Question 1

Bacterial lysogeny (phage conversion) — Which trait(s) are well-known results of lysogenic conversion by bacteriophages?

Accepted Answer

Introduction / Context: Lysogenic conversion occurs when a temperate phage integrates into a bacterial genome and brings genes that alter the phenotype of the host bacterium. This can include toxin genes or surface antigen variations, impacting virulence and epidemiology. Given Data / Assumptions: Corynebacterium diphtheriae requires a tox gene from corynephage for diphtheria toxin production. Certain Clostridium botulinum strains (types C and D) carry phage-encoded botulinum toxin genes. Phase variation, including antigenic shifts in some Salmonella serovars (e.g., anatum), can be influenced by phage elements. Concept / Approach: Because each listed trait is a classic example of phage-mediated conversion, the comprehensive answer is “All of the above.” Recognizing phage roles helps explain sudden acquisition of virulence in bacterial populations. Step-by-Step Solution: Identify temperate phage integration (prophage) as the mechanism.Associate each organism with a phage-encoded phenotype.Select the inclusive option summarizing all examples. Verification / Alternative check: Historical and molecular studies document prophage-encoded toxins and antigenic modifications in these bacteria. Why Other Options Are Wrong: Picking a single item ignores the breadth of documented lysogenic conversions. Common Pitfalls: Assuming all toxins are chromosomal; many key toxins are phage-borne. Final Answer: All of the above

Question 2

Phage architecture — Which capsid symmetry is exhibited by most bacteriophages (tailed phages)?

Accepted Answer

Introduction / Context: Bacteriophages display diverse virion structures. The majority of well-studied phages that infect bacteria are the tailed Caudoviricetes, whose overall virion organization is considered “complex.” Given Data / Assumptions: Tailed phages possess an icosahedral head plus a helical tail and baseplate/tail fibers. Symmetry classification considers the entire virion, not just the head. Non-tailed phages exist but are less common in classical teaching sets. Concept / Approach: Because tailed phages combine distinct symmetrical components (icosahedral head and helical tail), the composite virion is classified as having complex symmetry. Hence “Complex” best describes most phages overall, despite the icosahedral symmetry of their heads alone. Step-by-Step Solution: Recognize tailed phages as predominant.Note mixed architecture: head (icosahedral) + tail (helical) + accessories.Select “Complex” to reflect whole-virion symmetry. Verification / Alternative check: Electron micrographs of T-even phages and lambda phage illustrate the complex assembly. Why Other Options Are Wrong: Helical or icosahedral alone do not describe the combined structure. “None of these” ignores the well-accepted “complex” category. Common Pitfalls: Focusing solely on head symmetry; consider the entire virion. Final Answer: Complex

Question 3

Filamentous phage entry — A filamentous bacteriophage infects male E. coli by attaching specifically to which structure?

Accepted Answer

Introduction / Context: Host recognition by bacteriophages depends on precise receptor binding. Filamentous phages (e.g., M13, fd) target the F pilus on “male” E. coli cells, which carry the F plasmid and express conjugative pili. Given Data / Assumptions: Male E. coli cells present F pili on their surface. Filamentous phages initiate infection by binding the pilus tip. Attachment triggers DNA entry without lysing the host. Concept / Approach: The defining receptor for these phages is the F pilus tip. Binding and pilus retraction or dynamics promote delivery of the phage genome through the pilus into the bacterium, leading to chronic infection rather than immediate lysis. Step-by-Step Solution: Identify the F pilus as the male cell marker.Recall filamentous phage tropism for the pilus tip.Select “the tip of the pilus.” Verification / Alternative check: Classic M13 systems in molecular cloning rely on this pilus-specific entry mechanism. Why Other Options Are Wrong: LPS/cell wall/membrane can be receptors for other phages, but not for filamentous F-specific phages. Common Pitfalls: Confusing F-pilus-dependent phages with LPS-binding tailed phages. Final Answer: the tip of the pilus

Question 4

Phage gene expression timing — Which protein sets are typically synthesized from late mRNA during a lytic infection?

Accepted Answer

Introduction / Context: Lytic phage infections proceed through an ordered transcriptional program: early genes for takeover and replication functions, and late genes for particle construction and release. Knowing which proteins appear from late mRNA clarifies phage biology and biotechnology applications. Given Data / Assumptions: Late gene expression follows genome replication. Late mRNAs encode virion components and lysis machinery. Some late proteins assist assembly but are not retained in the mature virion. Concept / Approach: From late mRNA, phages synthesize capsid and tail proteins (structural), assembly-helper proteins (scaffolding, chaperones), and lysis proteins (e.g., endolysins, holins) that mediate host cell rupture. Therefore, all listed categories are produced from late transcripts. Step-by-Step Solution: Recall early vs. late gene roles.Map late mRNA to structural, assembly, and lysis functions.Select “All of the above.” Verification / Alternative check: Well-characterized phages (e.g., T4) show this transcriptional order; late promoters drive structural and lysis genes. Why Other Options Are Wrong: Picking only one subset ignores the full scope of late-phase products. Common Pitfalls: Assuming lysis proteins are early; they are typically expressed late to time particle release. Final Answer: All of the above

Question 5

Defining lysogeny — Which type of virus is specifically capable of establishing a long-term relationship with a host cell known as lysogeny?

Accepted Answer

Introduction / Context: Lysogeny is a hallmark of temperate bacteriophages, in which the viral genome integrates into, or persists within, the host genome as a prophage without immediate lysis. Understanding this state is key for phage genetics and bacterial evolution. Given Data / Assumptions: Lysogeny = stable, heritable association (prophage) with the host chromosome. Temperate phages can switch between lysogenic and lytic cycles. “Adsorbed virus” merely indicates attachment and does not define life-cycle strategy. Concept / Approach: Only temperate viruses are defined by their ability to form lysogens. While many temperate phages are DNA phages, “DNA phage” is not synonymous with temperate; some DNA phages are strictly lytic. Therefore, the precise term is “Temperate virus.” Step-by-Step Solution: Define lysogeny and prophage state.Match the definition to phage type that can enter lysogeny.Choose “Temperate virus.” Verification / Alternative check: Lambda phage is the classic temperate phage model demonstrating integration and induction. Why Other Options Are Wrong: Adsorbed virus: refers only to attachment. RNA phage: most known are lytic; lysogeny is uncommon in canonical RNA phages. DNA phage: too broad—includes both lytic and temperate phages. Common Pitfalls: Equating genome type (DNA vs RNA) with life-cycle strategy; temperateness is a behavioral category, not a genome-type category. Final Answer: Temperate virus

Question 6

Bacteriophage tail architecture: In which of the following classic phages is a contractile tail sheath present as part of the virion structure?

Accepted Answer

Introduction / Context: Contractile tail sheaths are hallmark features of many Myoviridae bacteriophages (for example, T2, T4, and T6). When the sheath contracts, it drives a rigid tail tube through the bacterial envelope to inject the phage genome. Recognizing which phages possess this mechanism is a frequent exam checkpoint in basic virology and microbiology. Given Data / Assumptions: T-even phages (such as T2) are classic contractile-tailed phages. T3 and P22 are short-tailed or non-contractile-tailed Podoviridae representatives. Only one option should be correct. Concept / Approach: Phage tails come in three broad morphotypes: Myoviridae (long, contractile), Siphoviridae (long, flexible, non-contractile), and Podoviridae (short, stubby, non-contractile). T2 is Myoviridae; T3 and P22 are Podoviridae. Therefore, the presence of a contractile sheath correctly applies to T2 but not to T3 or P22. Step-by-Step Solution: Classify each phage by family/morphotype. T2 → Myoviridae → contractile tail sheath present. T3 → Podoviridae → short, non-contractile tail. P22 → Podoviridae → short, non-contractile tail. Select T2 as the only correct option. Verification / Alternative check: Electron micrographs of T-even phages clearly show a sheath that shortens during infection, while Podoviridae display compact tails without a sheath capable of contraction. Why Other Options Are Wrong: T3 lacks a contractile sheath; P22 lacks a contractile sheath; “All of these” is incorrect because not all listed phages have contractile tails; “None of these” is wrong because T2 does. Common Pitfalls: Confusing general “tail” with “contractile sheath.” Many phages have tails, but only Myoviridae have the dedicated contractile sheath apparatus. Final Answer: T2.

Question 7

Phage head assembly: During bacteriophage capsid morphogenesis, the procapsid (prohead) is assembled with the aid of which helper proteins?

Accepted Answer

Introduction / Context: Assembly of icosahedral bacteriophage heads proceeds through a precursor called the procapsid (or prohead). This intermediate relies on transient helper proteins that guide correct geometry before DNA packaging and maturation. Knowing these helper proteins by name and function is foundational for phage assembly questions. Given Data / Assumptions: Procapsid forms prior to genome packaging. Helper proteins are not part of the final mature capsid. Only one response corresponds to standard terminology. Concept / Approach: “Scaffolding proteins” bind coat protein subunits during early assembly, enforcing correct angular relationships. After capsid maturation (often accompanied by proteolysis and expansion), scaffolding components are released or degraded, leaving a stable head shell ready for DNA packaging. Step-by-Step Solution: Identify the stage: procapsid formation precedes DNA packaging. Recall helper terminology: scaffolding proteins template geometry. Exclude terms not used in phage literature (ladder, framing, form). Select “Scaffolding proteins.” Verification / Alternative check: Classical models from phages like P22 and T7 document scaffolding proteins that are removed upon maturation, validating their transient role. Why Other Options Are Wrong: “Ladder,” “framing,” and “form” are not standard phage assembly terms; chaperonins assist general folding but do not define the procapsid templating function. Common Pitfalls: Assuming helper proteins remain permanently in the capsid; in most systems, they are removed during maturation. Final Answer: Scaffolding proteins.

Question 8

Early phage enzymes: Many RNA bacteriophages synthesize, very early after infection, an RNA-dependent RNA polymerase. What is the standard name for this enzyme?

Accepted Answer

Introduction / Context: Positive-sense RNA bacteriophages (and many RNA viruses) must copy their RNA genomes using an enzyme that uses RNA as a template to make RNA. In classical texts, the term “RNA replicase” refers to this RNA-dependent RNA polymerase activity encoded by the virus. Given Data / Assumptions: The enzyme template is RNA, and the product is RNA. “RNA replicase” is a historic but still widely recognized term for viral RNA-dependent RNA polymerase. Only one option names this function precisely. Concept / Approach: Enzyme names track template and product. DNA-dependent RNA polymerases transcribe DNA to RNA; RNA-dependent RNA polymerases replicate RNA to RNA. For RNA phages, this early enzyme is essential to amplify viral RNA and synthesize minus and plus strands. Step-by-Step Solution: Identify the template: RNA. Identify the product: RNA. Match to canonical name: RNA replicase (RNA-dependent RNA polymerase). Exclude ligases and reverse transcriptase (RNA → DNA). Verification / Alternative check: Biochemical purification from RNA phage-infected cells yields a virus-specific polymerase that copies RNA templates, classically termed RNA replicase. Why Other Options Are Wrong: “RNA polymerase” without qualifier usually implies DNA-dependent; “RNA transcriptase” is nonstandard; “RNA ligase” joins RNA ends; “reverse transcriptase” copies RNA to DNA. Common Pitfalls: Equating cellular transcription with viral RNA replication; they use different templates and enzymes. Final Answer: RNA replicase.

Question 9

Applications of phage typing: Which of the following bacterial pathogens have established phage-typing schemes used in epidemiology and strain differentiation?

Accepted Answer

Introduction / Context: Phage typing exploits the specificity of bacteriophages for particular bacterial surface receptors to differentiate strains. Historically, it has been valuable in outbreak investigations and surveillance of several pathogens including Staphylococcus aureus, Salmonella typhi, and Vibrio cholerae. Given Data / Assumptions: Phage panels are used to determine lytic patterns of bacterial isolates. Multiple human pathogens have well-described phage-typing systems. The question asks which listed pathogens can be typed this way. Concept / Approach: A strain’s susceptibility or resistance to standardized phage sets yields a lysis pattern code. S. aureus, S. typhi, and V. cholerae have each had phage sets curated for public health use, allowing fine-grained epidemiologic tracking before widespread genomic typing. Step-by-Step Solution: Identify pathogens historically typed by phages. Confirm S. aureus, S. typhi, and V. cholerae as classic examples. Choose the inclusive option “All of these.” Note that genomic methods now complement or replace phage typing in many labs. Verification / Alternative check: Public health manuals list standard phage panels and codes for these organisms, confirming their applicability. Why Other Options Are Wrong: Selecting a single organism ignores the broader historical usage; “None of these” is incorrect because phage typing has been widely applied. Common Pitfalls: Assuming modern genotyping eliminated the historical relevance; older questions still test these classic methods. Final Answer: All of these.

Question 10

Temperate phage life cycle: In a lysogenized bacterial culture, the phage reproductive cycle is triggered by a process known as what?

Accepted Answer

Introduction / Context: Temperate bacteriophages can integrate into the host genome as prophage and remain quiescent under the control of a phage-encoded repressor. Under stress, the prophage can be activated to enter the lytic cycle. This activation step is called induction and is central to understanding lysogeny–lysis switches. Given Data / Assumptions: Lysogeny: prophage maintained in the host chromosome. DNA-damaging conditions (e.g., UV) can inactivate repressors. Once repression is relieved, lytic genes are expressed. Concept / Approach: In models such as phage lambda, the CI repressor maintains latency. SOS responses (RecA-mediated) cleave the repressor, resulting in induction. The prophage excises, replicates, and packages its DNA, culminating in host lysis and virion release. Step-by-Step Solution: Define lysogeny vs. lytic growth. Identify the control protein (repressor) that prevents lytic gene expression. Recognize environmental triggers that disable repression. Name the switch event: induction. Verification / Alternative check: Classic experiments show UV exposure of lysogens yields phage production after prophage excision, consistent with induction. Why Other Options Are Wrong: Infection precedes lysogeny; integration is the establishment step; repression maintains dormancy; packaging is a late lytic event, not the trigger. Common Pitfalls: Confusing “induction” with initial infection; the term specifically refers to reactivation of a prophage. Final Answer: Induction.

Question 11

Bacterial defenses against phages: Which mechanism refers to host restriction of foreign DNA and is a classic bacterial defense against bacteriophage infection?

Accepted Answer

Introduction / Context: Bacteria possess several anti-phage defenses. A foundational system is restriction–modification, in which host-encoded restriction endonucleases cleave invading unmodified DNA, while host DNA is protected by methylation. Recognizing the terminology is essential for microbial genetics and biotechnology. Given Data / Assumptions: Restriction is enzymatic cleavage of specific DNA sequences. Modification (methylation) protects self DNA. Only one option names the defense mechanism itself. Concept / Approach: Restriction endonucleases survey DNA for defined sites. Foreign phage DNA lacking host methylation patterns is cut, preventing replication. This concept underpins many molecular cloning tools (type II restriction enzymes) and explains host-range barriers in phage infection. Step-by-Step Solution: Identify the defense mechanism: restriction–modification. Choose the term “restriction” as the defensive act. Exclude unrelated processes (concatamerization, polymerization). Note that lysogeny is a phage life cycle, not a host defense. Verification / Alternative check: Genetic studies show methyltransferase-deficient cells become hypersensitive to their own restriction enzymes, validating the specificity and protective role of modification. Why Other Options Are Wrong: Concatamerization describes DNA joining in phage packaging; polymerization is generic; lysogeny benefits temperate phages rather than host defense; autotransduction is unrelated. Common Pitfalls: Assuming CRISPR-Cas is the only defense; restriction–modification long predates CRISPR in textbooks and exams. Final Answer: Restriction.

Question 12

Phage adsorption forces: T-even coliphage binding to Escherichia coli most likely depends on which predominant type of interaction at the initial adsorption step?

Accepted Answer

Introduction / Context: The first step in bacteriophage infection is adsorption to the bacterial surface via tail fibers or spikes. Understanding the physicochemical nature of this contact clarifies why environmental conditions (pH, ionic strength) strongly affect phage attachment and host range. Given Data / Assumptions: T-even phages (e.g., T2, T4) target specific outer membrane receptors on E. coli. Initial binding is reversible and sensitive to ionic conditions. Only one option should reflect the primary initiating force. Concept / Approach: Initial phage–cell encounters are dominated by long-range, noncovalent forces (notably electrostatic attraction between charged surfaces). This reversible stage is followed by tighter, short-range contacts and conformational changes that lead to irreversible adsorption. Covalent bonding does not mediate routine adsorption; hydrophobic contacts may contribute secondarily but are not typically the initiating, dominant force for T-even phages. Step-by-Step Solution: Identify reversible adsorption as the first step. Recall dependence on ionic strength and pH, implicating electrostatics. Exclude covalent bonding as incompatible with rapid, reversible binding. Select electrostatic interaction as the best primary descriptor. Verification / Alternative check: Experimental modulation of divalent cations and salt concentrations profoundly alters T4 adsorption efficiency, consistent with charge-governed interactions at initial contact. Why Other Options Are Wrong: Hydrophobic forces may contribute later but are not the dominant, controllable variable in early reversible binding; covalent bonds and disulfide formation are not involved in normal adsorption events; “All of these” is incorrect because covalent bonding is not used. Common Pitfalls: Assuming any strong interaction must be covalent; biological adhesion commonly exploits multiple weak, reversible noncovalent forces coordinated in space. Final Answer: Electrostatic interaction.

Question 13

Plaque terminology: On a lawn culture of bacteria, the clear area produced by phage-mediated lysis is called a what?

Accepted Answer

Introduction / Context: When bacteriophages infect and lyse bacteria growing as a uniform lawn on agar, they produce localized clearings. These cleared zones are central to quantifying phage titers (plaque-forming units, PFU) and studying phage biology. Given Data / Assumptions: Bacterial lawn provides uniform host distribution. Each clearing arises from one infectious phage particle (assuming proper dilution). Standard virology terminology is required. Concept / Approach: The correct term is “plaque.” Counting plaques at suitable dilutions yields PFU per mL. Morphology (clear vs. turbid, size, halo) can inform phage traits such as lytic strength or depolymerase activity. Step-by-Step Solution: Plate host with soft agar and phage dilutions. After incubation, identify discrete clearings. Apply standard term: plaque. Use counts to calculate PFU/mL if needed. Verification / Alternative check: Virology manuals define PFU based on plaque counts; antibiotic susceptibility tests use “zones of inhibition,” a different concept. Why Other Options Are Wrong: “Pock” and “pox” are historical/animal virus terms in different contexts; “all of these” is inaccurate; zones of inhibition arise from antibiotics, not phages. Common Pitfalls: Confusing plaques with bacterial colony morphology or antibiotic halos; plaques reflect viral lysis and spread. Final Answer: Plaque.

Question 14

Genetic regulation in lysogeny: Which phage-encoded protein maintains the prophage in a dormant state by preventing lytic gene expression?

Accepted Answer

Introduction / Context: Temperate phages such as lambda rely on a regulatory protein to silence lytic genes while integrated into the host genome. This protein binds operator sequences to block transcription from lytic promoters, maintaining lysogeny and conferring immunity to superinfection by related phages. Given Data / Assumptions: Repressors are DNA-binding proteins that recognize operator sites. They prevent RNA polymerase from initiating lytic transcription. Terminology distinguishes proteins (repressor) from DNA elements (operator, promoter). Concept / Approach: In phage lambda, the CI repressor binds operator sites OL and OR, shutting down lytic promoters PL and PR. As long as repressor levels are maintained, the prophage remains quiescent. Stress-triggered repressor cleavage leads to induction and lytic growth. Step-by-Step Solution: Identify the functional role: block lytic transcription. Match function to protein: repressor. Exclude DNA elements (operator, promoter) and nonspecific terms (enhancer). Recognize integrase is needed for integration, not maintenance via repression. Verification / Alternative check: Genetic experiments show loss of repressor results in spontaneous induction; overexpression stabilizes lysogeny. Why Other Options Are Wrong: Operator and promoter are DNA sequences; enhancer is a eukaryotic regulatory concept; integrase catalyzes integration but does not suppress lytic transcription. Common Pitfalls: Confusing the repressor (protein) with operator (binding site) in terminology questions. Final Answer: Repressor.

Question 15

Viral envelopes and origin: For enveloped viruses, what is the correct statement about the origin of the envelope and the source of embedded glycoproteins?

Accepted Answer

Introduction / Context: Enveloped viruses acquire a lipid bilayer by budding through host cellular membranes (plasma membrane, ER, or Golgi). However, the viral spikes embedded in this membrane are encoded by the viral genome and are essential for attachment and entry. Distinguishing host contribution (lipids) from viral contribution (glycoproteins) is a core virology concept. Given Data / Assumptions: Envelope = host-derived lipid bilayer obtained during budding. Spike proteins = viral gene products targeted to budding sites. Single best statement is required. Concept / Approach: Viral glycoproteins are synthesized on host ribosomes, processed in secretory pathways, and trafficked to membranes where budding occurs. The lipid composition therefore reflects the host membrane; the protein identity reflects viral genetic information. Some host proteins may be incorporated nonspecifically, but the key functional spikes are viral. Step-by-Step Solution: Separate the origin of lipids (host) and spikes (viral). Evaluate each option for this division of labor. Select the statement that captures host-derived envelope with virus-encoded proteins. Exclude options claiming de novo viral lipid synthesis or wholly host-derived proteins. Verification / Alternative check: Electron microscopy and biochemical analyses show envelope lipid composition mirrors the host membrane, while viral spikes are immunologically specific to the virus. Why Other Options Are Wrong: Viruses do not synthesize lipids de novo; spike proteins are not generally host-coded; saying both envelope and proteins are host-derived neglects viral glycoproteins. Common Pitfalls: Assuming any membrane component must be viral; in reality, viruses hijack host membranes but decorate them with their own proteins. Final Answer: The envelope is derived from the host but it contains embedded proteins coded by the viral nucleic acid.

Bacteriophages Questions