Question 1

Cell culture — Which of the following are continuous (immortal) human cell lines used in virology labs?

Accepted Answer

Introduction / Context:Choosing the right cell line is critical for virus isolation and research. Continuous (immortal) lines divide indefinitely under culture, unlike primary or semi-continuous diploid strains that senesce after limited passages.Given Data / Assumptions:HeLa (cervical carcinoma), HEp-2 (laryngeal/epithelial carcinoma), and KB (epithelial carcinoma) are widely cited.Continuous lines are aneuploid and immortal.Concept / Approach:HeLa, HEp-2, and KB are classic continuous human lines, commonly permissive for a range of human viruses. In contrast, semi-continuous diploid lines include WI-38 and MRC-5, which have finite lifespans and near-diploid karyotypes.Step-by-Step Solution:Identify each listed line as continuous/immortal.Note broad laboratory use for cytopathic-effect assays and neutralization tests.Therefore, select “All of these.”Verification / Alternative check:Standard virology manuals categorize these three as continuous lines used for viral culture and research.Why Other Options Are Wrong:HeLa alone, HEp-2 alone, or KB alone: each is true but incomplete; the grouping answer captures all correct cases.Common Pitfalls:Confusing continuous lines with human diploid strains like WI-38/MRC-5; the latter are not immortal.Final Answer:All of these

Question 2

Phage–host interactions — When a virus enters a cell but does not replicate immediately, what is this non-productive state called?

Accepted Answer

Introduction / Context:Temperate bacteriophages can enter a dormant relationship with the host instead of immediately replicating and lysing the cell. Recognizing this state is essential for understanding bacterial virulence conversion, phage therapy, and prophage dynamics.Given Data / Assumptions:Virus enters cell and does not immediately replicate.Context fits classic temperate phage behavior.For animal viruses the analogous concept is latency, but in bacteriophages it is lysogeny.Concept / Approach:Lysogeny occurs when phage DNA integrates into (or persists in) the bacterial chromosome as a prophage, maintained by repressor proteins that silence lytic genes. The host replicates the prophage passively during cell division, conferring immunity to superinfection by the same phage type.Step-by-Step Solution:Interpret “no immediate replication” as repression of lytic functions.Map this to the prophage state termed lysogeny.Exclude unrelated biological terms (fermentation, symbiosis, synergism).Verification / Alternative check:Lambda phage models unequivocally define lysogeny as the nonproductive prophage state that can later switch (induce) to lysis.Why Other Options Are Wrong:Fermentation: microbial metabolism, not a viral lifecycle state.Symbiosis: broad ecological term, lacks genetic control implications.Synergism: interaction effect term, not a lifecycle state.Common Pitfalls:Confusing lysogeny (phages) with latency (animal viruses); both are dormancy but in different biological contexts.Final Answer:Lysogeny

Question 3

Induction triggers — A switch from lysogeny to lysis in temperate bacteriophages is commonly induced by which of the following?

Accepted Answer

Introduction / Context:Induction is the escape of a prophage from the lysogenic state into productive replication and cell lysis. It is classically tied to the bacterial SOS response following DNA damage.Given Data / Assumptions:External stressors that damage DNA can inactivate the phage repressor system.Multiple modalities can cause such damage: UV light, chemicals, and various forms of irradiation.Concept / Approach:DNA damage activates RecA, which promotes autocleavage of certain phage repressors (e.g., lambda cI), derepressing lytic genes. Therefore, any agent that triggers the SOS pathway can induce prophage excision and lytic growth.Step-by-Step Solution:Link UV, chemicals, ionizing radiation to DNA damage.Tie DNA damage to SOS response and repressor inactivation.Conclude that all listed triggers can cause induction.Verification / Alternative check:Classic experiments show increased phage titers after exposing lysogens to UV or mitomycin C, confirming induction by diverse genotoxic stresses.Why Other Options Are Wrong:Individual triggers alone are correct but incomplete; the comprehensive answer is “All of these.”Common Pitfalls:Assuming only UV light induces prophages; many chemical agents do so as well via the same SOS pathway.Final Answer:All of these

Question 4

Absolute requirement — What essential condition do viruses need for growth and replication?

Accepted Answer

Introduction / Context:Viruses are obligate intracellular parasites. They do not encode complete systems for energy production or protein synthesis; therefore, they must exploit a living cell's machinery to replicate their genomes and assemble progeny virions.Given Data / Assumptions:Virus replication depends on host ribosomes, nucleotides, ATP, and often host enzymes.Hosts can be bacteria, archaea, plants, animals, fungi, or protozoa.Concept / Approach:The universal requirement is not the host type but the “living cell” itself. Inert environments or cell-free media do not support complete viral replication cycles (with rare specialized exceptions requiring supplemented extracts), reinforcing the absolute need for living cellular systems.Step-by-Step Solution:Abstract away host taxonomy; focus on cellular status.Recognize dependency on active metabolic and translational machinery.Select “Living cells” as the only universally correct option.Verification / Alternative check:Laboratory propagation of viruses always employs living systems: cell cultures, embryonated eggs, or whole hosts, each providing active cellular processes.Why Other Options Are Wrong:Bacteria/plants/animals: too narrow; many viruses infect other domains.Common Pitfalls:Equating “animal viruses” with all viruses; bacteriophages and plant viruses demonstrate the broader host spectrum.Final Answer:Living cells

Question 5

Bacteriophage entry — What is the first step in infection of a bacterial host cell by a phage?

Accepted Answer

Introduction / Context:Phage infection is a multi-step process with defined order: adsorption, penetration, biosynthesis, assembly, and release. Mislabeling the first step confuses receptor biology and host-range concepts.Given Data / Assumptions:We consider tailed bacteriophages as canonical examples.Specificity is mediated by tail fibers or other receptor-binding structures.Concept / Approach:Adsorption (attachment) to host receptors such as LPS, teichoic acids, or transport proteins is the initiating interaction. Only after stable attachment does the phage inject its nucleic acid (penetration). Replication is later, and “absorption” refers to a physical process unrelated to infection steps.Step-by-Step Solution:Identify receptor-mediated binding as step one.Distinguish adsorption (binding) from penetration (injection).Place genome replication downstream in the timeline.Verification / Alternative check:Classical one-step growth experiments and EM studies confirm visible attachment prior to DNA ejection and intracellular replication events.Why Other Options Are Wrong:Absorption: not a virology lifecycle term; distractor.Penetration: follows adsorption.Replication: occurs after uncoating/penetration.Common Pitfalls:Swapping “adsorption” with “absorption”; in virology, adsorption = attachment.Final Answer:Adsorption (attachment to specific receptors)

Question 6

Lambda phage control — The lysogenic state is governed by a specific regulatory region of the λ (lambda) genome. What is this region traditionally called?

Accepted Answer

Introduction / Context:Lambda phage is a model for gene regulation. Texts distinguish between the immunity region (a genomic region encompassing operators and promoters controlling repressor expression) and the repressor protein itself (cI). Precision matters when naming DNA regions versus proteins.Given Data / Assumptions:The question asks for the region, not a protein.Common correct term is “immunity region,” containing operators OL/OR, promoters PL/PR, and cI locus control elements.Options provided do not include “immunity region.”Concept / Approach:Disambiguate terms: “immunity repressor” refers to the cI protein; “operon repressor” is a generic phrase; “immunity operon” is nonstandard. Since none accurately names the regulatory region, select “None of these.”Step-by-Step Solution:Identify the expected term: immunity region (not listed).Eliminate protein-level terms when a DNA region is asked.Choose “None of these” as the only precise answer.Verification / Alternative check:Lambda genetics maps label the “imm^λ” (immunity) region controlling lysogeny via cI expression and operator/promoter architecture; textbooks avoid calling it an “operon.”Why Other Options Are Wrong:Immunity repressor: a protein, not a region.Immunity operon: not standard nomenclature for λ regulatory DNA.Operon repressor: vague and incorrect.Common Pitfalls:Confusing the repressor protein name (cI) with the broader regulatory DNA elements that establish immunity to superinfection.Final Answer:None of these

Question 7

Viral taxonomy — Which of the following virus(es) belongs to the family Caliciviridae (as classically tested in many MCQ banks)?

Accepted Answer

Introduction / Context:MCQ items on Caliciviridae often probe recognition of “calici-like” viruses associated with fecal–oral transmission and gastroenteritis. Historically, Hepatitis E virus (HEV) was grouped by some sources as a calici-like virus; modern taxonomy places HEV in the family Hepeviridae. Many legacy question banks, however, still key HEV to Caliciviridae-type properties.Given Data / Assumptions:HBV (Hepadnaviridae) and HDV (Deltavirus) are not Caliciviridae.Legacy exam framing frequently lists HEV as the “calici-like” pick among hepatitis viruses.The stem asks “belong/s to family caliciviridae,” reflecting older MCQ convention.Concept / Approach:Answer per conventional MCQ expectation: choose HEV as the option associated with calici-like classification in older literature. Provide clarifying note so learners are aware of updated taxonomy where HEV = Hepeviridae, while true Caliciviridae include noroviruses and sapoviruses.Step-by-Step Solution:Eliminate HBV (partially double-stranded DNA; Hepadnaviridae).Eliminate HDV (satellite virus; requires HBV; Deltavirus).Select HEV as the traditionally “calici-like” choice tested in many exams.Verification / Alternative check:Modern references designate Norovirus and Sapovirus as Caliciviridae; HEV is Hepeviridae. Exams may still expect HEV when asked in this dated format.Why Other Options Are Wrong:Hepatitis B virus: different family and genome type.Hepatitis D virus: defective RNA virus, satellite of HBV.All of these: incorrect because the first two are not caliciviruses by any scheme.Common Pitfalls:Memorizing only modern taxonomy without being aware of older MCQ conventions; always read the examiner’s likely framing.Final Answer:Hepatitis E virus

Question 8

Virology — Which of the following viruses is susceptible to chloroform (i.e., inactivated by solvents that disrupt lipid envelopes)?

Accepted Answer

Introduction:Chloroform and other lipid solvents disrupt lipid envelopes. Enveloped viruses are generally sensitive to detergents, alcohols, and solvents that extract membrane lipids. This question evaluates recognition of envelope dependence for infectivity.Given Data / Assumptions:Choices include Herpes virus, Influenza virus, and Measles virus.Chloroform is a lipid solvent that can disrupt envelopes.Nonenveloped viruses are usually resistant to chloroform.Concept / Approach:Viral envelopes are host-derived lipid bilayers containing viral glycoproteins needed for attachment and fusion. Removal or disruption of this envelope inactivates the virion. Therefore, any classically enveloped virus is chloroform sensitive in standard laboratory conditions.Step-by-Step Solution:Identify which listed viruses are enveloped: Herpesviruses are enveloped.Influenza viruses are enveloped orthomyxoviruses.Measles virus is an enveloped paramyxovirus.Enveloped status implies chloroform susceptibility for all listed viruses.Verification / Alternative check:Textbook disinfection tables list enveloped viruses as more labile to solvents and detergents than nonenveloped viruses like adenovirus or poliovirus. Chloroform is a classic reagent demonstrating this differential sensitivity.Why Other Options Are Wrong:Herpes virus alone: true but incomplete because others are also susceptible.Influenza virus alone: true but incomplete.Measles virus alone: true but incomplete.Common Pitfalls:Assuming all viruses respond the same way to disinfectants; envelope presence is the key determinant of solvent sensitivity.Final Answer:All of these

Question 9

Vaccinology — In an attenuated (live-attenuated) vaccine, what is true about the vaccine viruses?

Accepted Answer

Introduction:Live-attenuated vaccines contain weakened versions of pathogens that retain the ability to replicate, but with markedly reduced virulence. This question checks understanding of how attenuation differs from inactivation and why attenuation elicits durable immunity.Given Data / Assumptions:Attenuated viruses are weakened, not killed.Chemical inactivation is associated with inactivated vaccines, not attenuated ones.Viruses are much smaller than bacteria and always require a genome to replicate.Concept / Approach:Attenuated strains replicate at low levels after vaccination, providing antigenic stimulation that mimics natural infection without causing disease in immunocompetent hosts. This limited replication enhances both humoral and cellular immune responses and often yields long-lasting protection after a single dose.Step-by-Step Solution:Exclude no-genome option because replication requires genetic material.Exclude larger-than-bacteria because viruses are subcellular and smaller.Exclude chemical inactivation because that describes killed vaccines.Select continued limited replication as the defining property of attenuation.Verification / Alternative check:Clinical examples include measles, mumps, rubella, varicella, and oral polio vaccine strains, all of which replicate transiently to induce robust immunity.Why Other Options Are Wrong:No genome: impossible for a replicating virus.Larger than bacteria: virology fundamentals contradict this.Chemically altered or killed: describes inactivated vaccines, not attenuated vaccines.Common Pitfalls:Confusing live-attenuated with inactivated vaccines and assuming replication is absent.Final Answer:They continue to replicate in the recipient to a limited extent

Question 10

Plant virology — Valid systems for cultivating plant viruses include which of the following?

Accepted Answer

Introduction:Plant viruses can be propagated in several experimental systems. Recognizing these systems helps in diagnostics, pathogenesis studies, and seed certification testing for virus-free stock.Given Data / Assumptions:Options include explant tissue culture, isolated cell or protoplast systems, and intact plants.Each method has specific use-cases based on virus host range and research goals.Concept / Approach:Viruses require living cells for replication. Depending on the virus and the desired readout, researchers may inoculate whole plants, use callus or tissue cultures, or infect isolated cells or protoplasts to study replication and movement.Step-by-Step Solution:Confirm that intact susceptible plants are a traditional propagation system.Note that tissue culture allows controlled growth and virus maintenance.Recognize that separated cells or protoplasts permit synchronized infection and mechanistic studies.Therefore, all listed systems are valid for cultivation.Verification / Alternative check:Standard plant pathology protocols employ mechanical inoculation on whole plants and protoplast infection for molecular analyses.Why Other Options Are Wrong:Single-method options are incomplete because multiple systems are well established.Common Pitfalls:Assuming only intact plants support virus growth; cell-based systems are widely used for controlled experiments.Final Answer:All of these

Question 11

Bacteriophage biology — The viral DNA of a temperate phage integrates into the host chromosome and becomes a prophage acting like a gene. This state is called:

Accepted Answer

Introduction:Temperate bacteriophages can choose between two developmental pathways. Integration of phage DNA into the host chromosome establishes a stable relationship with the bacterium. Knowing the terminology is fundamental to microbial genetics.Given Data / Assumptions:Temperate phage can integrate into host DNA.Integrated phage DNA is called a prophage.Question asks for the name of this integrated state.Concept / Approach:Lysogeny is the state in which a prophage is maintained and replicated with the host chromosome during cell division. Under certain triggers, the prophage can excise and enter the lytic cycle to produce new virions and lyse the cell.Step-by-Step Solution:Map integrated prophage state to the term lysogeny.Differentiate from lytic phase, which involves active replication and lysis.Recognize spontaneous induction as a separate event where prophage exits lysogeny without an external inducer.Verification / Alternative check:Classic lambda phage models define lysogeny as stable prophage carriage with repression of lytic functions by repressor proteins.Why Other Options Are Wrong:Spontaneous induction: describes exit from lysogeny, not the integrated state.Lytic phase: opposite program with phage production and cell lysis.None of these: incorrect because lysogeny precisely matches the description.Common Pitfalls:Confusing the state (lysogeny) with the transition out of it (induction).Final Answer:Lysogeny

Question 12

Cell culture — Which of the following is a semi-continuous human diploid cell line commonly used in virology?

Accepted Answer

Introduction:Human cell lines are categorized as primary, semi-continuous (diploid), or continuous (immortalized). This question assesses knowledge of classic lines used for viral isolation and vaccine research.Given Data / Assumptions:HeLa, HEp-2, and KB are well-known continuous lines.WI-38 is a human diploid fibroblast strain.Semi-continuous lines retain finite lifespan and normal karyotype features.Concept / Approach:Diploid strains such as WI-38 and MRC-5 are finite lines with limited passages and near-diploid chromosomes, making them suitable for certain vaccine production steps and for maintaining differentiated properties relative to immortalized lines.Step-by-Step Solution:Identify which option is human diploid: WI-38.Exclude HeLa (immortal cervical carcinoma).Exclude HEp-2 (carcinoma-derived, continuous).Exclude KB (epithelial carcinoma line).Verification / Alternative check:Standard virology references list WI-38 and MRC-5 as semi-continuous diploid fibroblasts with finite passage numbers, used historically for certain vaccines.Why Other Options Are Wrong:HeLa: continuous, aneuploid, immortal.HEp-2: continuous human epithelial line.KB: continuous carcinoma line.Common Pitfalls:Assuming all frequently used lines are diploid; many popular lines are immortalized and continuous.Final Answer:WI-38

Question 13

Temperate phages — When prophage DNA excises from the host chromosome and the phage enters the lytic cycle, the process is called:

Accepted Answer

Introduction:Induction is the switch from lysogeny to the lytic cycle in temperate bacteriophages. The term distinguishes how the prophage is activated to replicate and lyse the cell.Given Data / Assumptions:Prophage DNA can excise from the chromosome.Entry into the lytic cycle follows excision.If no external trigger is specified, the baseline term is spontaneous induction.Concept / Approach:Induction can be triggered by DNA damage (e.g., UV), chemicals, or occur at low frequency without external stimuli. The latter is termed spontaneous induction and reflects stochastic loss of repression or cellular stress fluctuations.Step-by-Step Solution:Define induction as transition from lysogeny to lytic growth.Without specified trigger, choose spontaneous induction.Reject distractor phrases not used in standard phage terminology.Verification / Alternative check:Lambda phage literature routinely uses spontaneous induction to describe prophage activation events in the absence of deliberate inducers.Why Other Options Are Wrong:Inductive infection: nonstandard term.Resultant induction: nonstandard term.Spontaneous infection: describes infection, not prophage activation.Common Pitfalls:Confusing induction with lysogenization, which is the establishment of lysogeny.Final Answer:Spontaneous induction

Question 14

Virus morphology — Enveloped viruses typically exhibit what overall particle shape under electron microscopy?

Accepted Answer

Introduction:Viral morphology can be icosahedral, helical, complex, or pleomorphic. Envelopes are host-derived lipid bilayers surrounding the nucleocapsid and often lead to variability in shape. This question examines recognition of envelope-associated morphology.Given Data / Assumptions:Enveloped particles acquire membranes by budding.Membrane flexibility allows size and shape variability.Internal symmetry can be helical or icosahedral even when the outer shape appears pleomorphic.Concept / Approach:Because the lipid envelope is deformable, many enveloped viruses look spherical or pleomorphic rather than strictly geometric. Classic examples include influenza (pleomorphic), togaviruses (spherical), and coronaviruses (spherical with surface projections).Step-by-Step Solution:Relate envelope presence to flexible particle contours.Recognize pleomorphism as a hallmark of many enveloped viruses.Select roughly spherical or pleomorphic as the best global descriptor.Verification / Alternative check:EM atlases consistently depict many enveloped virions as spheres with variable diameters or irregular outlines, unlike rigid nonenveloped icosahedral capsids.Why Other Options Are Wrong:Icosahedral: common for nonenveloped capsids; envelope masks strict geometry.Helical: describes nucleocapsid symmetry; the envelope often yields pleomorphism.Complex: typical for tailed bacteriophages, not enveloped animal viruses.Common Pitfalls:Conflating internal symmetry with overall particle outline; an enveloped virion can contain an icosahedral core but appear spherical externally.Final Answer:Roughly spherical or pleomorphic

Question 15

Flaviviridae taxonomy — Which viruses are members of the family Flaviviridae? (Select the option that correctly groups members.)

Accepted Answer

Introduction:Accurate viral classification is important for understanding transmission, pathogenesis, and antiviral targets. Flaviviridae includes mosquito-borne flaviviruses and the hepaciviruses, with important human pathogens across both genera.Given Data / Assumptions:Rubella is listed alongside Yellow fever virus and Hepatitis C virus.The family Flaviviridae comprises genera such as Flavivirus and Hepacivirus.Only one option should be entirely correct.Concept / Approach:Yellow fever virus is a prototypic Flavivirus. Hepatitis C virus belongs to the genus Hepacivirus within Flaviviridae. Rubella virus, however, is a Rubivirus placed in the Togaviridae family, not Flaviviridae. Therefore the correct grouping must include Yellow fever and Hepatitis C but exclude Rubella.Step-by-Step Solution:Confirm Yellow fever virus as Flaviviridae.Confirm Hepatitis C virus as Flaviviridae.Identify Rubella as Togaviridae.Choose the option that includes the first two and excludes Rubella.Verification / Alternative check:Standard taxonomy charts list Flaviviridae members such as dengue, yellow fever, West Nile, Zika (Flavivirus) and hepatitis C (Hepacivirus). Rubella is separated under Togaviridae.Why Other Options Are Wrong:Rubella virus only: wrong family.Yellow fever virus only: incomplete because it omits Hepatitis C virus.Hepatitis C virus only: incomplete because it omits Yellow fever virus.None of these: incorrect because two members are indeed Flaviviridae.Common Pitfalls:Memorizing only arthropod-borne members and forgetting that Hepatitis C is also in Flaviviridae.Final Answer:Both Yellow fever virus and Hepatitis C virus

Question 16

Viral enzymes — Which virus carries the enzyme neuraminidase as a surface glycoprotein?

Accepted Answer

Introduction:Some viruses package or express characteristic enzymes and glycoproteins that are central to their life cycle and serve as drug targets. Neuraminidase is a hallmark enzyme of influenza virions used in viral release from infected cells.Given Data / Assumptions:We are asked to identify the virus associated with neuraminidase.Candidates include RNA and DNA viruses with distinct biology.Concept / Approach:Influenza A and B have two major surface glycoproteins: hemagglutinin and neuraminidase. Neuraminidase cleaves terminal sialic acid residues, facilitating virion release and preventing reattachment to the same cell. This enzyme is the target of oseltamivir and zanamivir.Step-by-Step Solution:Recall influenza surface proteins: HA and NA.Match neuraminidase presence to influenza.Exclude other viruses lacking neuraminidase as a defining feature.Verification / Alternative check:Drug classes named neuraminidase inhibitors are clinically used for influenza, confirming the association.Why Other Options Are Wrong:HIV: carries reverse transcriptase, integrase, and protease, not neuraminidase.Epstein–Barr virus: herpesvirus with different glycoprotein set.Adenovirus: nonenveloped DNA virus without NA.Common Pitfalls:Confusing neuraminidase with neuraminic acid binding by hemagglutinin; HA binds sialic acid, NA cleaves it.Final Answer:Influenza virus

Question 17

Virus replication — Which event is essential for a virus to replicate inside a host cell?

Accepted Answer

Introduction:All viruses are obligate intracellular parasites. Despite diverse entry pathways, a universal requirement is delivery of the viral genome to a permissive intracellular site where replication and expression can proceed.Given Data / Assumptions:Different viruses enter cells by endocytosis, membrane fusion, or direct injection.Some uncoat at the plasma membrane, others in endosomes, and some at nuclear pores.Mitotic state of the host is not universally required.Concept / Approach:Replication cannot begin until the viral nucleic acid is uncoated and becomes accessible to host or viral enzymes. Whether the capsid itself enters fully is not a constant; bacteriophages inject nucleic acid, leaving capsids outside. Therefore, the reliable, generalizable requirement is genome release inside the cell.Step-by-Step Solution:Identify common denominator: genome delivery to cytoplasm or nucleus.Reject options that depend on specific entry modes.Select genome release as the essential event preceding replication and gene expression.Verification / Alternative check:Uncoating is a named step in all standard viral life cycle diagrams, preceding replication, transcription, and translation.Why Other Options Are Wrong:Capsid must enter intact: not required for many viruses such as tailed phages.Host mitosis required: many viruses replicate in nondividing cells.Host must lack membrane: biologically impossible for animal cells; membranes mediate entry.Common Pitfalls:Equating endocytosis of a capsid with a universal rule; mechanisms vary widely across virus families.Final Answer:The viral genome must be released inside the cell to access replication machinery

Question 18

Virology fundamentals – Unit of measurement: In routine electron microscopy and microbiology, the size of viruses is usually expressed in which unit?

Accepted Answer

Introduction:Knowing the typical scale of viruses is a foundational concept in microbiology. Virus particles are smaller than most bacteria and far below the resolving power of light microscopy, which is why electron microscopy and nanometer-scale measurements are commonly used. This question tests whether you can recall the correct unit used for reporting viral dimensions in standard references and laboratory reports.Given Data / Assumptions:Most animal and plant viruses have diameters roughly between 20 nm and 300 nm.Light microscopes resolve down to about 200 nm under ideal conditions.Electron microscopy routinely measures structures in nanometers.Concept / Approach:The metric system offers several units: millimeter (10^-3 m), micrometer (10^-6 m), and nanometer (10^-9 m). Viral dimensions are so small that nanometers are the most practical unit for direct description, comparison, and imaging analysis.Step-by-Step Solution:Step 1: Recall that bacteria are typically 0.5–5 µm; viruses are far smaller.Step 2: Many standard examples: parvoviruses ~20–25 nm; adenoviruses ~90–100 nm; poxviruses ~200–300 nm.Step 3: Because 1 µm = 1000 nm, reporting a 90 nm virion as 0.09 µm is less conventional in virology literature.Step 4: Therefore, the best unit is nanometers (nm).Verification / Alternative check:Textbooks, CDC/WHO fact sheets, and electron microscopy atlases consistently list virion diameters in nanometers, confirming discipline-wide convention.Why Other Options Are Wrong:Centimeters: far too large for microscopic entities.Micrometers: more common for cells and bacteria, not for precise viral sizing.Millimeters: inappropriate scale for microscopic particles.Angstroms as the primary unit: sometimes used for atomic-scale detail (1 Å = 0.1 nm) but not the standard unit for whole virions.Common Pitfalls:Conflating bacterial and viral size ranges; assuming micrometers suffice for all microbes; mixing nm and Å without context.Final Answer:Nanometers (nm).

Question 19

Virology technique: viruses can be purified on the basis of both size and density using which method?

Accepted Answer

Introduction / Context: Purifying viruses from complex biological mixtures requires separating particles based on physical properties such as size and buoyant density. The technique chosen affects purity and yield. This question asks which method allows separation based on both size and density.Given Data / Assumptions:Viruses vary in diameter, mass, and capsid composition, which affect sedimentation behavior.Common lab methods include differential centrifugation, gradient centrifugation (rate-zonal and isopycnic), and precipitation (for example, with polyethylene glycol).Goal: obtain a more homogeneous viral preparation while removing cellular debris and macromolecules.Concept / Approach: Gradient centrifugation uses a preformed gradient (sucrose, CsCl, iodixanol) so particles migrate at rates determined by size and density (rate-zonal) or band at the position where their buoyant density equals the gradient (isopycnic). This enables fine separation of virions from contaminants. Differential centrifugation uses sequential spins at increasing g-forces to sediment larger components first; it is cruder and primarily size-based. Precipitation concentrates particles nonspecifically and is not selective for precise size/density differences.Step-by-Step Solution:Clarify target properties: size and buoyant density.Match technique: gradient centrifugation (rate-zonal or isopycnic) addresses both properties.Contrast alternatives: differential centrifugation is mostly size-based; precipitation is non-selective.Therefore choose gradient centrifugation.Verification / Alternative check: Literature and protocols show viruses banding at distinct densities (for example, CsCl gradients) and fraction collection yielding purified virions.Why Other Options Are Wrong:Differential centrifugation: Coarse fractionation; insufficient density resolution.Precipitation: Concentration method; lacks discriminative separation.None of these: Incorrect because gradient centrifugation fits perfectly.Common Pitfalls: Overloading gradients causing band overlap; using gradients incompatible with virus stability; misinterpreting rate-zonal vs isopycnic goals.Final Answer: gradient centrifugation

Question 20

Bacteriophage replication: the yield of phage particles produced from a single infected bacterium is called what?

Accepted Answer

Introduction / Context: In one-step growth experiments with bacteriophages, key time points and quantities describe viral replication dynamics. Understanding these terms helps interpret growth curves and infection kinetics. This item asks for the term describing the number of phage progeny produced per infected host cell.Given Data / Assumptions:Single-cycle (one-step) growth conditions are assumed.Standard terms: eclipse period, latent period, rise period, and burst size.Measured using plaque assays or quantitative titers over time.Concept / Approach: The burst size is defined as the average number of mature phage particles released from one bacterium at lysis. It depends on phage type, host physiology, and conditions. The eclipse period is when no mature intracellular phage are detectable; the latent period spans from adsorption to the first release of mature phage; the rise period is when extracellular titer increases to a plateau.Step-by-Step Solution:Plot phage titer vs time during synchronous infection.Identify plateau titer and initial adsorbed count.Compute average progeny per infected cell = burst size.Confirm definition: particles per bacterium released upon lysis.Verification / Alternative check: Perform multiplicity-of-infection–controlled assays and compare counts pre- and post-lysis to derive the same number.Why Other Options Are Wrong:Eclipse size: Not a standard term; eclipse refers to a time period with no detectable mature phage.Latent size: Not a standard term; latent refers to a time interval.None of these: Incorrect because “burst size” is well-established.Common Pitfalls: Confusing time intervals (eclipse/latent) with quantitative yield; ignoring partial infections or superinfection effects.Final Answer: burst size

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