Question 1

Measles (paramyxovirus) inclusion bodies: where are the characteristic inclusions typically found within infected cells?

Accepted Answer

Introduction / Context: Inclusion bodies are accumulations of viral components or altered host structures visible under light microscopy with appropriate stains. For measles virus (a member of the Paramyxoviridae family), inclusion bodies help pathologists and virologists recognize infection in tissues and cell culture. Given Data / Assumptions: Measles virus is an enveloped, negative-sense RNA virus. Cytopathic effects include multinucleated giant cells (Warthin–Finkeldey cells) and characteristic inclusions. Question asks for the location(s) of inclusions. Concept / Approach: Measles infection can produce both cytoplasmic and nuclear inclusion bodies. Cytoplasmic inclusions reflect sites of nucleocapsid accumulation and replication complex components; nuclear inclusions can also be observed in infected lymphoid tissues. Recognition of inclusions is part of classic histopathological diagnosis, although modern diagnosis relies on serology and molecular testing. Step-by-Step Solution: Recall measles cytopathic effect: syncytia (giant cells) and inclusions.Identify inclusion locations reported for measles: cytoplasm and nucleus.Select the option representing both compartments.Confirm that “both” is the best match for classical descriptions. Verification / Alternative check: Histology texts describe Warthin–Finkeldey giant cells with both intranuclear and intracytoplasmic inclusions in measles-affected lymphoid tissues. Why Other Options Are Wrong: Intracytoplasmic only or intranuclear only: Each is incomplete for measles, which can display both. None of these: Incorrect because inclusions are indeed observed. Common Pitfalls: Confusing measles with rabies (Negri bodies are cytoplasmic) or CMV (prominent intranuclear inclusions); assuming a single compartment for all RNA viruses. Final Answer: both (a) and (b)

Question 2

Phage one-step growth curve: the interval during which extracellular phage titer rises to a plateau is called what?

Accepted Answer

Introduction / Context: The one-step growth experiment dissects phage replication into characteristic stages by plotting extracellular phage count over time. Correct terminology helps interpret curves and quantify kinetics. The item asks for the term describing the phase when extracellular titer increases and then reaches a constant level. Given Data / Assumptions: Multiplicity of infection is controlled to synchronize infection. Phage adsorption is rapid, followed by intracellular replication. Sampling measures extracellular infectious particles at fixed intervals. Concept / Approach: After the eclipse period (no detectable mature intracellular phage), lysis begins and infectious particles are released into the medium. The rise period is the interval during which extracellular titer increases rapidly. When lysis completes across the population, the curve approaches a plateau. The latent period spans adsorption to the first appearance of extracellular phage and includes the eclipse period; it is not the rising interval itself. “Burst size” is a yield, not a time period. Step-by-Step Solution: Map phases: adsorption → eclipse → onset of lysis → rise → plateau.Identify the requested phenomenon: extracellular titer increases to a constant level.Match to terminology: “rise period.”Exclude latent period (earlier, before extracellular appearance) and burst size (a number, not a time). Verification / Alternative check: Classic Delbrück–Luria phage growth curves illustrate these intervals and definitions. Why Other Options Are Wrong: Eclipse period: No detectable mature phage; occurs earlier. Latent period: Ends at first extracellular detection; not the rising interval. Burst size: A yield per cell, not a time interval. Common Pitfalls: Mixing up latent and rise periods; treating “burst size” as a temporal metric. Final Answer: rise period

Question 3

Oncogenic viruses history: which virus was the first tumor-inducing (oncogenic) virus to be detected?

Accepted Answer

Introduction / Context: Oncogenic viruses are capable of initiating or promoting tumor formation in animals or humans. The historical sequence of their discovery is foundational knowledge in virology and cancer biology. This question asks which virus was first recognized as oncogenic. Given Data / Assumptions: Peyton Rous reported a transmissible agent causing sarcomas in chickens in the early 20th century. Later discoveries included Epstein–Barr virus (EBV) and human tumor viruses such as HTLV. The question is about the first detected oncogenic virus, not the first human oncogenic virus. Concept / Approach: Rous demonstrated that a cell-free filtrate from chicken tumors could induce sarcomas when injected into healthy birds. The agent, later known as Rous sarcoma virus (RSV), is an avian retrovirus and is historically credited as the first tumor virus discovered. EBV (a gammaherpesvirus) was linked later to Burkitt lymphoma and nasopharyngeal carcinoma; HTLV and HSV-2 associations came even later or are more limited/controversial in humans. Step-by-Step Solution: Identify candidate viruses and their timelines.Recall that RSV was described by Rous in 1911 as a transmissible sarcoma agent.Compare with EBV (1960s), HTLV (late 1970s/1980s), HSV-2 associations (later and not considered the first).Conclude that RSV is the earliest detected oncogenic virus. Verification / Alternative check: Historical reviews of tumor virology consistently cite RSV as the first tumor-causing virus discovered. Why Other Options Are Wrong: Epstein–Barr virus: Discovered later; not first. HSV-2: Associations are not the earliest and remain complex. HTLV: Identified later as a human oncovirus; still not the first. Common Pitfalls: Confusing “first detected” with “first human tumor virus”; assuming human relevance is implied by “oncogenic.” Final Answer: Rous sarcoma virus.

Question 4

Virion properties: which statement is NOT true about virions (complete virus particles)?

Accepted Answer

Introduction / Context: A virion is the complete, infectious form of a virus outside a host cell, typically composed of nucleic acid (DNA or RNA), a protein capsid, and sometimes an envelope. Knowing what virions can and cannot do clarifies viral life cycles and the distinction between viruses and cellular life. Given Data / Assumptions: Virions carry either DNA or RNA (never both simultaneously as their genetic material). Virions are metabolically inert outside host cells. Replication requires host cellular machinery after entry and uncoating. Concept / Approach: The key question is to find the statement that is not true. Virions can be found extracellularly; they indeed exist as particles outside the cell while seeking new hosts. Some viruses contain DNA; others contain RNA—either possibility is true, depending on the virus family. However, virions do not reproduce independently: they lack ribosomes, energy metabolism, and the enzymatic systems necessary for autonomous replication. Step-by-Step Solution: Evaluate “Are extracellular”: true—virions are extracellular particles between infections.Evaluate “Contain DNA” and “Contain RNA”: each is true for different viruses but not simultaneously in one virion.Evaluate “Reproduce independently”: false—viruses require host cells.Thus select “Reproduce independently” as the statement that is not true. Verification / Alternative check: Standard virology texts characterize virions as obligate intracellular parasites for replication. Why Other Options Are Wrong: Contain DNA / Contain RNA: Each is correct in the appropriate viral lineage. Are extracellular: Correct description of the virion state. Common Pitfalls: Thinking “contain DNA” and “contain RNA” are mutually exclusive in the answer key; both can be true statements broadly across viruses, but only one applies to any given species. Final Answer: Reproduce independently

Question 5

Helical capsid example: which bacteriophage is a rod-shaped filament with capsomeres arranged helically rather than in stacked rings?

Accepted Answer

Introduction / Context: Virus capsid symmetry is commonly icosahedral or helical. Filamentous bacteriophages are classic examples of helical symmetry, where identical capsid subunits wrap around the nucleic acid to form a rod-like particle. Recognizing exemplars helps connect morphology to life cycle and applications (for example, phage display). Given Data / Assumptions: Rod-shaped viruses with helical symmetry have capsomeres arranged in a helix along the genome. T-even phages (T2, T4) are tailed, complex icosahedral heads, not simple helical rods. M13 is a filamentous (Ff) phage infecting E. coli bearing F pili. Concept / Approach: M13’s coat protein subunits polymerize around circular single-stranded DNA to form a flexible filament with helical symmetry. In contrast, T2/T4 possess icosahedral heads and contractile tails; their capsid proteins form facets, not continuous helices around the genome. Therefore, the correct helical rod example among the choices is M13. Step-by-Step Solution: Identify capsid symmetries: helical vs icosahedral vs complex.Match candidates: T2/T4 → complex (icosahedral head + tail); M13 → filamentous helical rod.Exclude MV-L2 (not a standard textbook exemplar).Select M13 as the canonical helical rod-shaped phage. Verification / Alternative check: Structural images and cryo-EM reconstructions show M13 as a long filament with helical arrangement of coat proteins. Why Other Options Are Wrong: Bacteriophage T2/T4: Complex morphology; not helical rods. MV-L2: Not the classic rod-shaped helical example compared with M13. Common Pitfalls: Confusing “helical symmetry” with “stacked ring” descriptions of some rod-like viruses; assuming all bacteriophages are tailed and icosahedral. Final Answer: Bateriophage M13

Question 6

In virology, which virus is known to “rescue” (i.e., enable productive replication of) adenovirus in simian cells by providing missing helper functions?

Accepted Answer

Introduction / Context: This question probes your understanding of helper functions and “rescue” phenomena in virology. Certain viruses can complement missing functions of another virus within a specific host cell, permitting productive replication. In simian (monkey) cells, simian virus 40 (SV40) is historically noted for its ability to assist adenovirus replication by providing helper activities the adenovirus lacks in that cellular context. Given Data / Assumptions: Adenovirus requires specific host and viral factors for efficient replication. Simian cells may not naturally supply all factors for adenovirus to complete its cycle. SV40 expresses early proteins (notably large T antigen) that can modulate host replication machinery. Concept / Approach: “Rescue” here means that coinfection or prior infection with a helper virus supplies functions enabling another virus to replicate. SV40 large T antigen drives the host into S phase–like conditions, activates or sequesters key cell-cycle regulators, and can enhance DNA replication environments. Historically, this complementation permits adenovirus to produce progeny in simian cells where it otherwise would be restricted. Step-by-Step Solution: Identify the candidate viruses in the options and their known host ranges.Recall that SV40 is a polyomavirus adapted to simian cells and expresses potent replication helpers (e.g., large T antigen).Understand that these helper functions can nonspecifically promote replication of DNA viruses such as adenoviruses.Conclude that the known helper in simian cells for adenovirus rescue is SV40. Verification / Alternative check: Classic virology literature and vector systems reference SV40 “helper” effects in primate cell lines, contrasted with other viruses that lack such complementation in this setting. Why Other Options Are Wrong: Vaccinia: a poxvirus with cytoplasmic replication; it does not provide the nuclear helper functions required for adenovirus in simian cells. Cytomegalovirus: human betaherpesvirus; its helper roles are host-specific and not known to rescue adenovirus in simian cells. Rabies: a negative-sense RNA virus without relevant DNA-replication helper activities. Common Pitfalls: Assuming any co-infecting DNA virus will rescue another; helper functions are specific to replication requirements and host context. Final Answer: Simian virus 40

Question 7

In geometry and biophysics, the most efficient shape for enclosing the maximum volume with a given surface area is which of the following?

Accepted Answer

Introduction / Context: This fundamental optimization problem appears across mathematics, physics, biology, and engineering: given a fixed surface area, which shape encloses the greatest possible volume? The answer reveals why many natural structures—drops, bubbles, certain organelles—tend toward a particular shape to minimize surface energy. Given Data / Assumptions: Surface area is fixed and identical for all candidate shapes. We compare idealized, perfectly regular shapes without defects. We are not imposing constraints such as packing efficiency or boundary conditions. Concept / Approach: The isoperimetric (3D) principle states that among all bodies with a given surface area, the sphere encloses the maximum volume. Equivalently, for a given volume, the sphere has the minimum surface area. This emerges from variational calculus and symmetry arguments: the sphere distributes curvature uniformly and minimizes surface energy in systems where surface tension dominates. Step-by-Step Solution: Frame the optimization: maximize volume subject to constant surface area.Recall the isoperimetric inequality in 3D: S^3 ≥ 36πV^2, with equality only for a sphere.Equality implies the sphere uniquely maximizes V for given S.Therefore, among options, the sphere is the most efficient enclosure. Verification / Alternative check: Observe nature: soap bubbles and droplets become spherical to minimize energy; any deviation increases surface area for the same volume. Why Other Options Are Wrong: Icosahedron: a near-spherical polyhedron but still has greater surface area for the same volume than a sphere. Cube: has edges and flat faces, resulting in higher surface area for the same enclosed volume. Helix: not a closed enclosing surface; it cannot define a volume on its own. Common Pitfalls: Confusing packing efficiency (how shapes fill space) with surface-area efficiency of a single shape; polyhedra approximate spheres but never surpass them. Final Answer: Sphere

Question 8

Clinical therapeutics: Which of the following is NOT useful for the treatment of viral infections (select the agent that is ineffective against viruses)?

Accepted Answer

Introduction / Context: The question distinguishes antiviral strategies from antibacterial agents. Effective management of viral diseases relies on antivirals, immune modulators, and passive or active immunization—not on antibiotics that target bacterial structures such as cell walls or ribosomes. Given Data / Assumptions: Acyclovir is a nucleoside analog used against herpesviruses. Interferon refers to cytokines that modulate antiviral defenses. Antibodies (e.g., monoclonal antibodies or convalescent plasma) can neutralize viruses. Penicillin targets bacterial peptidoglycan synthesis, which viruses lack. Concept / Approach: Viruses use host-cell machinery and have no cell wall or independent metabolism. Antibiotics like penicillin have no viral targets. In contrast, acyclovir inhibits viral DNA polymerase after phosphorylation by viral thymidine kinase, interferon enhances innate antiviral responses, and antibodies can bind and neutralize virions or block entry. Step-by-Step Solution: List each option’s mechanism and target.Identify which mechanisms act on viral processes versus bacterial structures.Penicillin has no effect on viruses because they lack peptidoglycan and independent cell walls.Therefore, penicillin is NOT useful against viral infections. Verification / Alternative check: Clinical guidelines reserve antibiotics for bacterial coinfections; overuse in viral illness risks antimicrobial resistance without therapeutic benefit against the virus itself. Why Other Options Are Wrong: Acyclovir: active against herpes simplex and varicella-zoster; clearly antiviral. Interferon: used in certain chronic viral infections and for immune modulation. Antibodies: neutralizing monoclonal antibodies are established antivirals in several diseases. Common Pitfalls: Assuming “antibiotic” is a synonym for “antimicrobial”; antibiotics are a subset targeting bacteria, not viruses. Final Answer: Penicillin

Question 9

In the one-step growth curve of bacteriophages, the interval from infection until the first release of progeny by cell lysis is known as the:

Accepted Answer

Introduction / Context: Understanding the one-step growth curve is essential in phage biology. It partitions viral replication into defined phases that are measured experimentally to characterize timing and yield of phage production in infected bacteria. Given Data / Assumptions: An infection is synchronized so all bacteria are infected at approximately the same time. Parameters include eclipse period, latent period, rise period, and burst size. Cell lysis marks the initial release of mature virions into the medium. Concept / Approach: The eclipse period spans from infection until the appearance of mature, intracellular, assembly-complete virions. The latent period spans from infection until the first extracellular appearance of phage—typically at lysis. The rise period is the subsequent rapid increase in free phage concentration as more cells lyse. Burst size is the average number of virions released per lysed cell. Step-by-Step Solution: Define each term in the growth curve.Map the event “first release of progeny by lysis” to the corresponding interval.Recognize that this event marks the end of the latent period and the start of the rise period.Therefore, the interval is the latent period. Verification / Alternative check: Experimental curves plotting plaque-forming units in the medium vs. time show zero extracellular phage until the end of the latent period, followed by the rise. Why Other Options Are Wrong: Eclipse period: ends before lysis; mature virions exist intracellularly but are not yet released. Rise period: begins after lysis as free phage accumulates. Burst size: a number (yield), not a time interval. Common Pitfalls: Confusing eclipse and latent periods; the key difference is extracellular detectability of phage. Final Answer: Latent period

Question 10

Microbiology fundamentals: Which of the following organisms are obligate intracellular parasites (i.e., must live and reproduce within host cells)?

Accepted Answer

Introduction / Context: Obligate intracellular parasites cannot complete their life cycles outside host cells. Recognizing these organisms is crucial for diagnostics, therapeutic choices, and understanding transmission and pathogenesis. Given Data / Assumptions: Viruses lack cellular machinery and rely entirely on host cells for replication. Chlamydia spp. require host-derived ATP and exist as elementary/reticulate bodies. Rickettsia spp. are small bacteria that replicate within host cytoplasm and require intracellular environments. Concept / Approach: Evaluate each organism’s biology and dependence on host cells. Viruses, by definition, are intracellular obligates. Chlamydia and Rickettsia, although bacteria, also have strict intracellular requirements for replication and survival, classifying them as obligate intracellular pathogens. Step-by-Step Solution: Assess viruses: absolute dependence on host transcription/translation → obligate.Assess Chlamydia: biphasic life cycle; cannot grow on standard media → obligate.Assess Rickettsia: replicate only inside eukaryotic cells → obligate.Therefore, all listed groups fit the definition. Verification / Alternative check: Culturing requirements (cell culture, eggs) and clinical treatments reflect intracellular lifestyles (e.g., tetracyclines for rickettsial diseases). Why Other Options Are Wrong: Each single-organism choice is incomplete; the comprehensive, correct choice is “All of these.” Common Pitfalls: Assuming all bacteria are free-living; several clinically important bacteria are obligate intracellular. Final Answer: All of these

Question 11

Virology terminology: By which fundamental biological process do viruses reproduce inside living host cells?

Accepted Answer

Introduction / Context: Correct terminology matters in virology. While lay usage might refer to “multiplication,” the precise biological term for how viruses copy their genomes and produce progeny within host cells is “replication.” Given Data / Assumptions: Viruses rely on host cellular machinery for many steps. They must synthesize new genomes and proteins and assemble them into virions. We are seeking the standard scientific term used in virology texts and research. Concept / Approach: “Replication” denotes the biological copying of nucleic acids (DNA or RNA). Viral replication encompasses entry, uncoating, genome replication, protein synthesis, assembly, and release. “Duplication” is not standard in this context, and “multiplication” is colloquial, sometimes used descriptively but not as the formal mechanistic term. Step-by-Step Solution: Identify the precise term used in virology to describe genome copying: replication.Consider alternative words: duplication is a genetics term for chromosomal events, not standard for viral life cycles.“Multiplication” may describe the numerical increase but lacks mechanistic specificity.Therefore, the correct technical term is replication. Verification / Alternative check: Standard virology curricula and textbooks (e.g., basic virology chapters) consistently use “viral replication cycle.” Why Other Options Are Wrong: Duplication: typically refers to a type of mutation or gene dosage change, not an infectious cycle. Multiplication: descriptive but non-technical; not the canonical term in virology. All of these: incorrect because the precise term is replication. Common Pitfalls: Conflating everyday language with technical nomenclature used in scientific literature. Final Answer: Replication

Question 12

Oncogenic viruses: Approximately what proportion of human tumours worldwide are associated with a viral risk factor?

Accepted Answer

Introduction / Context: Cancer etiology includes infectious causes. Several human viruses are classified as oncogenic or cancer-associated, contributing to a significant fraction of global cancer burden through chronic infection, inflammation, and direct oncogene expression. Given Data / Assumptions: High-burden viruses include HPV, HBV, HCV, EBV, HTLV-1, KSHV, and Merkel cell polyomavirus. Global estimates aggregate across regions with varied prevalence (e.g., higher HBV/HCV in some areas). We are asked for a broad, widely cited upper-bound estimate. Concept / Approach: Epidemiological studies estimate that approximately 15–20% of human cancers have an infectious (often viral) component, with variation by geography and income level. This figure captures cancers such as cervical (HPV), hepatocellular carcinoma (HBV/HCV), certain lymphomas and nasopharyngeal carcinoma (EBV), adult T-cell leukemia/lymphoma (HTLV-1), Kaposi sarcoma (KSHV), and Merkel cell carcinoma (MCV). Step-by-Step Solution: List known oncogenic viruses and associated cancers.Recall global burden estimates converging near one-fifth of cases.Select the option that matches the typical “up to ~20%” figure.Therefore, “Up to 20%” is the best supported answer. Verification / Alternative check: International cancer agencies (e.g., IARC) and global burden studies regularly cite ~15–20% worldwide, higher in certain regions. Why Other Options Are Wrong: Up to 10%: underestimates the aggregate burden. Up to 30% or 40%: exceed commonly accepted global estimates. Common Pitfalls: Confusing regional peaks (where infection-related cancers are more prevalent) with the global average. Final Answer: Up to 20% of human tumours have a viral risk factor

Question 13

Laboratory methods: Which type of embryo is classically used for viral assays, isolation, and propagation in embryonated eggs?

Accepted Answer

Introduction / Context: Before widespread cell culture systems, and still today for specific applications, embryonated eggs provide a convenient, sterile, living system to grow and assay viruses. Understanding which eggs are used and why remains relevant for diagnostics, vaccine production, and basic virology labs. Given Data / Assumptions: Embryonated eggs provide multiple inoculation sites (chorioallantoic membrane, allantoic cavity, yolk sac, amniotic cavity). Common target viruses include orthomyxoviruses (e.g., influenza), poxviruses, and others. The question asks which embryo is “often used” in this context. Concept / Approach: Fertilized chicken eggs (usually 9–12 days old) are the standard for many viral assays. They are economical, readily available, and offer compartmentalized environments that support viral growth and visualization of pocks or hemagglutinating virus production. Step-by-Step Solution: Identify the widely used system: embryonated chicken eggs.Recall applications: influenza vaccine production and pock assays for poxviruses.Contrast with other embryos (mouse, rat, cat), which are not standard egg-based assay systems.Select “Chicken” as the correct choice. Verification / Alternative check: Standard lab manuals and vaccine manufacturing protocols cite 9–11 day embryonated chicken eggs as the workhorse system. Why Other Options Are Wrong: Mouse, Rat, Cat: not used as embryonated egg assay systems; while animal models exist, they are not the classic egg-based platform. Common Pitfalls: Confusing animal infection models with egg-based propagation; the question specifically refers to embryos used for viral assays in eggs. Final Answer: Chicken

Question 14

Phage morphology: Which bacteriophages are described as having binal (dual) symmetry, with an icosahedral head and a helical tail?

Accepted Answer

Introduction / Context: Bacteriophages (phages) exhibit diverse morphologies. A common architecture among tailed phages is “binal symmetry,” combining two structural symmetries: an icosahedral capsid (head) attached to a helical tail apparatus for adsorption and genome injection. Given Data / Assumptions: The question focuses on classic Escherichia coli T-even/T-series phages. “Binal” (sometimes misspelled as “banal”) refers to dual symmetry. We consider T2, T4, and T6 morphologies. Concept / Approach: Tailed dsDNA phages, including T2, T4, and T6, share the canonical structure: icosahedral head containing genomic DNA and a contractile or non-contractile tail with baseplate and tail fibers. This dual-symmetry design underlies their infection mechanism: tail fibers bind receptors, the tail sheath may contract, and DNA is injected into the bacterial cytoplasm. Step-by-Step Solution: Identify structural classes: head–tail phages have binal symmetry.Recall that T2, T4, T6 are tailed coliphages with similar architecture.Therefore, each listed T-series phage exhibits binal symmetry.Choose the inclusive option “All of these.” Verification / Alternative check: Electron micrographs and standard microbiology texts depict T-even phages as icosahedral-headed with distinctive tails and fibers. Why Other Options Are Wrong: Each single-phage option is only partially correct; all three share the morphology. Common Pitfalls: Confusing “binal” with “bilateral”; binal specifically refers to combined icosahedral and helical symmetry in phages. Final Answer: All of these

Question 15

Environmental stability: Which of the following viruses is relatively thermostable (i.e., can better withstand heat compared with many other enveloped respiratory viruses)?

Accepted Answer

Introduction / Context: Virion stability in the environment varies with structure and composition. Enveloped viruses are generally more labile to heat, desiccation, and detergents, whereas many nonenveloped, icosahedral RNA viruses are more resistant. Identifying thermostable viruses informs disinfection practices and food/water safety. Given Data / Assumptions: Hepatitis A virus (HAV) is a nonenveloped, positive-sense RNA picornavirus. Influenza virus, HIV, and rubella virus are enveloped and relatively heat-labile. “Relatively thermostable” implies comparative robustness, not absolute indestructibility. Concept / Approach: The presence or absence of a lipid envelope is a key determinant of environmental stability. Nonenveloped viruses like HAV possess sturdy capsids that resist temperature and pH changes better than lipid-enveloped viruses. HAV’s stability underlies transmission via the fecal–oral route and the need for adequate heating and chlorination in food and water handling. Step-by-Step Solution: Classify each virus by envelope status.Recall that HAV is nonenveloped; influenza, rubella, and HIV are enveloped.Nonenveloped capsids confer greater heat resistance.Therefore, HAV is the relatively thermostable option. Verification / Alternative check: Public health guidelines emphasize heating shellfish and proper sanitation to inactivate HAV due to its resilience compared with enveloped respiratory viruses. Why Other Options Are Wrong: Influenza virus: enveloped orthomyxovirus; heat and detergent sensitive. Rubella virus: enveloped togavirus; environment-labile. Human immunodeficiency virus: enveloped retrovirus; readily inactivated by heat and disinfectants. Common Pitfalls: Assuming medical severity correlates with environmental stability; stability is a structural property, not a measure of virulence. Final Answer: Hepatitis A virus

Question 16

In virology, identify the morphological class of bacteriophages described as the most complex type, with a hexagonal head, a rigid tail that has a contractile sheath, and distinct tail fibers.

Accepted Answer

Introduction / Context: This item tests recognition of classical bacteriophage morphology. Early electron microscopy led to a practical scheme (commonly attributed to Bradley) that groups tailed bacteriophages by tail structure. Correct classification is important in understanding attachment, genome injection mechanisms, and even phage therapy selection. Given Data / Assumptions: Head: hexagonal outline (icosahedral symmetry). Tail: rigid tail equipped with a contractile sheath. Accessories: distinct tail fibers are present. We are choosing a morphological class label rather than a specific species. Concept / Approach: In Bradley’s morphology-based scheme, three major tailed groups are highlighted: Type A (contractile tail), Type B (long, flexible, noncontractile tail), and Type C (short, noncontractile tail). The presence of a sheath that actively shortens to drive the tail tube through the bacterial envelope is the hallmark of Type A phages (typified by the family Myoviridae). Step-by-Step Solution: Identify the diagnostic feature: a contractile sheath around the tail.Map to class: contractile tail corresponds to Bradley type A.Confirm supportive features: hexagonal head and tail fibers are consistent with tailed phages of type A.Select the option that explicitly states type A / contractile tail. Verification / Alternative check: Review reference micrographs: Type A phages show extended and contracted tail states; the sheath visibly shortens during genome injection. Why Other Options Are Wrong: Type B and C describe noncontractile tails; they lack a sheath. The ”no tail” option refers to entirely different, nontailed icosahedral viruses. Common Pitfalls: Confusing “rigid” with “noncontractile”; assuming all tailed phages contract—only type A does. Final Answer: Bradley type A (contractile tail; Myoviridae-like)

Question 17

Virus quantification methods: What is the most popular indirect method used to estimate the number of virus particles in a sample?

Accepted Answer

Introduction / Context: Virologists often need to estimate how many virions are present in a preparation. Methods vary by whether they measure infectious units (functional) or total particles/indirect properties. Understanding which techniques are direct versus indirect is foundational in laboratory virology. Given Data / Assumptions: Some viruses bind to red blood cells (RBCs) via surface proteins (e.g., influenza hemagglutinin). Hemagglutination can be observed as visible RBC lattice formation in microtiter plates. Plaque-based methods quantify infectious units, not merely particle presence. Concept / Approach: Hemagglutination assay (HA) is an indirect particle counting method. It does not require infection of cells to produce plaques; instead, it detects the ability of viral particles to cross-link RBCs. The readout is the hemagglutination titer (e.g., HA units), which correlates with particle numbers when the virus efficiently agglutinates RBCs. Step-by-Step Solution: Recognize that “indirect” implies not strictly limited to counting infectious virions.Recall that plaque assays and PFU counts are direct measures of infectious virus.Identify hemagglutination assay as the classic indirect approach.Exclude colony counting (used for bacteria, not viruses). Verification / Alternative check: Compare a preparation’s HA titer with PFU/ml; often PFU is lower because not every particle is infectious. Why Other Options Are Wrong: Plaque assay and “counting plaque-forming units” directly quantify infectious units, not total particles. Colony counting is a bacteriological method. Common Pitfalls: Assuming HA applies to all viruses—only those that agglutinate RBCs are suitable; misinterpreting HA as a measure of infectivity rather than particle-associated activity. Final Answer: hemagglutination assay

Question 18

Core roles of the viral capsid: Which statement best describes the functions served by a virus capsid?

Accepted Answer

Introduction / Context: The capsid is the protein shell enclosing viral nucleic acid. Beyond passive containment, its design underpins stability, host recognition, and environmental survival, making a comprehensive view of capsid functions essential for understanding infection biology and vaccine design. Given Data / Assumptions: Capsid subunits (capsomeres) self-assemble into icosahedral, helical, or complex forms. Viruses must protect their genome outside the host and then locate and enter susceptible cells. Transmission between hosts often occurs in harsh environments (desiccation, enzymes, UV). Concept / Approach: Capsids are multifunctional. They physically protect RNA/DNA from shear, pH, and nucleases; they present receptor-binding motifs or, in enveloped viruses, underlie and organize glycoproteins that mediate attachment and entry; and they stabilize virions during environmental transit, enabling efficient host-to-host spread. Step-by-Step Solution: Evaluate option A: true—capsids shield the genome from physical/enzymatic damage.Evaluate option B: true—capsid or associated proteins contribute to receptor binding and tropism.Evaluate option C: true—capsids create a robust particle for transmission.Therefore, the inclusive answer is “all of the above.” Verification / Alternative check: Nonenveloped enteric viruses (e.g., poliovirus) illustrate extreme capsid robustness and receptor specificity. Why Other Options Are Wrong: Each single-function option is incomplete; the capsid performs all listed roles. Common Pitfalls: Assuming only enveloped viruses have receptor-binding proteins; in many nonenveloped viruses, the capsid itself carries the attachment determinants. Final Answer: all of the above

Question 19

Source of the viral envelope: The membrane envelope present on many animal viruses is typically derived from which host-cell structure during budding?

Accepted Answer

Introduction / Context: Enveloped viruses acquire a lipid bilayer as they exit host cells. Identifying the typical origin of this membrane helps explain viral stability, entry pathways, and the composition of viral surface proteins targeted by immunity. Given Data / Assumptions: Many animal viruses bud through a host membrane to acquire their envelope. Viral glycoproteins are inserted into the donor membrane before budding. The exam-style question asks for the most common, canonical source. Concept / Approach: Most classic examples (e.g., orthomyxoviruses, paramyxoviruses, coronaviruses at the plasma membrane or other secretory membranes) obtain their envelope by budding through the host cell (plasma) membrane, incorporating host lipids and viral proteins. While some viruses bud into intracellular membranes (ER/Golgi) and are exocytosed, the standard teaching answer when options are limited is the cell (plasma) membrane. Step-by-Step Solution: Identify budding as the mechanism for envelope acquisition.Recall that the plasma membrane is the prototypical donor membrane.Select “the cell membrane” as the best single answer from the provided choices. Verification / Alternative check: Examine EM images showing virions budding from the cell surface with continuity of membranes. Why Other Options Are Wrong: Mitochondrial membranes are not used for viral envelopes. ER can be used by certain viruses, but the question singles out the typical case; “none of these” is therefore incorrect. Common Pitfalls: Overgeneralizing special cases (ER/Golgi budding) as the common rule when a single best answer is expected. Final Answer: the cell membrane

Question 20

Bacteriophage one-step growth curve: The early interval after phage DNA injection during which no intracellular infectious phage can be recovered, even if cells are disrupted, is called the ______.

Accepted Answer

Introduction / Context: In the classic one-step growth experiment, phage replication proceeds through definable phases. Correctly naming these phases is essential for interpreting kinetics, burst size, and intracellular events. Given Data / Assumptions: Immediately after adsorption and genome injection, virions lose infectivity as particles and disassemble. No infectious phage can be detected inside cells by lysis during this interval. Later, progeny assemble and infectious particles reappear. Concept / Approach: The eclipse period spans the time from genome entry to the first appearance of mature, intracellular infectious phage. The latent period extends from infection to first extracellular release (lysis). The rise period is when extracellular phage count increases, and burst size is the number of virions released per infected cell. Step-by-Step Solution: Match the description “no recoverable infectious phage despite cell disruption” to the intracellular assembly gap.Identify this gap as the eclipse period.Exclude latent period (concerns extracellular detection) and rise period (release phase). Verification / Alternative check: Plot intracellular vs. extracellular infectivity over time; intracellular infectivity reappears before extracellular counts rise. Why Other Options Are Wrong: Latent period includes the eclipse but is defined by first release; rise period is the increase in extracellular phage; burst size is a value, not a time interval. Common Pitfalls: Confusing eclipse (intracellular undetectability) with latent (pre-release) because both occur before lysis. Final Answer: eclipse period

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