & EPIDEMIOLOGY:
- via respiratory droplets
- occurs world-widee with peak incidence in winter
- spreads airborne (coughing, sneezing), saliva (kissing, sharing drinks) and touching contaminated surface
- occurs in 5-15 years, rarely <1 years

PATHOGENESIS:
- infects upper respiratory tract and then spreads through blood to infect parotid glands, testes, ovaries, pancreas and sometimes meninges
- Lifelong immunity occurs in those who have had it

SYMPTOMS:
- Fever + malaise
- Tender swelling of parotid glands
- Loss of appetite
- Pain when eating, in ears, jaw and chin and on both sides of face

DIAGNOSIS:
- Clinically (symptoms)
- Laboratory tests

TREATMENT:
- No antiviral therapy

PREVENTION:
- Live, attenuated vaccine
- Two immunisations: at 15 months then at 4-6 years
[vaccine should not be given to immunocompromised people or pregnant women]

45
Q

What are the differences between Orthomyxoviruses and Paramyxoviruses?

A

ORTHOMYXOVIRUSES:
- No giant cell formation
- Hemagglutinin and neuraminidase on DIFFERENT spikes

PARAMYXOVIRUSES:
- Giant cell formation
- Hemagglutinin and neuraminidase on SAME spike

MICROBIOLOGY (14 decks)

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