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VIROLOGY JK > EXAM I > Flashcards

EXAM I Flashcards

1
Q

Which of the following is NOT true about Innate immunity?

A. Provide critical first line of defense

B. Constant presence

C. Occurs immediately following infection

D. Innate immunity lasts for up to 12 hours.

E. Does not have antigen specificity or memory.

A

D. Innate immunity lasts for up to 12 hours.

Innate immunity lasts for a few days.

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2
Q

T/F. Primary physical and chemical defenses include skin, mucous membranes, GIT, respiratory tract, NK cells.

A

True.

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3
Q

T/F. NK cells have antigen specific receptors.

A

False. They are not antigen specific.

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4
Q

What are the two factors that are needed to activate NK cells?

A

Differential engagement of cell surface receptors + pro-inflammatory cytokines.

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5
Q

What is the correct statement about the reaction between NK cells and virus infected cells?

A. Decreased in Class I MHC molecule expression > inhibitory receptors are not engaged and ligands for activating receptors are expressed in virus infected cells > NK cells activated > APOPTOSIS

B. Decreased in Class I MHC molecule expression > inhibitory receptors are not engaged and ligands for activating receptors are expressed in healthy cells NK cells activated > APOPTOSIS

C. NK cells are usually attached to normal/healthy cells.

D. When both healthy cells and virus infected cells are recognized > APOPTOSIS

A

A. Decreased in Class I MHC molecule expression > inhibitory receptors are not engaged and ligands for activating receptors are expressed in virus infected cells > NK cells activated > APOPTOSIS

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6
Q

T/F. Pattern recognition receptors (PRR) recognize specific (PAMPs), which are present in viruses and host cells, such as Toll-Like Receptors (TLRs).

A

False. NOT ON HOST CELLS!

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7
Q

T/F. PRR are expressed endothelial cells and mucosal epithelial cells, as well as other phagocytic cells.

A

True.

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8
Q

Find the statement that is false.

A. Phagocytic cells and endothelial cells = increased production of inflammatory mediators and cell-surface expression of adhesion molecules.

B. Macrophages = initiate chemotaxis to bring neutrophils to site of action.

C. Adaptive immune response initiates expression of IFNs and inflammatory cytokines (TNF and IL1, 12).

A

C. Adaptive immune response initiates expression of IFNs and inflammatory cytokines (TNF and IL1, 12). INNATE IMMUNE!

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9
Q

T/F. Persistent activation of PPRs by viruses can cause continuous production of inflammatory mediators and chemotaxix > IMMUNOPATHOLOGY

A

TRUE

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10
Q

Find the incorrect statement about NK cells.

A. Important in localized infection.

B. Non-specific resistance against viral infections.

C. Eliminate infected cells by apoptosis.

D. Use perforin and granzymes, and release cytoplasmic granules.

E. Acquire cytokines from lymphocytes to proliferate.

F. The important function of interleukins is for growth and proliferation.

G. Produced within a few hours after viral invasion.

A

E. Acquire cytokines from lymphocytes to proliferate. They can synthesize and release their own cytokines to grow and proliferate!

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11
Q

What is the correct statement regarding Interferons?

A. A group of cytokines that are secreted by epithelial cels in response to infections.

B. Virus specificity.

C. RNA viruses are stronger inducers of interferon than DNA viruses.

D. Should be administered orally.

A

C. RNA viruses are stronger inducers of interferon than DNA viruses. A. secreted by somatic cells. B. NOT virus specific. D. IV!!

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12
Q

Describe components of Type I Interferon.

A

2 MAJOR TYPES

IFN-aa: Leukocyte interferon. Produced in large quantities by dendritic cells. Produced in small quantities by macrophages, lymphocytes, monocytes. Not host specific

IFN-bb: Fibroblast interferon Host specific

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13
Q

Describe components of Type II Interferon

A

IFN-gg: Immuno-regulatory, Produced by antigen-stimulated (T cells, NK cells), Labile at pH 2, Host specific

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14
Q

Describe components of Type III Interferon

A

IFN-II1, II2, II3: Immuno-regulatory, Recent Viral infections, activation of TLRs

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15
Q

Which of the following is not correct statement about roles of type-I IFNs?

A. Inhibit virus replication in host cells and activate NK cells.

B. Decrease expression of MHC-I molecules and antigen presentation.

C. Stimulate and maturation of macrophage release.

D. Stimulates memory T cell proliferation.

A

B. Decrease expression of MHC-I molecules and antigen presentation. INCREASE.

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16
Q

Matching game!

A. Latent ribonuclease (RNAse L. RNAse)

B. Synthesis of Mx proteins.

C. Synthesis of Protein Kinase R (PKR)

  1. bind and trap viral nucleocapsid and inhibit virus assembly.
  2. degrades viral RNA.
  3. prevents initiation of translation of viral RNA.
A

A - 2 B - 1 C - 3

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17
Q

What is NOT true about RNAi (Gene silencing)?

A. Small, interfering, RNA molecules.

B. regulating normal developmental and physiological processes and to interfere with virus replication.

C. Initiate formation of RNA-silencing complex.

D. Protease: degrades mRNAs that are complementar to RNAi

A

D. Protease: degrades mRNAs that are complementar to RNAi ENDONUCLEASE

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18
Q

KNOW THE GENERAL THINGS ABOUT ADAPTIVE IMMUNITY!

A

Humoral and cellular components. Cellular immunity: T lymphocytes, Antigen specific; response take a few days, mediated by lymphocytes that have surface receptors that are specific to each pathogen. Long term memory.

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19
Q

What is incorrect about granulocytosis?

A. due to increased number of granulocytes in peripheral blood.

B. Affected by viral infections.

C. cells that are involved are neutrophils, eosinophils, basophils, mast cells.

A

B. Affected by viral infections.

Viral infections DO NOT provoke granulocytosis.

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20
Q

T/F. Humoral immunity is involved in recognizing viral capsid and envelope, which are antigenic.

A

True.

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21
Q

T/F. Antibodies may be directed against viral proteins on free virions or against viral proteins expressed on surface of infected cells.

A

True.

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22
Q

What is the difference between virus neutralization and opsonization?

A

Virus neutralization: antibodies prevent virus attachment and entry into host cells (bind to capsid or envelope). Opsonization: coating of virions with antibodies > recognized and phagocytosed by macrophages and neutrophils.

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23
Q

What is not a component of activation of complement system?

A. Opsonization B. Chemotaxis C. Neutralization D. Lysis E. Agglutination

A

C. Neutralization

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24
Q

What is the process called when antibodies bind to viral antigens expressed on surface of host cells and the antigens are destroyed by phagocytes?

A

Antibody-Dependent Cell-mediated cytotoxicity (complement mediated cytolysis)

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25
Q

What is immuno-complex formation (antiviral effects of antibodies)?

A

Decreased number of viral particles available for cell invasion.

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26
Q

Which cells are involved in cell mediated immunity and what are their roles?

A

Helper T lymphocyte: activation of macrophages, inflammation, stimulation of B lymphocytes.

Cytotoxic T lymphocytes: killing of infected cell.

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27
Q

What are the roles of cytotoxic T lymphocytes? (choose all that apply)

A. Produced in the cytosol and transport to the ER where they associated with class I MHC molecules.

B. Recognized by Antigen-Specific Cytotoxic T lymphocytes.

C. Recognize MHC-I complexes by TCRs and CD8 molecules and kill the cells.

D. Release pore-forming proteins called perforins.

E. Granzymes and chemokines are proteolytic enzymes, which are involved in apoptosis.

A

ALL OF THEM!!

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28
Q

T/F. (Evasion of immune system) Antigenic plasticity is rapid changes in the structure of the viral antigen, which may be the result of mutation (drift), reassortment, (shift) or recombinaton. This will increase resistance.

A

TRUE

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29
Q

T/F. (Evasion of immune system) Antigenic multiplicity is antigenic variants with many or cross-reactivity (100 serotypes > antigenically different). Immunity against one serotype is not enough.

A

False. LITTLE OR NO CROSS-REACTIVITY.

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30
Q

Match the correct statement.

A. Risk Group I B. Risk Group 2 C. Risk Group 3 D. Risk Group 4

  1. Cause disease to animals and humans; unlikely to cause serious hazard; moderate individual risk; spread of infection is limited; Herpes virus, SLOW virus.
  2. Causes serious human and animals diseases; increased individual and community risk; can spread readily (indirect/direct); Foot and mouth disease.
  3. Unlikely to cause diseases; no individual/community risk; Adeno-associated virus.
  4. Cause serious human and animals diseases; increased individual risk; HIV, rabies.
A

A - 3 B - 1 C - 4 D - 2

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31
Q

What is incorrect about BSL-4 lab?

A. Maximum containment lab due to dangerous and exotic pathogens belonging to highest risk groups.

B. Wear negatively air-pressurized, HEPA filtered (incoming and outgoing air is filtered), supplied-air suit.

C. Negative air-pressure in the room.

D. Sterilization through double door autoclaving system and suit decontamination shower when leaving.

A

B. Wear negatively air-pressurized, HEPA filtered (incoming and outgoing air is filtered), supplied-air suit.

POSITIVELY air-pressurized. everything else is true.

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32
Q

Match the correct statement.

A. Biosafety cabinets (BSC) B. Biosecurity C. Biohazard D. Aerosol

  1. Biological substances that pose a threat to the health of living organisms, primarily that of humans.
  2. Protection, control and accountability for valuable biological materials (prevent their unauthorized access, loss, theft, misuse, diversion or intentional release).
  3. Small droplets of fluid that can spread via air.
  4. An enclosed, ventilated lab for safely working with materials contaminated with pathogens requiring a defined biosafety level.
A

A - 4 B - 2 C - 1 D - 3

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33
Q

Which is incorrect?

A. Systemic disease > blood, nasal and urogenital swab; feces > Blood sample, tissues from affected system.

B. Respiratory and; ocular disease > nasal and conjuctival swabs, blood > tissues from affected tissue and lymph nodes.

C. Gastroenteritis > feces, blood > intestinal contents, lymph nodes, tissues from affected system.

D. Central nervous system disease > blood, CSF, urogenital swabs > tissues from affected system and lymph nodes.

E. Disease of urinary tract > urogenital swab, urine, blood > tissues from affected system, lymph nodes.

F. Abortion > blood from dam, vaginal mucus > tissues from placenta and fetus, blood from fetal heart, intestinal contents.

A

A. Systemic disease > blood, nasal, and urogenital swab; feces > Blood sample, tissues from affected system.

DON’T NEED A BLOOD SAMPLE.

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34
Q

Choose 3 potential hazards associated with transportation of pathogens.

A. Breakage of containers results in spilage.

B. Exposure to possible infection due to breakage.

C. Not sealing the sample 2 times.

D. A delay in package delivery > serious during outbreak situation.

A

A, B, D

YOU WANT TO USE TRIPLE PACKAGING SYSTEM for transportation

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35
Q

Choose all that apply. Successful detection of viruses from a sample depends upon:

A. Collection of the sample from the right site, right time, appropriate animal.

B. Proper transport and storage.

C. Performing correct diagnostic test and interpretation of results.

D. Temperature of the site and the animal.

A

A, B, D.

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36
Q

What are 3 factors that diagnostic lab require data on?

A

Epidemiological data, histories, clinical signs.

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37
Q

T/F. Virus specimens should be collected during the first three days after onset (maximum titers).

A

True.

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38
Q

When are 2 blood specimens collected for serological tests? What kind of diagnostic is used for the sample?

A

Acute phase and Convalescence period (10-14 days after 1st sample or even more); Molecular diagnostic (PCR: during acute period).

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39
Q

What is incorrect about transportation and storage of samples?

A. delivered to the lab as soon after collection as possible.

B. should be kept cold and moist.

C. virus samples must be frozen and avoid refrigeration due to temperature.

D. histopath specimens should never be frozen.

E. fix in 10% buffered formalin.

A

C. virus samples must be frozen and avoid refrigeration due to temperature.

Refrigerate (2-8C) or place them on wet ice or cold pack; if need to freeze > -20 to -70C.

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40
Q

What are essential in viral transport medium (VTM)?

A

Buffered salt solution (added protein, antimicrobials) -> helps to maintain viability and retards growth of microbial contaminants.

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41
Q

What are the five factors that are helpful for diagnosis of viral infections?

A

Clinical signs, necropsy, histopathology, Cultivation/Isolation (tissue culture/inoculation of eggs), Electron microscopy.

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42
Q

What are the three ways to process samples?

A. Tissue homogenization: Rinse and mesh

B. Feces: liquefy the fecal > vortexed and centrifuged.

C. Swabs: Twirl the swab and vortex.

D. Blood: Hemottiglutinzation

A

A, B, C

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43
Q

How does Negative-stain electron microscopy work?

A

Solution of heavy metal salt that is highly opaque to electrons (sodium phosphotungstate, uranyl acetate) > spread on a thin layer (Carbon-cated copper grid) >bombardment with an electron beam > stain absorbs e-> increased amount than the sample

Viral particles not penetrated: electron-lucent (low affinity, less e- density). Opaque background (high affinity, electron-dense).

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44
Q

What is incorrect about TEM?

A. Transmitted electrons (inside or beyond the surface).

B. Produce higher magnification and Greater resolution.

C. 2-D images.

D. SEM is preferred over TEM because SEM portrays 3-D images.

A

D. SEM is preferred over TEM because SEM portrays 3-D images. SEM lacks magnification and resolution.

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45
Q

What color tube do you use for a serum sample? How about for a plasma sample?

A

Serum: Red top Plasma: Lavender top

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46
Q

What is the difference between serum and plasma?

A

Plasma - clotting factors = serum

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47
Q

Find the mismatched one regarding ELISA.

A. Direct ELISA - Antigens are immobilized and use of primary antibodies to detect antigen concentration; specificity of the primary antibody is important.

B. In-Direct ELISA - Primary antibodies are labeled and therefore, antigens are detected with primary antibodies.

C. Sandwich ELISA - antigen is present between two antibodies (AB’s must be chosen that do not cross-react or competitively bind).

D. Competitive ELISA - More antigens present in the well represents more Ab-Ag reaction, therefore, weaker signal indicates presence of antigens in sample.

A

B. In-Direct ELISA - Primary antibodies are labeled and therefore, antigens are detected with primary antibodies. Secondary antibodies are labeled and therefore, antigens are detected with secondary antibodies.

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48
Q

What do you see in fluorescence antibody test (FAT)? What are the two subtypes of FAT? (be able to explain each)

A

AB’s are labeled with fluorescent dye; visible fluorescence appears when there is Ag-Ab reactions.

Direct FAT: One type of AB’s is labeled. Indirect FAT: secondary AB is labeled recognizes primary AB.

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49
Q

What is immunohistochemistry? What are the two subtypes?

A

Antibody is tagged with enzyme (HORSERADISH PEROXIDASE) > enzyme reacts with substrate > colored product > light microscope

Direct assay: primary AB that binds to Ag > color product. Indirect assay: secondary AB that is specific against primary AB.

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50
Q

What is immunochromatography (lateral flow devices)? What test is used for this?

A

does not require specialized equipment (Easy) POINT OF CARE (POC): test near the site of care; liquid sample dropped on the sample pad > Ag reacts with Ab that has been labeled with colloidal gold > contact with Ab immobilized on the membrane > immuno-complex > red purple line (positive result)

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51
Q

What is the agglutination test?

A

Specific AB’s bind to many Ag’s > single clumps, forming large complexes. Precipitation can be mascroscopically or microscopically visible.

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52
Q

What is hemagglutination and hemagglutination inhibition test?

A

Relies on the property of some pathogens to non-specifically agglutinate erythrocytes > no clumps > button-like formation (presence of AB’s). Avian infleunza, Peste Des Petits Ruminants

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53
Q

What is Agar Gel Immunodiffusion Test?

A

Ag and Ab placed in separate wells > diffuse toward each other > a thin white line is formed (Ag-Ab complex) Avian influenza, Equine infectious Anaemia (Coggins Test) and Enzootic Bovine Leukosis

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54
Q

What is Complement Fixation Test?

A

Serum sample from viral infection > treat with regimen antigen > Ag+Ab complex > add complement > utilize all complement > add sheep RBC’s > No Ab’s then cannot destroy sheep RBC’s > settle down like a button reaction. Hemolysis if complement is available.

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55
Q

What is Immunoblotting? what is Hemadsorption?

A

Ag samples > nitrocellulose sheet (blot) > labeled Ab’s with fluorescent dye > Ag+Ab > autoradiography > Ag bands visualized.

The adherence of an agent or substance to the surface of a red blood cell (glycoproteins are inserted into host cell membrane at sites of budding of enveloped viruses).

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56
Q

What is hemadsorption-Inhibition Assay?

A

Same as Hemaglutination and Hemagglutination inhibition test.

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57
Q

What is Neutralization Assay?

A

Loss of infectivity through reaction of the virus with specific AB. Virus + serum (AB’s) are mixed > inoculated into cell culture, eggs or animals > Ag-Ab reaction > no desired effect

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58
Q

What is IgM Class-Specific Antibody Assay?

A

Indicative of recent infection (usually drop within 1-2 months and disappear within 3 months)

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59
Q

Match the following.

A. Cell transformation B. Neoplasia C. Oncology D. Benign Neoplasm E. Malignant Neoplasm/Metastasis F. Oncogenic viruses G. Neoplasms

  1. Abnormal tissue overgrowth that may be either localized or disseminated (Syn. carcinogenesis)
  2. Growth produced by abnormal cell proliferation that remains localized and does not invade adjacent tissue.
  3. Viruses that cause of give rise to tumors.
  4. A consequence of the dysregulated growth of cells derived from a single, genetically altered progenitor cell.
  5. Study of neoplasia and neoplasms.
  6. Changing of a normal cell into a cancer cell.
  7. Locally invasive and may also be spread to other parts of the body by bloodstream or lymph system.
A

A - 6 B - 1 C - 5 D - 2 E - 7 F - 3 G - 4

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60
Q

Match the following.

A. Proto-onco genes B. Oncogenes C. Tumor Suppressor gene

  1. Involve in growth signaling and anti-apoptotic pathways. Encodes growth factor proteins, growth factor receptors, transcription factors, intracellular signaling proteins, signal transducers.
  2. Mutated forms of Proto-Oncogenes or abberantly expressed proto-oncogenes. Encode proteins that somewhat resemble product of proto-oncogenes but differ.
  3. Keep cell division in check. Encodes proteins that regulate and inhibit uncontrolled growth.
A

A - 1 B - 2 C - 3

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61
Q

What is signal transduction cascade?

A

Carefully regulated event where mitosis (cell division) is regulated by activating one protein to activate another. Controlled by Proto-Onco Genes

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62
Q

Which of the following is NOT a regulation by Oncogenes?

A. Synthesis of aberrant growth factors, growth factor receptors, which trigger uncontrolled growth.

B. Failure to undergo Apoptosis.

C. Minimizing protein synthesis to inhibit the viral attachment.

D. Defective differentiation of cells.

A

C. Minimizing protein synthesis to inhibit the viral attachment. I don’t even know what this is saying.

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63
Q

T/F. Proto-onco genes and oncogenes require regulatory step of ligand binding to be active.

A

FALSE. Oncogenes DO NOT required ligand binding.

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64
Q

What is the correct statement about Tumor Suppressor Genes?

A. Promotes the expression of genes that are essential for the continuing of the cell cycle.

B. Repair and apoptosis if repair fails.

C. Adhesion proteins, Metastasis suppressors, induce spread of cancer cells or metastasis.

A

B. Repair and apoptosis if repair fails.

A. Inhibits C. Prevent spread

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65
Q

Match three important proteins involved in tumor suppressor genes with their functions. A. Retinoblastoma protein (Rb) B. P16 C. P53

  1. Blocks Cdk so Cdk cannot phosphorylate Rb. This binds to E2F so cell division does not occur.
  2. Blocks G1->S when it’s unphosphorylated. Loss of control when lose this.
  3. Activates the DNA repair system and stops the cell cycle at the G1 checkpoint (before DNA replication).
A

A - 2 B - 1 C- 3

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66
Q

T/F. A loss of control when loss of Rb function.

A

True

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67
Q

Choose all that apply. What is the correct statement about oncogenic viruses?

A. Oncogenic viruses have a DNA genome or generate a DNA provirus after infection.

B. Cells transformed by oncogenic viruses have viral DNA integrated into host genome, which is a part of viral genome.

C. Viral genome may remain Episomal, replicating each step with host cell chromosome.

D. Viral genome that never gets integrated into host genomes will fail.

A

A, B, C.

D. the genome may have an autonomous replicating system.

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68
Q

What is induce transformation?

A

The process where DNA oncogenes that alter patterns of gene expression and regulation of cell growth.

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69
Q

What is the MOST important oncogenic viruses in animals? A. Papilomaviruses B. Retroviruses C. Polyomaviruses D. Herpesviruses

A

B. Retroviruses

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70
Q

T/F. Oncogenes of DNA viruses have homologue or direct ancestors (c-onc genes) among cellular genes of the host.

A

False. NO homologue or direct ancestors.

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71
Q

What are the two ways DNA tumor viruses interact with cells?

A
  1. Productive infection in permissive cell (virus completes its replication cycle). 2. Non-productive infection in non-permissive cells (virus transforms the cell without completing its replication cycle).
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72
Q

How does non-productive infection occur?

A

Viral genome or truncated version of viral genome is integrate into the cellular DNA > complete genome persists as an autonomously replicating plasmid (episome).

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73
Q

Explain how papillomaviruses can cause cervical carcinoma in woman.

A

Produce papillomas (warts) on the skin and mucous membranes > these benign neoplasms are hyperplastic epithelial outgrowths that can regress spontaneously > however, occasionally, may progress to malignancy (a property of specific virus strains).

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74
Q

T/F. Papillomaviruses: Benign warts DNA is episomal and not integrated into the host-cell DNA and persists as an autonomously replicating episome. Induced malignant cancers the viral DNA is integrated into host.

A

TRUE

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75
Q

T/F. Integration of viral DNA into host DNA disrupts one of the Early Genes, E2, which is a viral suppressor. When viral oncogenes (E6 and E7) remain intact and cause malignant transformation.

A

True.

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76
Q

What are the two ways oncogenic RNA viruses can infect host cells?

A
  1. Mutation: proto-oncogenes become oncogenes.
  2. Recombination: between provirus and proto-onco genes
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77
Q

T/F. All RNA Tumor viruses belong to the family REOVIRUS.

A

FALSE. Retrovirus.

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78
Q

Which statement is incorrect about acutely transforming retroviruses (oncogenic RNA viruses)?

A. Retroviruses are directly oncogenic by carrying an additional viral oncogene, V-onc.

B. Retroviral V-onc is encoded from itself and inserted into the virus genome by recombination events between provirus DNA and host DNA.

C. V-Onc genes are separated from the cellular machinery that normally controls gene expression (lacks introns) as they have power of unregulated expression.

D. C-onc/Proto-oncogene mutates accentuating its transformation activity.

E. V-onc genes are under the control of the Viral Ltrs, which are strong promoters.

A

B. Retroviral V-onc is encoded from itself and inserted into the virus genome by recombination events between provirus DNA and host DNA.

Originates from a shot C-onc gene/proto-oncogene

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79
Q

What are two genes involved in chronic transforming retrovirus and what are their functions?

A

Promoter: DNA sequence at which DNA-dep RNA polymerase binds to initiate transcription. Enhancer: a transcription regulatory sequence located some distance from the promoter (increases the rate of initiation of transcription).

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80
Q

What is the outcome of chronic transforming retrovirus?

A

Malignant transformation of cell > neoplastic ells (loss of contact inhibition and cells are more spindle-shaped).

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81
Q

What is incorrect about chronic transforming retrovirus?

A. Virus genes DO NOT contain V-onc gene.

B. The integration of Retroviral genes into host can occur at promoter or enhancer sites that increase in proto-oncogene/c-onc gene expression, results in malignant transformation of the cell.

C. This can be an irreversible change, where NK cells attack neoplastic cells.

A

C. This can be an irreversible change, where NK cells attack neoplastic cells. Made this up.

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82
Q

What are tumor antigens? Who are they products of? What is the outcome?

A

New antigens appear on the surface of tumor cells that may provoke an immune response; mutated oncogenes, tumor suppressor genes, other mutated genes; abnormal molecules are not appropriately present to cells of immune system (cytotoxic T cells)

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83
Q

What are the 5 types of classifications of tumor antigens?

A

Differentiation antigens, Excessive amount of normal proteins, Mutated proteins, Viral coded proteins, Cancer/testis antigens.

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84
Q

What are the routes of entry of viruses into host?

A

Mucous membrane, Respiratory Tract Defenses, Cut or Breach/trans-cutaneous injection (skin), GIT

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85
Q

Describe respiratory tract defenses.

A

Muco-ciliary blanket, BALT (bronchus associated lymphoid tissue), Temperature gradient (nasal: 33C, alveoli: 37C).

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86
Q

What are the ways that a virus can spread in a host?

A
  1. Local spread in epithelial surfaces. 2. Sub-epithelial invasion and lymphatic spread. 3. Spread via blood stream. 4. Spread via nerves.
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87
Q

How does virus spread in epithelial surface?

A

Replicate in epithelial cels at the site > local spread infecting contagious cells > produce localized infections (SHEDDING) > may or may not proceed to adjacent sub epithelial tissue.

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88
Q

What is incorrect about sub-epithelial invasion and lymphatic spread?

A. Facilitated by inflammatory response in epithelium or destruction of epithelium (exposure of virus) or transcytosis.

B. Viruses should overcome local host defenses.

C. Viruses can go into lymphatics, phagocytes, and tissue fluids and go back to sub-epithelial tissues, which will increase chances of infection.

A

C. Viruses can go into lymphatics, phagocytes, and tissue fluids and go back to sub-epithelial tissues, which will increase chances of infection. Virus does not go back to sub-epithelial tissues.

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89
Q

What is the difference between disseminated infection and systemic infection during sub-epithelial invasion/lymphatic spread?

A

Disseminated infection: spread beyond the primary site of infection. Systemic infection: number of organs or tissues are infected.

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90
Q

There are apical release and basolateral release as a part of directional shedding. What do they mean? Also, what is directional shedding?

A

Directional shedding: viruses from the infected epithelium is critical to sub-epithelial spread. Apical release: facilitates virus dispersal. Basal release: provides access to underlying tissues, facilitating systemic spread.

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91
Q

After viruses are spread to lymphatics, how do they enter bloodstream? Choose the incorrect statement.

A. Migration and replication within phagocytic leukocytes (dendritic cells, macrophages, lymphocytes).

B. Synthesize proteins in order to use extravastation.

C. Pass straight through lymph nodes and enter bloodstream.

D. Go directly into blood through bites, syringes.

A

B. Synthesize proteins in order to use extravastation.

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92
Q

Matching. A. Viremia B. Primary viremia C. Secondary viremia D. Passive viremia E. Active viremia

  1. virus has replicated in major organs and once more entered the circulation.
  2. presence of virus in the blood (free in blood or in lymphocytes).
  3. Initial entry of virus into the blood after infection.
  4. Direct inoculation of virus in the blood (arthropod or syringe) NO INITIAL REPLICATION
  5. Viremia following initial virus replication in host LYMPHATICS or EPITHELIUM OF INTESTINES
A

A - 2 B - 3 C - 1 D - 4 E - 5

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93
Q

T/F. viruses can be free in plasma (short duration) or multiply in monocytes or lymphocytes (prolonged)

A

True.

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94
Q

Which is incorrect about virus interaction with macrophages?

A. Macrophages fail to phagocytose host (prolong viremia).

B. Virions may be phogocytosed and destroyed.

C. Phagocytosed and transferred passively to adjacent cells.

D. Virions synthesize proteins to break down engulf macrophages.

E. Tissue invasion (macrophages emigrate through walls of blood vessels) Trojan Horse

F. Virions may be phagocytosed and may replicate in them.

A

D. Virions synthesize proteins to break down engulf macrophages. I don’t even know if this EVER happens.

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95
Q

What are the three ways to clear virus from blood stream?

A

Mononuclear phagocytes in spleen, liver, and bone marrow; Antibodies; complement-mediated clearance.

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96
Q

Match. A. Neurotropic virus B. Neuroinvasive virus C. Neurovirulent virus

  1. Viruses that cause disease of the nervous tissue; neurological symptoms and death may occur.
  2. Viruses that aggressively can infect neural cells; infection occurs by neural or hematogenous spread.
  3. Enter the CNS after infection of a peripheral site.
A

A - 2 B - 3 C - 1

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97
Q

Match. A. Herpes Simplex Virus B. Mumps Virus C. Rabies Virus

  1. Neuroinvasive, not neurovirulent, most infections lead to CNS invasion, doesn’t cause severe damage to CNS.
  2. Neuroinvasive, neurovirulent, infects peripheral nervous system, spreads to CNS and 100%.
  3. low neuroinvasive, high neurovirulent, enters peripheral nervous system, rarely enters CNS (if does, fatal).
A

A - 3 B - 1 C - 2

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98
Q

What is the difference between retrograde and anterograde spread?

A

Retrograde: travel opposite direction of nerve impulse flow. Axons -> dendritic cell body > crosses synapse > axon terminal Anterograde: travel IN direction of nerve impulse flow. Dendrites or cell bodies > spread by axon terminal > crosses synapse > next neuron

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99
Q

What are two ways that viruses spread through CNS?

A
  1. Olfactory routes (anterograde) 2. Blood Brain Barrier
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100
Q

Explain the methods when viruses go through BBB.

A
  1. Increase permeability of endothelial cells through secretion of TNF. 2. Breakdown of cell junctions through Matrix metalloproteinase. 3. Trojan Horse (trafficked by monocytes).
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101
Q

Match. A. Localized acute infections. B. Systemic acute infections.

  1. Site of pathology: portal of entry, incubation period: short, No viremia, Duration: variable (can be short), Secretory IgA: VIMP
  2. Site of pathology: distant sites, incubation period: long, Presence of viremia, Duration: lifelong
A

A - 1 B - 2

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102
Q

What is incorrect about virus shedding?

A. Crucial to maintain infection in population.

B. Acute infection and persistent infection are involved.

C. Viruses shed at different sites.

D. Virus shedding is important for living in the host.

A

D. Virus shedding is important for living in the host. Important for disease transmission.

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103
Q

What are determinants of viral tropism?

A

Receptors of host cells, viral attachment proteins, viral enhancers, protease, temperature, acid lability and protease digestion, transcription control, anatomic barriers.

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104
Q

What is viral tropism? what are pantropic viruses?

A

Viral tropism: specificity/affinity of a virus for a particular host tissue (Enteric virus, Respiratory virus). Pantropic viruses: replicate in more than one host organ/tissue.

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105
Q

Match. Injuries to SKIN

A. Rash B. Vesicles C. Ulcer D. Nodule/Tumor E. Warts F. Papules G. Erythema

  1. Opening in the skin caused by sloughing of necrotic tissue (extending past epidermis)
  2. Skin growths that appear when a virus infects the top layer of the skin (Cauliflower like)
  3. Reddening of skin (systemic viral infections: endothelial injury in blood vessels).
  4. Solid elevations without fluid (sharp borders).
  5. Temporary eruption on the skin; shade of red; Lyme disease; varies with disease in question.
  6. Palpable, solid, elevated mass, distinct borders, extending deep into dermis.
  7. Small distinct elevation with fluid.
A

A - 5 B - 7 C - 1 D - 6 E - 2 F - 4 G - 3

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106
Q

What is the common way to injure GIT by viruses?

A

Destruction of enterocytes due to viral replication > hypersecretion > GIT disease, mal absorption, diarrhea > dehydration > acidosis > hemoconcentration. Enterotoxin: nonstructural protein made by viruses can increase peristalsis and diarrhea.

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107
Q

What is Viral-Bacterial synergism?

A

Secondary bacterial infections, due to viral infections, will increase mortality rate significantly and more rapidly.

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108
Q

What are the organs that are injured by viruses?

A

Skin, GIT, respiratory tract, CNS

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109
Q

Which of the following statement is incorrect about injury to CNS caused by viruses?

A. Leads to encephalitis or encephalomyelitis

B. Neural necrosis can occur.

C. Phagocytosis of neurons (neuronphagia)

D. Perivascular infiltrations of inflammatory cells (perivascular cuffing).

E. The statement is false; they are all true.

A

E. The statement is false; they are all true.

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110
Q

What are 4 outcomes that is caused by viral infection of hematopoietic system?

A
  1. Petechial and ecchymatic hemorrhages. 2. DIC 3. Edema 4. Infarction (ischemic necrosis)
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111
Q

Which statement is incorrect about disseminated intra-vascular coagulation?

A. Clotting cascade that results in blood clots in small blood vessels throughout the body.

B. Clots can cut off blood supply (liver, brain, kidneys)

C. Result: ischemia or necrosis

D. Clotting proteins will accumulate, helping blood flow to important organs.

A

D. Clotting proteins will accumulate, helping blood organ to important organs. Clotting proteins are used up > severe bleeding from various sites.

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112
Q

What is teratogenesis?

A

Abnormal development or arrests in development of the embryo/fetus > death/malformation during antenal period.

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113
Q

Which of the following are the outcomes of teratogenesis or viral infection of fetus?

A. Cerebellar hypoplasia

B. Porencephaly

C. Arthrogryposis

D. Congenital Hydranencephaly

E. All of the above

A

E. All of the above

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114
Q

Match. When the virus infects pregnant cow during:

A. Month 1 B. Month 2-4 C. Month 5-9

  1. Persistent infection (immuno-tolerance calves)
  2. Embryo death
  3. Abortion/deformities or normal calves.
A

A - 2 B - 1 C - 3

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115
Q

How does mucosal disease develop from persistent infection in CALVES?

A

Calf recognizes virus as self (no immune response against the virus) > virus mutates and become cytopathic > systemic disease > mucosal disease > secondary infection (pneumonia)

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116
Q

Which of the following is incorrect about virus-induced immuno-pathology?

A. Tissue injury mediated by viruses.

B. Depends on balance between protective and destructive effects of the host immune response to virus.

C. Caused by viruses that are non-cytolytic and persistent.

D. Infected cells are not immediately destroyed and immune response becomes chronic.

E. No permanent damage if immune response clears a small number of infected cells.

F. Immune mediated destruction can cause fatal pathological consequences if not infected cells are not cleared.

A

A. Tissue injury mediated by viruses. Mediated by host immune response TO virus infection.

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117
Q

What is NOT related to immuno-pathology?

A. The premise is false. Everything is related to immuno-pathology.

B. Tissue damage mediated by Hypersensitivity RXN’s.

C. Inflammation mediated tissue damage (fibrosis).

D. Immunodeficiency disorders.

E. Auto-immune diseases.

A

A. The premise is false. Everything is related to immuno-pathology.

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118
Q

What mechanism is NOT involved in virus-induced immuno-pathology?

A. Role of T cells.

B. Role of NK cells.

C. Role of toxicity from antibody response.

D. Infection and damage to mononuclear phagocytes.

A

B. Role of NK cells.

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119
Q

T/F. T cells can directly destroy virus-infected cells or release cytokines (TNF).

A

True.

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120
Q

T/F. Cytotoxic cell mediated lysis/killing of infected host cells with non-cytopathic virus infections such as HCV and HBV.

A

True.

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121
Q

What is the main cause of liver damage during cytotoxic cell mediated lysis/killing of infected cells?

A

CD8+ effector T cells.

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122
Q

T/F. Cytokines never become chronic against persistent virus infections.

A

False. It DOES become chronic.

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123
Q

What is incorrect about cytokines?

A. The premise is false. Everything is true.

B. Small proteins that are important in cell signaling.

C. Mediators and regulators that can cause inflammation.

D. Can directly destroy virus infected cells.

E. Include monokines, lymphokines, interleukines.

A

D. Can directly destroy virus infected cells.

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124
Q

T/F. Innate immunity: invading viruses and replicative intermediate can be recognized by several innate immune receptors expressed only on the host cell (TLRs).

A

False. OR within cells.

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125
Q

T/F. Innate immunity: persistent activation of receptors of innate host cells by virus causes production of pro-inflammatory cytokines and interferons as well as signals that recruit and activate cells involved in inflammation.

A

True.

126
Q

What is the role of free radicals (NO and superoxide) produced during innate immunity?

A

Inhibit viral replication but cause cell damage in abundance.

127
Q

What are the two ways of toxicity from antibody response can occur?

A
  1. IgG + Fc receptors on inflammatory cells > inflammatory mediator release. 2. Viral Ag-Ab complexes in capillary beds > activation of complement cascade (damage to blood vessels).
128
Q

What is special about Feline Infectious Peritonitis Virus (FIPV) when it binds to Ab’s?

A

Spikes bind to Ab’s > fails to neutralize the virus > activates complement cascade > Feline Infectious Peritonitis (vasculitis and edema).

129
Q

What are the two outcomes when infected macrophages interact with T-lymphoctyes?

A
  1. Macrophages release IL-10 > cell mediated immunity and humoral immunity 2. Macrophages release TNF > apoptosis of lymphocytes
130
Q

What happens during infectious bursal disease due to viral replicaton?

A

Atrophy of bursa + severe B-lymphocytes deficiency > immuno-suppression. Infected birds become susceptible to other pathogens.

131
Q

Match the terms.

A. Inapparent infection. B. Acute infection C. Persistent infection D. Latent infection E. Chronic infection F. Slow infection

  1. Prolonged incubation period (months-years), quantities of virus increases during long pre-clinical phase, slow and progressive lethal disease.
  2. Not demonstrable except when reactivation occurs; stimulated by immuno suppression, cytokine and hormone action).
  3. Clinical signs and symptoms not evident, too few cells are infected, stimulate immune response, source of virus spread.
  4. virus is continuous whether or not there is ongoing disease, pathogen is not cleared efficiently by adaptive immunity, recurrent episodes of diseases, continuous shedding.
  5. Virus is continuously shed from or is present in infected tissue, host unable to clear virus, foot and mouth disease.
  6. Short clinical course, rapid clearance by host immunity.
A

A - 3 B - 6 C - 4 D - 2 E - 5 F - 1

132
Q

How is viral latency maintained?

A
  1. restricted suppression of genes prevents the expression of proteins, which would have killed the infected cells. 2. Virus genome maintained in cell by integration of viral nucleic acid into host DNA. 3. Carriage of viral nucleic acid in episomal form.
133
Q

How does a disease develop late with persistent infection?

A

Immunologic, Neoplastic, No manifestation of clinical signs.

134
Q

What are the three outcomes of cytopathic effects (CPE)?

A
  1. Complete destruction of cells. 2. Subtotal destruction of cells. 3. Focal destruction f cells.
135
Q

Match the terms.

A. Complete destruction of cells. B. Subtotal destruction of cells. C. Focal destruction f cells.

  1. Consists of detachment (death) of some, but not all of the cells in the monolayer.
  2. Produce localized areas of infection.
  3. Most severe form of CPE. Monolayer rapidly shrinks, become dense (pyknosis) and detach from the glass within 72 hours.
A

A - 3 B - 1 C - 2

136
Q

What is pyknosis?

A

A degenerative condition of a cell nucleus marked by clumping of the chromosomes, hyperchromatism, and shrinking of the nucleus.

137
Q

What are the visible effects of virus-induced cell damage?

A
  1. Cell fusion (syncytium or polykaryon formation). 2. Inclusion bodies in host cells during viral infections.
138
Q

What is incorrect about cell fusion?

A. fusion of the plasma membrane of four or more cells of infected or uninfected cells to produce an enlarged cell with 4 or more nuclei.

B. Prone to premature cell death.

C. Enveloped viruses direct the insertion of their surface glycoproteins into host cell membrane as part of their budding process leading to membrane fusion and syncytium formation.

D. Syncytia formation may be the only detectable CPE of some Parvovirus.

A

D. Syncytia formation may be the only detectable CPE of some Parvovirus. Paramyxoviruses.

139
Q

What is incorrect about inclusion bodies in host cells during viral infection?

A. An abnormal structure in a cell nucleus or cytoplasm or both, such as aggregates of proteins.

B. Staining properties and associated with certain viral infections.

C. Inclusion bodies are only found in the liver.

D. Help ID certain viral infections.

A

C. Inclusion bodies are only found in the liver.

140
Q

What is correct about inclusion bodies?

A. Accumulation of viral components, such as Negri bodies consist of Ribonuclear Proteins produced by the Rabis virus.

B. Result from synthetic changes of proteins in cells.

C. Fibrious formation of virions such as adenovirus.

A

A. Accumulation of viral components, such as Negri bodies consist of Ribonuclear Proteins

Correct: B. Result from degenerative changes in cell. C. Crystalline aggregates of virions.

141
Q

What is incorrect about inhibition of host-cell protein synthesis?

A. Production of viral enzymes that degrade cellular mRNAs.

B. Alteration of the intracellular ionic environment favoring the translation of cellular mRNAs over viral mRNAs.

C. Production of factors that bind to ribosomes and inhibit cellular mRNA translation.

D. Production of large excess of viral mRNA that outcompetes cellular mRNA for host ribosomes.

E. Some viruses cause lysosomes to release hydrolytic enzymes, which then destroy the host cell.

A

B. Alteration of the intracellular ionic environment favoring the translation of cellular mRNAs over viral mRNAs.

VIRAL mRNAs over cellular mRNAs.

142
Q

What is apoptosis?

A

The process of programmed cell death, cell suicide that those activates as a last resort to eliminate viral virus BEFORE progeny virus production is complete.

143
Q

What is lysis?

A

Viral replication is complete and host cell is destroyed and new virions are released.

144
Q

What is correct about interference with cellular membrane function? Choose all that apply.

A. The premise is false. Everything is false.

B. Promotion of cell fusion (syncytium formation).

C. Affect ion exchange and membrane potential.

D. Induce synthesis of new intracellular membranes or the rearrangement of previously existing ones.

E. Damage to the cytoskeleton resulting in changes in cell shape.

A

B, C, D, E.

145
Q

What is the difference between intrinsic (mitochondrial) and extrinsic (Death receptor) pathway?

A

Intrinsic: increased permeability of mitochondrial membrane subsequent to cell injury. Extrinsic: engagement of specific cell membrane receptors (TNF receptors).

146
Q

T/F. Binding of Cytokine TNF to cellular receptor can trigger apoptosis. Cytotoxic T lymphocytes can bind Fas receptor to trigger the executioner caspase pathway.

A

True.

147
Q

T/F. Only NK cells can utilize perforin and granzyme that activates caspases in the target cell.

A

False. Cytotoxic T lymphoctyes can as well.

148
Q

What is the pathogenesis of non-cytocidal changes in virus infected cells?

A

No immediate cell death > persistent infection > infected cells grow and divide > affects crucial functions caused by pathophysiologic changes (may not affect the host). Neurons (terminally differentiated cells) will not be replaced > cannot carry out specialized functions.

149
Q

T/F. Retroviruses will ultimately lead to cell death due to slow progressive changes.

A

True

150
Q

Match the terms.

A. Virions B. Virus C. Virioid D. Variolation/inoculation

  1. Infectious particle smaller than any virus (certain plant diseases); contain extremely smell circular RNA molecule; no protein coat of a virus.
  2. Broad term that describes any aspect of infectious agent (infectious virion, inactivated virus particle, viral nuclei acid + protein in infected cell).
  3. Complete virus particle with RNA or DNA core + protein coat + external envelope > extracellular infective form of virus.
  4. 1st method used to immunize an individual against smallpox.
A

A - 3 B - 2 C - 1 D-4

151
Q

Match the scientist and what they have discovered.

A. Edward Jenner B. Louis Pasteur C. Dmitri Iwanoski D. Martinus Beijerinck E. Friedrich Loeffler and Paul Frosch F. Walter Reed G. Peyton Rous

  1. To find tobacco mosaic disease, filtered the sap of the tobacco plant in hopes to capture disease agent > went through the filter > not a bacteria but something else.
  2. Infectious agent of tobacco mosaic disease was different from bacteria.
  3. First to document concept of a vaccination; inoculated into 8 year old boy > became immune to smallpox.
  4. Found the cause of foot and mouth disease.
  5. Isolated the first tumor causing animal virus.
  6. Demonstrated why vaccine worked, developed fowl cholera vaccine, used infected rabbit brain and injected into 2 boys bitten by a rabid dog > both recobered.
  7. Yellow fever was spread by mossies.
A

A - 3 B - 6 C - 1 D - 2 E - 4 F - 7 G - 5

152
Q

Match virus morphology determination and equipments used

A. Electron microscopy B. Cryo-microscopy C. X-Ray Crystallographic method D. Nuclear Magnetic Resonance (NMR)

  1. Allows to observe biological specimens in their native environment at cryogenic temperatures (-180C liquid -269 He), not stained or fixed, resolution: good and detailed.
  2. Imaging technique (see DNA/RNA genes, Capsid, Envelope, molecules of protein).
  3. Negative staining with electron dense material (sodium phosphotungstate and uranyl acetate), resolution: 50-70A, not always reliable.
  4. More detailed to see reconstruction of virus structure after using computer + graphics.
A

A - 3 B - 1 C - 4 D - 2

153
Q

Which statement is incorrect about capsid?

A. Capsomere: basic protein that surrounds capsid and held by non-covalent bonds.

B. Encases the viral nucleic acids or genome.

C. Most viruses have 1 capsid EXCEPT reovirus (2 layered capsid).

D. Functions: structure, protections of DNA/RNA, attachment-receptors, contain enzymes, lipid envelope (budding), uncoating, antigenic.

A

A. Capsomere: basic protein that surrounds capsid and held by non-covalent bonds. Capsomere: basic protein subunit of capsid (capsomeres held together by non-covalent bonds).

154
Q

What is correct about Nucleo-capsid?

A. Capsid with enclosed capsomeres.

B. Cubic symmetry (icosahedron): pentagon (icohedral virions with 4 neighbors) and hexgonal capsomeres (12 corners, 20 facets, 15 edges).

C. Always have 12 hexons but pentons vary.

D. Triangulation number: T= h^2+hk+k^2

A

D. Triangulation number: T= h^2+hk+k^2

Correct: A. capsid with enclosed nucleic acid B. 5 neighbrs; 30 edges C. 12 PENTONS and hexons vary

155
Q

T/F. h and k in triangulation number system is the distances between successive pentagons on the virus surface of each axis.

A

True.

156
Q

T/F. As the triangulation number increases , there are more pentagons present than hexagons.

A

False. more HEXAGONS present than PENTAGONS.

157
Q

Which statement is incorrect about helical (all coiled and enveloped) virus?

A. All animal viruses with helical nucleo-capsid are enveloped (lipo-protein).

B. In nucleo-capsid-capsomeres + nucleic acid are bound together in a helical structure > incomplete helical virions cannot form (no empty helical capsid).

C. Naked-helical nucleo-capsid are only present in human and plant viruses.

A

C. Naked-helical nucleo-capsid are only present in human and plant viruses. ONLY PLANT VIRUSES (tobacco mosiac virus)

158
Q

T/F. Pox virus and bacteriophages are two components that are related to complex virus.

A

True.

159
Q

What is pleomorphic?

A

Some viruses can change shape depending on situation/environment they are placed in.

160
Q

T/F. Most viruses are either bullet-shaped or ROD.

A

False. Spherical shaped or ROD.

161
Q

What are the three ways to cultivate viruses?

A
  1. Cultured cells 2. Embryonated hens egg 3. Lab animals
162
Q

What are cell cultures? what are two types of cell cultures?

A

Removal of cells from plant or animal, then grown in artificial environment, dispersed animal cells grow in vitro (suspension or monolayer). Primary cell cultures and serially propagated cell cultures.

163
Q

What are the advantages of primary cell cultures?

A

Best culture for isolation and propagation of viruses, heterogeneous (many cell types), closest to animal tissue cells, used for producing viruses.

164
Q

What are the disadvantages of primary cell cultures?

A

Difficult to obtain, short life span (5-20 subcultures), susceptible to contamination, does not act the same as parent media (environment is not identical).

165
Q

Which statement is correct about primary cell cultures?

A. Established from human or plant cells.

B. Same number of chromosome.

C. Primary culture can never be detached from the flask no matter what solution is used.

D. Capable of culturing 100 subcultures.

A

B. Same number of chromosomes.

Correct: A. Human or animal cells. C. Can use trypsin or EDTA to detach from flask. D. only 5-20 cultures.

166
Q

What are the two types cell lines?

A
  1. Diploid/finite cell lines 2. Continuous cell lines
167
Q

Which statement is incorrect about secondary culture/transfer culture/cell lines?

A. Primary culture is sub-cultured.

B. Transfer from one vessel to the other > to provide fresh nutrients and growing space for cells.

C. Suspension cultures mostly used.

A

C. Suspension cultures mostly used. Made this up.

168
Q

Match. May use A or B more than once.

A. Diploid/finite cell lines B. Continuous cell line/immortal/heteroploid cell lines

  1. Homogenous population of a single cell type.
  2. No contact inhibition, density limitation, achorage dependence.
  3. Slow growth, double time = 24-96 hrs.
  4. Furthest from animal, abnormal morphology and chromosome number.
  5. Used to make viruses.
  6. MOST homogenous cell culture of a single cell type.
  7. Derived from human embryos or sub-culture of primary culture.
  8. Derived from cancer cells, indued transformation of primary cultures or diploid cell lines.
  9. Contact inhibition, density limitation, anchorage dependence; fibroblast tissue.
  10. Cannot be used to make viruses.
  11. Example: WI-38
  12. Divide indefinitely.
  13. Example: Henrietta Lack, HeLa cells
  14. Limited life span, sub-culture up to 100x before growth stops.
  15. Rapid growth, double time = 12-24 hrs.
  16. Retain original morphology and diploid number of chromosomes.
A

1 - A 2 - B 3 - A 4 - B 5 - A 6 - B 7 - A 8 - B 9 - A 10 - B 11 - A 12 - B 13 - B 14 - A 15 - B 16 - A

169
Q

Which is the incorrect statement regarding morphology of cell in culture?

A. Fibroblastic-like: bipolar or multipolar, elongated, grow attached to substrate.

B. Lymphoblastic-like: spherical, grown in suspension WITHOUT attaching to surface.

C. Epithelial-like: polygonal, without attached to surface and makes a discrete patch.

A

C. Epithelial-like: polygonal, without attached to surface and makes a discrete patch. Polygonal; grow attached to substrate in discrete patches.

170
Q

T/F. Cell culture provides basic nutrients, such as amino acids, inorganic salts, vitamins, and glucose. The examples of media are Eagle’s Basal Medium, Leibovitz L-15 medium.

A

True.

171
Q

Which statement is incorrect about serum in culture media?

A. source of adhesion factors, hormones, spreading factors, growth factors.

B. Has carrier proteins for lipoid and trace elements.

C. Regulates membrane attachment.

D. Most common: Fetal Bovin Serum (FBS).

E. Growth medium: 5-10% antibodies and maintenance medium: 0-2% antibodies.

A

C. Regulates membrane attachment. Membrane permeability.

172
Q

Which of the following regarding phenol red (ph indicator) is true?

A. The premise is false. Everything is false.

B. All of the below.

C. tissue culture media is normally maintained at pH 7.35-7.45.

D. pH change > culture is not healthy due to overgrowth, waste accumulation, contamination.

E. Phenol red is normally red but when pH decreases, it turns yellow.

A

B. All of the above.

173
Q

Why is antimicrobial agents added to cell culture media?

A

Prevent contamination with bacteria, mycoplasma, yeast, molds.

174
Q

Find the incorrect statement regarding temperature of cell culture media.

A. human and mammals: 36-37C

B. insect cells: 17C

C. Avian cell lines: 38.5C

D. Cold-blooded animals: 15-26C

A

B. insect cells: 17C 27C

175
Q

T/F. Hydrolase is responsible for dissociating primary cell culture to sub-culture.

A

False. Protease.

176
Q

T/F. Cell lines are maintained if exposed to trypsin with EDTA-Ca2+ for a long time.

A

False. Long exposure to trypsin will damage cells.

177
Q

What are the two ways to exam cell culture?

A
  1. Inverted microscope. 2. ID cytopathic effects.
178
Q

Explain the cytopathic effects of rotavirus in Caco-2 cell monolayer.

A

48 hrs post infection: cellular vacuolization, opening of intra-cellular junctions, cell detachment. 96 hrs post infection: extensive cellular detachment, only few pyknotic cells present.

179
Q

How do you use the shell vial technique to RAPIDLY grow cell culture?

A

incubation > virus grows > antibodies tagged with florescent dye > added to cover slip > check under florescent microscope > Ag-Ab reaction.

180
Q

What is co-cultivated cells? What are some advantages of this method?

A

Single monolayer, consisting multiple cell types, using Fluorescein-Labeled Monoclonal antibodies. Isolation of multiple viruses an detection of viral antigens.

181
Q

What is R-mix? Why is this method used?

A

Monolayer of mink lung cells and human adnocarcinoma cells; ID and isolate different kinds of viruses (UNIQUE). Support a large number of viruses (respiratory group viruses: influenza A and B, RSV, Adenovirus, Parainfluenza viruses 1 + 2 + 3)

182
Q

Which statement is incorrect about Cultivation of viruses in eggs?

A. Egg candling to check for crack or embryo development (if not, cannot be used)

B. Can be drilled right away after checking the egg for a damage.

C. Drill - perforate egg 100-200uL.

D. Seal with molten wax.

A

B. Can be drilled right away after checking the egg for a damage. Antiseptic solution (keep sterile)

183
Q

Match.

A. Yolk Sac Inoculation B. Allantoic Cavity Inoculation C. Amniotic Cavity Inoculation D. Chorioallantoic Membrane (CAM)

  1. 26G, drill hole in eggshell OVER air sac.
  2. 22G, drill hole in eggshell, inoculum below embryo and within yolk material, seal hole.
  3. 26G, drill 2 holes (one on the side and another ABOVE air sac), move air sac to side of eggy by gentle sunction using rubber bulb.
  4. 26G, drill hole in eggshell ABOVE and BELOW air sac.
A

A - 2 B - 4 C - 1 D - 3

184
Q

Name some evidence that can tell you whether the virus is growing in the egg.

A

Death of embryo, paralysis, stunted growth, crystal deposits, hemorrhage and congestion, hemagglutins in embryonic fluids, extracellular membrane lesions, pocks on chorioallantoic membrane.

185
Q

What are two ways to inoculate lab animals?

A

Intra-cerebral, intra-peritoneal.

186
Q

To purify and concentrate viruses, this played a vital role in virology because they provided sufficient gravitational force to efficiently sediment even the smallest viruses.

A

Ultracentrifuge (60,000RPM and 200,000 x g to 150,000 RPM and 1,000,000 x g)

187
Q

This method of virus purification and concentration results in the sample being layered as a narrow zone on top of a density gradient, such as sucrose, of different densities; particles move at different rates depending on their MASS.

A

Rate-zonal centrifugation

188
Q

________________ refers to the object having the same density as the fluid, resulting in its buoyancy equaling its weight; it will neither sink nor float.

A

Buoyant density

189
Q

This refers to the point where the buoyant density of a particle equals that of the surrounding density gradient medium

A

Isopycnic point

190
Q

What are methods for virus purification and concentration?

A

Ultracentrifuge, rate-zonal centrifugation, isopycnic centrifugation, and membrane chromatography

191
Q

What are suitable density gradient mediums for isopycnic centrifugation?

A

Sucrose, cesium chloride

192
Q

This method of virus purification and concentration starts with a uniform mixture of sample and a density gradient medium; after ultracentrifugation, the particles separate solely on the basis of their buoyant density; the particles will never sediment to the bottom of the tube, no matter how long the centrifugation time.

A

Isopycnic separation/ buoyant separation/ equilibrium separation

193
Q

This method of virus purification uses a macroporous ion exchange membrane to allow large viruses to enter and bind to the inner pore surface easily.

A

Membrane chromatography (binding depends on the charge distribution on the virus)

194
Q

This is the lowest concentration of virus that still infects cells; it is also defined as the number of infectious units per mL of the sample.

A

Virus titer

195
Q

Plaque assays, pock assays, and various endpoint titration methods are what type of viral quantification tests? A. Biological B. Physical

A

A. Biological (depends on a virus particle initiating a successful replication cycle)

196
Q

Electron microscope particle counts, hemagglutination, ELISA, PCR, and flow cytometry are what type of viral quantification tests? A. Biological B. Physical

A

B. Physical (do not depend on any biological activity of the virus particle)

197
Q

What are methods used to directly count viral particles in solution?

A
  1. Transmission electron microscopy- the most direct method to determine concentration of virus particles in a sample
  2. Virus Counter 2100- a type of flow cytometer that measures intact virions; each sample is stained with 2 different fluorescent dyes, one for nucleic acid channel and the other for a protein channel; they are analyzed as they flow through a laser beam
198
Q

How are viruses quantified based on antigen concentration?

A

Hemagglutination assay, ELISA, High Performance Liquid Chromatography (HPLC; via UV analysis), and Single Radial Immunodiffusion (SRID)

(img: SRID)

199
Q

The inverse of the greatest dilution that completely agglutinates red blood cells is defined as the _____________________.

A

HA titer (example: if the viral dilution of allantoic fluid is 1/64, the original allantoic fluid contained 64 hemagglutinating units)

200
Q

How are viruses quantified based on gene expression?

A

Quantitative PCR (amplifies viral DNA or RNA and quantified by fluorescence)

201
Q

What are traditional assays/biological assays that are used to quantify viruses?

A

Monolayer plaque assay (most simple and accurate assay), pock assay, transformation assay, and quantal assay

202
Q

_________________ is a circular zone of necrotic cells surrounded by viable cells in a monolayer.

A

Plaque

203
Q

T or F. Only viruses that cause visible cell damage of cultured cells can be quantified using the monolayer plaque assay; it is a functional measurement, and has no relation to actual number of viruses.

A

True

204
Q

What are the units used for the monolayer plaque assay?

A

PFU = plaque-forming units/mL (it measures the number of virus particles capable of forming plaques per unit volume; example: if a solution has a PFU of 1,000 PFU/mL, then every mL of solution contains enough viruses to form 1000 plaque)

205
Q

Each plaque represents cell lysis initiated by how many viral particles?

A

One. Principle of Plaque assay = the agar restricts movement so that the virus can infect only contiguous cells

206
Q

What are the plaques stained with to be observed under the inverted tissue culture microscope?

A

Crystal Violet

207
Q

How do you determine the titer (PFU/mL)?

A

Average plaque count x reciprocal of the dilution selected

208
Q

How do you calculate PFU/mL?

A

KNOW THIS IMAGE

209
Q

Pocks are necrotic areas on the _______________________ membrane of embryonated egg.

A

Chorioallantoic membrane (CAM) (ex. titration of herpesvirus and poxvirus)

210
Q

What are the units for pock assay?

A

Pock-forming units/mL

211
Q

Transformation assay is the quantitative determination of titers of what type of viruses?

A

Oncogenic viruses (transformed cells lose contact inhibition; example: Rous sarcoma virus in avian cells)

212
Q

What are the units for transformation assay?

A

Focus-forming units/mL

213
Q

What does quantal assay measure?

A

The presence or absence of infection (used for certain viruses that do not form plaques or for determining the virulence of a virus in animals or eggs)

214
Q

What is the endpoint of a quantal assay?

A

A virus dilution that affects 50% of the test subjects, tissue culture infectivity dose 50 (TCID 50)

215
Q

What is TCID50?

A

Tissue culture infectivity dose; it is the dose which will infect 50% of the cell monolayers challenged with the defined inoculum.

216
Q

How is TCID50 calculated?

A

Using the Reed and Muench method; KNOW HOW TO SOLVE THIS EXAMPLE FROM THE IMAGE

217
Q

The average number of virus particles infecting each cell is called the _______________________.

A

Multiplicity of infection (MOI)

218
Q

T/F. A permissive cell is a cell which virus is able to replicate and a non-permissive cell is a cell which is lacking a factor necessary for viral replication.

A

True.

219
Q

Which of the following statement is incorrect about one-step virus growth curve?

A. A monolayer cell culture can be infected to perform sequential sampling of virus at different time intervals.

B. Can examine titer by measuring of PFU/ml of only intracellular virions.

C. Can measure both intracellular and extracellular virions.

A

B. Can examine titer by measuring of PFU/ml of only intracellular virions. Can examine titers of both intracellular and extracellular virions.

220
Q

Match the terms.

A. Adsorption B. Eclipse period C. Latent period D. Burst size.

  1. Virus attaches and enters the cells; free of titers.
  2. Number of infectious virions released.
  3. Time BEFORE new infectious virus appears in the medium; time from uncoating to just prior to release of 1st extracellular virions.
  4. Time interval between uncoating and appearance of 1st infectious progeny virions, no infectious virus is detected, ranges 2-12 hours.
A

A - 1 B - 4 C - 3 D - 2

221
Q

T/F. Most DNA viruses transcript and replicate in cytoplasm. Most RNA viruses replicate in nucleus.

A

False. DNA viruses - nucleus RNA viruses - cytoplasm

222
Q

Which of the following is incorrect about attachment to host cell surface?

A. Mediated by interactions between the virus and complementary receptor on host surface.

B. Cells that lack the appropriate receptor will synthesize protein to make receptors.

C. An additional co-receptor (cell surface molecule) is needed for the virus to be able to enter the cell.

D. Some viruses may use more than one host cell receptor (HIV).

A

B. Cells that lack the appropriate receptor will synthesize protein to make receptors. These cells won’t be able to be infected by virus.

223
Q

What are the four general ways to penetrate the host cell by a virus?

A

Endocytosis, surface/membrane fusion, pore-mediated penetration, antibody-mediated penetration.

224
Q

Be able to explain Clathrin-mediated endocytosis.

A

Virions attach to host receptor and induces cytoplasmic tail of receptor > adaptor proteins bind to Clathrin > increase in adaptor proteins on the inside will multimerize clathrin to form CCP (Clathrin Coated Pit) > Dynamin pinch off the CCP from the host membrane > Clathrin Coated Vesicle (CCV) is released > Clathrin Basket released from vesicle > vesicle delivers viral content to endosomes > pH in endosome changes (become acidic) > genome is released into host cell

225
Q

Match the following regarding Clathrin-Mediated Endocytosis.

A. Enveloped viruses B. MOST non-enveloped viruses C. SOME non-enveloped viruses

  1. LYSIS occurs when a viral capsid induces rupture of Endosomal membrane > releases viral capsid or genome.
  2. LOCAL PERMABILIZATION of host endosomal membrane to allow virus capsid penetration into cytoplasm.
  3. FUSION of virus with Host Endosomal membrane, then pH decreases and releases viral genome.
A

A - 3 B - 1 C - 2

226
Q

What are endosomes?

A

Membrane bound compartment in host cell cytoplasm.

227
Q

T/F. Caveolin-mediated endocytosis uses lipid rafts.

A

True.

228
Q

T/F. Membrane fusion occurs for both enveloped and non-enveloped viruses.

A

False. ONLY enveloped!!!

229
Q

What are three methods of membrane fusion? (choose all that apply)

A. Antibody-dependent cell mediated cytotoxicity

B. pH independent fusion proteins

C. pH dependent-acidic fusion proteins

D. Temperature dependent fusion proteins.

A

A, B, C

230
Q

Which of the following is incorrect about antibody-dependent cell mediated cytotoxicity relating to membrane fusion?

A. NK cells are involved in killing the infected cell by apoptosis.

B. There are no antigens found and therefore, memory cells will induce release of cytokines.

C. Glycoproteins are retained on cell surface and the cell can become the target.

A

B. There are no antigens found and therefore, memory cells will induce release of cytokines. Glycoproteins are antigenic.

231
Q

What is an important factor for pH independent fusion proteins related to membrane fusion? What is their role? What are two viruses that use this method?

A

F proteins (fusion) Catalyzes membrane fusion at the cell surface at neutral pH > viral nucleo-capsid is realsed into cytoplasm. HIV and measles.

232
Q

T/F. pH dependent-acidic fusion proteins related to membrane fusion use the same method as receptor mediated Endocytosis-enveloped viruses. The example of a virus is HA-Influenza virus.

A

True.

233
Q

T/F. Pore-mediated penetration of viral genome into host cell is a method that is used by non-enveloped viruses, which they inject their genomes into the host cytoplasm through creation of a pore.

A

True.

234
Q

Which of the following is incorrect about Antibody mediated attachment and penetration related to membrane fusion?

A. Seen in Feline Infectious Peritonitis Virus (FIP).

B. Antibodies against spike protein FIP virus cannot clear the virus > facilitate entry of virus.

C. Antibody-IgG-Fcgamma receptor are involved to facilitate the entry of virus.

D. FIP enters the host macrophages attachment of its spike protein to CD13 receptor.

E. All of the above.

A

E. All of the above.

235
Q

What is uncoating? What are the three methods that are used by viruses to uncoat?

A

Release of virus genome into host cell, “eclipse period”. 1. Uncoating of naked virus by endocytosis 2. Uncoating within endosome 3. Uncoating at nuclear membrane

236
Q

T/F. The method used for uncoating of naked virus by endocytosis is the same as receptor mediated endocytosis - enveloped viruses.

A

False. The same as receptor mediated endocytosis - non-enveloped viruses.

237
Q

What is the study of determinants, frequency, dynamics, and distribution of viral diseases in populations?

A

Virus epidemiology

238
Q

Why are we even studying epidemiology of viral diseases?

A

The risk of infection/disease in the animal is determined by virus, the host, and the environment (also behavior and ecology)

239
Q

What numbers are we interested in based on the outcome of disease in populations?

A

Case fatality rate, mortality rate, and morbidity rate.

240
Q

What is the % of deaths among the clinically ill animals?

A

Case-fatality rate

241
Q

If an animal population of 100 had 25 sick animals and 10 dead animals, what is the case-fatality rate?

A

40% (10/25 x 100)

242
Q

What is the % of animals in a population that die from a particular disease over a specified period of time?

A

Mortality rate

243
Q

If an animal population of 100 had 25 sick animals and 10 dead animals, what is the mortality rate?

A

10% (10/100 x 100)

244
Q

What is the % of animals in a population that develop clinical signs attributable to a particular virus over a defined period of time?

A

Morbidity rate

245
Q

What is the # of new cases that occur in a population over a specified period of time?

A

Incidence

246
Q

How do you calculate the incidence rate?

A

(# of cases x 10^n) / (population at risk) in a specified period of time

247
Q

What is the # of occurrences of disease (old and new cases), infection, or related attributes (antibodies) in a population, at a particular point of time?

A

Prevalence

248
Q

How do you calculate the prevalence rate?

A

(# of cases x 10^n) / (population at risk) at a particular time; The ratio, at a particular point in time of the # of cases currently present in the population divided by the # of animals in the population

249
Q

For chronic diseases, it is customary to determine the _______________________. A. Incidence B. Prevalence

A

B. Prevalence

250
Q

This type of disease occurs occasionally, singly, or in scattered instances, and in an irregular and haphazard manner.

A

Sporadic viral disease

251
Q

This type of disease refers to the constant presence of viral disease within a given geographic area or population, such as Dengue virus in the tropic and Louping Ill disease in the British Isles.

A

Enzootic viral disease (endemic in humans)

252
Q

This type of disease refers to the occurrence of more cases of viral diseases than expected in a given area or among a specific group of people/animals over a particular period of time.

A

Epizootic viral disease (epidemic in humans)

253
Q

This is a viral epidemic occurring over a very wide area (several countries or continents) and usually affecting a large proportion of the population.

A

Panzootic viral disease (pandemic in humans)

254
Q

A __________________ is an animal that has contracted an infectious viral disease, but display no clinical symptoms.

A

Carrier (however, they are continuous or intermittent shedders of the disease)

255
Q

This type of carrier refers to an animal that sheds the virus during the incubation period of the disease.

A

Incubatory (acute) carrier

256
Q

This type of carrier refers to an animal that sheds the virus during recovery from disease.

A

Convalescent (chronic) carrier

257
Q

This carrier state may exist in an animal with an infection that is inapparent throughout its course.

A

Inapparent carrier

258
Q

Who is the inapparent carrier of African Horse Sickness caused by the orbivirus?

A

Zebra

259
Q

This is a disease that spreads from one person or organism to another by direct or indirect contact.

A

Contagious disease (period of contagiousness is when the infected animal sheds the virus)

260
Q

This is a disease that is not known to occur in a particular country or geographical area.

A

Exotic disease

261
Q

This is the habitat in which an infectious agent normally lives, grows and multiplies; it may be animate or inanimate.

A

Reservoir

262
Q

This is the systemic collection, analysis, interpretation, and dissemination of health data on an ongoing basis, to gain knowledge of the pattern of disease occurrence and potential in a community, in order to control and prevent disease in a community.

A

Surveillance

263
Q

What are 2 methods to study epidemiology of viruses?

A

Seroepidemiology (have to determine prevalence or incidence; study of duration of viral infection) and molecular epidemiology of viruses (important in identifying new viruses, viral load in host, vaccines, diagnostics, and zoonoses)

264
Q

Most viruses are transmitted this way. It is the spread of an infectious agent from one person/animal or group to another person/animal or group.

A

Horizontal (lateral) transmission

265
Q

Biting, fucking, licking, rubbing, sneezing, and coughing (saliva/mucus traveling less than 1 meter from the source to the susceptible host) are all examples of what type of virus transmission?

A

Direct contact horizontal transmission

266
Q

Sharing eating containers, bedding, restraint devices, clothing, and the use of improperly sterilized surgical equipment/syringes are all examples of what type of virus transmission?

A

Indirect contact horizontal transmission (ex. contaminated farm boots/equipment > gastroenteritis virus > coronavirus in piglets)

267
Q

The spread of infectious agents by droplet nuclei in dust that travel more than 1 meter to the susceptible host is what type of virus transmission?

A

Airborne

268
Q

The passive transport of the infectious agent on the feet or other body part of an arthropod vector is what type virus transmission?

A

Mechanical vector transmission/ mechanical arthropod-borne transmission (ex. mosquitos > Fowlpox virus)

269
Q

An infectious agent that undergoes either a necessary part of its life cycle, or multiplication in the vector before transmission to a susceptible host is what type of virus transmission?

A

Biological vector transmission/ biological arthropod-borne transmission

270
Q

The ___________________________________ is the period when replication of the ingested virus takes place in the insect gut, and is spread to the salivary glands.

A

Extrinsic incubation period

271
Q

________________________ transmission is when the virus is transmitted from the mother tick through infected eggs to the next generation of ticks.

A

Transovarial transmission

272
Q

________________________ transmission is when the virus is transmitted from larva or nymph to the next stage of development (adult or nymph), but is not transmitted vertically. (ex. tick borne flavivirus)

A

Trans-stadial transmission

273
Q

T or F. Arboviruses are a class of viruses transmitted to humans by arthropods such as mosquitoes and ticks.

A

True (Arthropod-borne virus)

274
Q

The natural transmission of virus between wild animals/birds (vertebrate hosts) and primary insect vectors.

A

Enzootic cycle (sylvatic or jungle cycle)

275
Q

The virus is transmitted between non-wild or domestic animals and the primary or accessory insect vectors.

A

Epizootic cycle (rural cycle)

276
Q

The virus cycles between humans and insect vectors.

A

Urban cycle

277
Q

This is a type of host from which infectious agents are not transmitted to other susceptible hosts. They do not develop sufficient viremia to be picked up by the insect vectors.

A

Dead-end host or incidental host

278
Q

This is an arthropod that acquires a virus from an infected wild animal and subsequently transmits the agent to human or secondary host.

A

Bridge vector

279
Q

This type of transmission includes fecal contamination of food and water supplies and virus-contaminated meat or bone products.

A

Common vehicle transmission (ex. Classical Swine fever and BSE)

280
Q

This is an infection that is transferred during medical or surgical practice.

A

Iatrogenic transmission (ex. Equine Infectious Anemia via multiple use needles and the presence of porcine circovirus genome in a Rotavirus vaccine)

281
Q

This type of infection occurs while an animal is in a veterinary hospital or clinic.

A

Nosocomial infection

282
Q

This type of transmission is usually used to describe infection that is transferred from dam to embryo, fetus, or newborn before, during, or shortly after parturition (colostrum, milk, or fecal contamination of teats).

A

Vertical transmission

283
Q

This is a type of infection that is transmissible from animals to humans.

A

Zoonosis

284
Q

Be able to explain Replication of DOUBLE-STRANDED DNA viral genome and production of Viral mRNA

A
285
Q

Be able to explain replication of SINGLE STRANDED DNA viral genome and production of Viral mRNA

A
286
Q

Be able to explain replication of DOUBLE-STRANDED RNA viral genome and production of Viral mRNA

A
287
Q

Be able to explain replication of SINGLE STRANDED (-) RNA Viral genome and production of viral mRNA

A
288
Q

Be able to explain replication of SINGLE STRANDED (+) RNA viral genome and production of viral mRNA

A
289
Q

Be able to explain replication of SINGLE STRANDED (+) by REVERSE TRANSCRIPTASE

A
290
Q

Be able to explain replication of DOUBLE STRANDED DNA viral gnome and production of proteins by REVERSE TRANSCRIPTASE

A
291
Q

What is incorrect about processing of primary RNA transcription (Pre-mRNA)?

A. viral mRNA is translated by cellular protein synthetic apparatus.

B. Viral mRNA must conform requirements of the host cell translation system (host cell should be able to recognize).

C. Cap5’7 methy-gppp and attach the poly-A tail must occur.

D. After processing, mRNA’s are translated in the nucleus.

E. Viral mRNA produced in the nucleus is exported to the cytoplasm.

A

D. After processing, mRNA’s are translated in the nucleus.

Translated in cytoplasm

292
Q

Match the terms.

A. Capping B. Adding 3’Poly-Adenylated tails C. Splicing

  1. Removes introns and joins exons in a primary transcript.
  2. Offers stability of mRNA, binding of mRNA to ribosomes, marks as self mRNA
  3. Cleavage occurs at 10-35 nucleotides downstream from specific signal sequence. A second signal is located about 50 nucleotides downstrea from the cleavage site.
A

A - 2

B - 3

C - 1

293
Q

How do these viruses synthesize their cap?

Retrovirus, adenovirus, poxvirus, reovirus, influenza virus.

Host cell enzymes, viral enzymes, cap snatching.

A

Host cell enzymes: retrovirus and adenovirus

Viral enzymes: poxvirus and reovirus

Cap snatching: infleunza virus

294
Q

T/F. mRNA’s can be polyadenylated by host or viral enzymes. Poly-A acid polymerase is an important enzyme when adding 3’poly-adenylated tails.

A

True.

295
Q

T/F. Poly-A tail contains ~250 A residues in mammals. The major signal for the 3’ cleavage is the sequence AAUAAA.

A

TRUE

296
Q

What are two important ways of splicing? What is the purpose of splicing?

A

Constitutive splicing: every intro out and every exon in.

Alternative splicing: all introns out and only selected exons in.

mRNA’s having different coding information from a single gene.

297
Q

What is the difference between polycistronic and monocistronic mRNA? What is an important enzyme for polycistronic mRNA and what is its function?

A

Monocistronic: mRNA that encodes for one polypeptide

Polycistronic: mRNA that encodes for several polypeptide.

Proteases (can come from virus or host): cleave up the poly-proteins into structural and non-structural proteins.

298
Q

Match

A. Lysins B. Retroviral integrase C. Reverse transcriptase D. Nucleic acid polymerase E. Neuraminidases

  1. Enzyme produced by a retrovirus that enables its genetic material to be integrated into DNA of the infected cell.
  2. Needed for viral genome replication.
  3. Enzymes that cleave glycosidic bonds > allows release of viruses from host cell.
  4. Hyrolytic enzymes produced by bacteriophages to cleave the host’s cell wall.
  5. Enzyme used to generate complementary DNA (cDNA) from a RNA template.
A

A - 4

B - 1

C - 5

D - 2

E - 3

299
Q

T/F. VP7 and VP4 protines of rotaviruses form the viral capsid.

A

True.

300
Q

What is incorrect about non-structural proteins?

A. Proteins encoded by a viral genome that are produced in the organisms they infect but not packaged into the virus particles.

B. Play roles within the infected cell during virus replciation or act in regulation of virus replication or virus assembly.

C. V7P and V5P genes of Rotavirus.

D. None of the above.

A

C. V7P and V5P genes of Rotavirus.

NSP1 - NSP5

301
Q

Which statement is incorrect about regulatory proteins?

A. Indirect roles in the biological processes and activities of viruses.

B. Regulate the expression of viral genes or are involved in modifying host cell functions.

C. Multiple functions.

D. Products of the retroviral NEF gene.

E. None of the above.

A

E. None of the above.

302
Q

Which of the following is incorrect about assembly and maturation of viruses?

A. Assembly follows a specific order.

B. Nucleic acids and proteins are packaged to form mature virions.

C. Takes place only in cytoplasm.

D. Naked virions use lysis of host cell and enveloped virions use budding to escape.

A

C. Takes place only in cytoplasm.

Takes places in nuclues, cytoplasm, plasma cell membrane (most enveloped viruses)

303
Q

What is exocytosis and when/who is it used by?

A

Budding through the membranes of golgi apparatus or ER; migrate to the plasma membrane and are released by exocytosis.

Flaviviruses, Arteriviruses, Coronaviruses, and Bunyaviruses

304
Q

Why is integrase important in replication of retroviruses?

A

DNA is integrated into host DNA > virus replication > maturation occurs > progeny are made

305
Q

Match. Can use A and B more than once.

A. Extracellular spread B. Intercellular spread C. Nuclear spread

  1. Released from cells (already infected) by budding or lysis to infect the next cell.
  2. Without contact with extracellular environment.
  3. Advantages include: rapid dissemination of virus, evasion of host immune system, persistent infection.
  4. The most efficient way of spreading.
  5. Seen in HIV, herpes, and measles.
  6. Integrated in the host cell genome and passed to next progeny/generation of host cells.
  7. Seen in retrovirus.
A

1 - A

2 - B

3 - B

4 - B

5 - B

6- C

7 - C

306
Q

Which is not the route for intercellular spread?

A. Plasma membrane fusion (herpes, paramoxyvirus, retrovirus)

B. Tight junctions (herpes)

C. Neural synapse (rabies)

D. Actin or tubulin structures (poxvirus)

E. Subverion of Actin-containing structure (retrovirus)

F. Non-tube subversion (HIV)

G. Virological synapses (retrovirus)

H. Desmosomes (paramoxyvirus)

A

H. Desmosomes (paramoxyvirus)

307
Q

Match the words.

A. Pathogenicity B. Pathogenesis C. Pathogen D. Virulence E. Avirulent

  1. Manner/mechanism of development of a disease.
  2. Quantitative or relative measure of the degree of pathogencitiy of the infecting virus.
  3. Not virulent (not harmful to the host).
  4. Ability of a virus to cause diases in host.
  5. The virus that causes a disease.
A

A - 4

B - 1

C - 5

D - 2

E - 3

308
Q

T/F. The higher ID50 and LD50, the more virulent the organism

A

False. The lower.

309
Q

Which one is NOT the way to assess virulence?

A. Degree of severity of illness (clinical signs)

B. Experimental animals

C. Incubation period

D. Location, distribution of gross, histologic or ultrastructural lesions in affected animals (the extent of lesion distribution).

E. Zoonoses

A

E. Zoonoses

Made it up

310
Q

Which is incorrect about typical acute infection by a virus?

A. Innate immunity comes into play when infection is established.

B. Virus has to overcome the host’s innate defenses.

C. Adaptive immune response is activated and the infection is cleared.

D. Immune and memory cells remain after infection is cleared and if host is infected again, the immune response is stronger.

E. The presmise is false. Everything is true.

A

E. The presmise is false. Everything is true.

VIROLOGY JK (1 decks)

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