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Microbiology II > General Virology (Dustin) > Flashcards

General Virology (Dustin) Flashcards

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1
Q

General description of viruses

A
  • Infectious genetic information: either DNA or RNA
  • Obligate intracellular parasite: independently cannot reproduce, make energy, or synthesize proteins
  • 20-300nm
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2
Q

5 structural aspects of viruses

A
  1. Capsid: protein shell enclosing the nucleic acid genome
  2. Capsomeres: outer covering proteins on the capsid
  3. Nucleocapsid: protein-nucleic acid complex representing packaged form of viral genome
  4. Viral nucleic acids
  5. (optional) Envelope: host lipids, carbs + viral peptides (peplomers). Much more protective.
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3
Q

How are nucleocapsids categorized?

A

By symmetry:

  • Helical: proteins bound periodically to viral nucleic acid, winding it into a helix. Flexible or rigid.
  • Cubical: icosahedral pattern. Capsomeres arranged in 20 triangle faces.
  • Complex: pox virus
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4
Q

6 properties of viruses used for classification

A
  1. RNA or DNA
  2. Single vs Double-Stranded
  3. Circular or Linear nucleic acids
  4. Capsid symmetry
  5. Enveloped or not
  6. Size (nm)
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5
Q

5 features of viral nucleic acids

A
  1. RNA or DNA
  2. SS or DS
  3. Circular or Linear
  4. Segmented or not
  5. Usually only single copy of genome (haploid) except retrovirus are diploid
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6
Q

What is a viroid?

A

Smallest infectious agent of virus. Naked, closed circles of SS RNA, 300-400 nucleotides. Form diseases in plants but not known in humans

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7
Q

What is a prion?

A

Infectious protein particle, capable of self-reproduction. 50-100 kDa.

Examples: scrapie, CJD, BSE, Kuru

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8
Q

How do viruses propagate / what are the steps?

A
  1. Attachment: with specific receptor on host cell (specific to cells of various species or tissues)
  2. Penetration: receptor-mediated endocytosis, membrane fusion (if enveloped), or bacteriophage mode (attach tail and use lysozyme to degrade cell wall)
  3. Uncoating: viral nucleic acid freed
  4. Eclipse period: intense synthetic activity
  5. Assembly: viral genomes and capsids are put together
  6. Release: either by rupture (non-enveloped) or budding (enveloped, cell may survive)
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9
Q

Molecular bases of the biosynthesis of viruses: productive infection

A

Need mRNA to make structural proteins for (new) progeny viruses.

  • RNA viruses: positive strand ones work as mRNA and synth proteins right away, neg strand ones must first be converted to pos RNA by RNA-dependent RNA polymerase
  • DNA viruses: DNA transcribed to mRNA
  • Retrovirus: viral RNA -> DNA by reverse transcriptase, then from DNA -> mRNA
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10
Q

Latent and persistent viral infections

Risks of latency?

A

Persistent: virus remains for a long period of time either intact or in the genome

Latent: after initial infection, virus is persistent by laying dormant (“lysogenic viral life cycle”). Infection can recur at some point. Different than chronic infection (virus is constant problem). Latency is typical feature of herpes virus family.

Besides recurring, latent viruses can cause uncontrolled cell proliferation / neoplasia (HPV). Latency in some cells infected with HIV is important as it maintains a reservoir that it is not yet possible to eliminate.

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11
Q

Congenital viral infections: 6 important examples

A
  1. Rubella: classic triad of cataracts, heart defect, sensory-neural deafness
  2. CMV: most common. Often causes mental retardation and various other CNS or organ problems
  3. Varicella-Zoster: rare but great risk of CNS and eye defects
  4. Neonatal Herpes Simplex: HSV1 or 2, infection during delivery. Can become disseminated.
  5. HIV: somewhat low chance of transmission but severe consequences
  6. Parvovirus B19: often causes abortion
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12
Q

Two classes of tumor viruses and most important examples of viruses that cause tumors:

Common function:

A
  1. DNA viruses: HPV 16 and 18, EBV, HBV, HHV-8
  2. RNA viruses (retroviruses with ss positive-sense RNA): Human T-lymphotropic virus, HCV

Both types integrate into host genome

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13
Q

What is the difference between acute and slowly transforming tumor viruses?

A

Acute: overactive oncogene (v-onc) that alters the infected cell as soon as v-onc is expressed.

Chronic: not v-onc, but cause transformation long after infection by insertional mutagenesis. Usually cause leukemia

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14
Q

Some specifics on genes/proteins by which these types of viruses can cause neoplasia, and what types of neoplasia they cause:

  • HPV
  • EBV
A
  • HPV: encode proteins that bind/inactivate cell growth regulatory proteins (e.g. p53, RB). HPV 16 and 18 cause cervical carcinoma.
  • EBV: stimulates cell growth (B-mitogen) and inducing Bcl-2 oncogene, preventing apoptosis. Has c-myc oncogene, causing t(8:14). Causes Burkitt lymphoma, Nasopharyngeal carcinoma, Hodgkin lymphoma
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15
Q

3 broad mechanisms of any viral tumor formation

the same as all tumor formation, answer is easy but just putting it for completeness sake

A
  1. Activation of oncogenes: provide stimulating growth gene
  2. Elimination of tumor suppressor genes / proteins that limit cell growth
  3. Inhibiting apoptosis / blocking apoptotic signals
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16
Q

What are the host defense mechanisms for viruses?

A
  1. Barriers: skin, mucous, gastric acid, etc.
  2. Non-specific innate immune system: fever, interferons, NK cells, macrophages
  3. Later, the specific immune system responds with antibody formation and memory B and T cells
17
Q

What stimulates interferon production? What are the functions?

A
  • Stimulated by dsRNA, viral glycoproteins, or LPS
  • Function: inside the cell it has RNA endonuclease activity and inhibits cell growth (increase p53 activity). Outside the cell it activates neighboring cells to also have anti-viral properties: increasing MHC-I viral peptide presentation, also activating Tc and NK cells to kill virus-infected cells.
18
Q

What are the 3 different types of interferons?

A

INF-alpha: produced by leukocytes. Induced by viral nucleic acids, proteins, etc. Especially dsRNA.

INF-beta: produced by fibroblasts, epithelial cells, etc. Induced by viral nucleic acids, especially dsRNA

INF-gamma: produced by unsensitized lymphoid cells or sensitized Th1 cells. Strongest INF. Induced by foreign antigens.

(alpha and beta also called type 1 interferons; gamma is type 2)

19
Q

How do viruses react with T lymphocytes?

A
  • Cytotoxic T cells recognize viral MHC-I peptides, NK cells also kill related to MHC-I presentation.
  • Helper T cells produce cytokines, especially INF-gamma, which stimulates strong anti-viral response from various cells
20
Q

How do viruses react with B lymphocytes?

A

B cells produce antibodies specific for certain viral antigens, which is only really effective if the viral antigens are present in the extracellular spaces.

Antibodies block extracellular viruses from interacting with new cells (prevents viremia), or they can sometimes attack virus-infected cells that are presenting viral antigens (antibody-dependent cell-mediated cytotoxity)

21
Q

How do viruses react with RBCs?

A
  • Influenza, parainfluenza, and mumps have Haemagglutinin (H) antigen, which binds RBCs of various animal species. Used in viral diagnostics.
  • Mumps and measles can cause hemolysis of agglutinated cells
  • Hemadsorption: certain virally-infected (influenza, parainfluenza, mumps) cell cultures bind to added RBCs, used in viral diagnostics
22
Q

What is viral interference?

What are some known mechanisms for viral interference?

A

When a cell is infected with one virus, it becomes resistant to infection from other types of viruses.

Mostly works because INF-gamma is being produced in relation to the virus-infected cell, and so it’s already resistant to infection. May also work because the viruses have to compete to use various cellular components.

23
Q

Immune suppressing effect of viruses: 4 examples of viruses and how they alter host’s ability to respond to infection

A
  1. CMV: viral protein inhibits NK cell activity
  2. Measles: depresses ability of uncommitted lymphocytes to begin replication and differentiation, also inhibits APC effect by blocking IL-12 secretion
  3. HIV: destroys CD4+ T cells and disrupts macrophage function
  4. HBV: can infect thymus, causing clonal deletion of maturing virus-specific T cells (especially in peri-natal infection)
24
Q

Immune suppressing effect of viruses: examples how viruses evade T cell recognition
(6 are listed)

A
  1. HSV and VZV remain latent in neurons, undetected
  2. Measles, rubella also persist in neurons, and neurons won’t have MHC-I presentation
  3. EBV, CMV persist in the salivary gland, which is not accessible to the immune system
  4. EBV is latent in B cells, only producing EBNA-1 and no other viral peptides, so there is no cytotoxic T cell response
  5. CMV, HSV, HIV suppress expression of MHC-I
  6. CMV, HIV, and measles suppress expression of MHC-II
25
Q

4 potential interactions between viruses and host cells

A
  1. Cytolytic productive infection: host cell is killed
  2. Non-cytolytic productive infection: virus released by budding. May be persistent infection as a result.
  3. Abortive / non-productive: virus can’t replicate because either the virus is defective or the cell is resistant (“non-permissive”)
  4. Latency: Virus is maintained in the cell but doesn’t replicate. (HSV, VZV, CMV, EBV, HIV). Some types cause malignant transformation.
26
Q

4 types/patterns of viral infections

A
  1. Acute
  2. Chronic
  3. Slow infections: takes a while after infection for disease to develop, e.g. measles encephalitis (SSPE). More typical of prions.
  4. Latent

Can also be grouped as symptomatic vs asymptomatic

27
Q

4 stages of a typical virus infection

A
  1. Incubation: asymptomatic
  2. Prodromal: non-specific symptoms, e.g. fever
  3. Specific-illness period: has some sort of pattern used to identify the disease
  4. Recovery: depends on virulence and host susceptibility. Potentially remains in chronic, latent, or carrier state
28
Q

5 portals of entry for viruses, and some examples of viruses for each

A
  1. Skin / skin puncture: papilloma viruses, rabies, HBV, HCV, HDV, HIV
  2. Respiratory tract: influenza, rhinovirus, MMR, hantavirus, adenovirus
  3. GI tract: adenovirus, rotavirus localized in GI. HAV and polio become systemic. Anus for HIV.
  4. Genital tract / STIs: papillomavirus, HBV, HIV, HSV-2
  5. Transplacental: CMV, Rubella, VZV, HBV, HIV, Parvovirus B19
29
Q

Ways that viruses are shed from the body and can be spread + some examples of viruses for each

(there are 8 listed, really too many but just try to remember some examples)

A
  1. Skin lesions: HSV, papillomaviruses
  2. Respiratory secretions
  3. Saliva: mumps, EBV, rabies
  4. Feces: enteric viruses, rotaviurs, HepA
  5. Urine: adenoviruses
  6. Genital secretions: HIV, HepA/B, papillomaviruses, HSV-2
  7. Milk: HIV, CMV
  8. Blood: HBV, HCV, CMV, EBV, HIV
30
Q

4 pathogenesis mechanisms that must occur for a viral disease to develop

A
  1. Implantation
  2. Replication
  3. Dispersal: spreads to other target cells
  4. Shedding: virus spreads to outside environment
31
Q

Mechanisms for prevention of viral diseases

A

Vaccines: necessary because few drugs are effective against viruses.

  • Live vaccine/attenuated virus: greater protection but risk of virulence. MMR, Polio, Rabies, Influenza, HepA
  • Subunit vaccines: e.g. HBV surface antigen, made with recombinant genetic engineering

-Passive immunity: inject immunoglobulins. Rabies. HBIg: neonate with mother HBV carrier. VZIg: immunocompromised person exposed to VZV. HAIg: travelers exposed to HepA

Microbiology II (8 decks)

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