Question 1

In bacteriophages, lysozyme (endolysin) that lyses the bacterial cell to release mature virions is encoded by which phase of viral gene expression?

Accepted Answer

Introduction: Bacteriophage replication is temporally regulated. Distinct waves of gene expression (immediate-early, early, delayed-early, and late) accomplish host takeover, genome replication, assembly, and release. The timing of endolysin expression explains when cell lysis occurs to liberate progeny virions. Given Data / Assumptions: We are focusing on phage lysozyme (endolysin), which degrades peptidoglycan. Endolysin must act after virion assembly to release progeny. Options cover temporal classes of gene expression. Concept / Approach: Phages typically express structural proteins and lysis proteins during the late phase. Late genes include capsid proteins, tail components, scaffolding factors, holins, and endolysins. Holins form membrane lesions allowing endolysins to access the cell wall, coordinating lysis after assembly is complete. Step-by-Step Solution: Relate function to timing: lysis should follow assembly. Structural and release functions cluster in the late gene class. Therefore, endolysin is a late gene product. Verification / Alternative check: Genetic maps of classic phages (e.g., T-even phages, lambda under lytic conditions) place lysis genes in late transcriptional units, ensuring lysis occurs only after successful assembly. Why Other Options Are Wrong: Immediate-early / Delayed-early: Involved in host takeover and DNA metabolism, not final lysis. All of these: Incorrect because expression is temporally restricted. Non-coding regulatory region only: Lysis requires a protein product. Common Pitfalls: Assuming any essential function must be early; in fact, precise timing prevents premature cell death and maximizes burst size. Final Answer: Late genes encode endolysin for phage release.

Question 2

Oncogene theory: What does it explain in the context of virus–host interactions and cancer biology?

Accepted Answer

Introduction: The oncogene theory underpins modern tumor virology and molecular oncology. It addresses how viral elements or dysregulated cellular genes can drive uncontrolled proliferation, loss of growth control, and malignant phenotypes. Understanding this theory clarifies viral carcinogenesis (e.g., retroviruses, DNA tumor viruses) and even non-viral oncogene activation. Given Data / Assumptions: The question asks for the core idea of the oncogene theory. Oncogenes can be viral (v-onc) or cellular (proto-oncogenes that become activated oncogenes). Transformation refers to conversion of normal cells into tumor cells. Concept / Approach: Oncogene theory proposes that certain genes, when introduced by viruses or aberrantly activated within host cells, can induce transformation. Retroviruses may carry v-onc genes or activate host proto-oncogenes via insertional mutagenesis. DNA tumor viruses can disrupt cell-cycle regulators (e.g., p53, Rb) using viral oncoproteins, tipping the balance toward proliferation and away from apoptosis. Step-by-Step Solution: Identify the focus: transformation of normal cells. Relate viral mechanisms: v-onc carriage, promoter insertion, enhancer activation, or disruption of tumor suppressors. Conclude that the theory explains viral induction of tumors. Verification / Alternative check: Classical examples include Rous sarcoma virus (v-src), human papillomavirus (E6/E7 impacting p53/Rb), and HBV/HTLV mechanisms influencing oncogenesis. Why Other Options Are Wrong: Chemical inactivation: Disinfection, not oncogenesis. Viral replication: General virology, not transformation-specific. None of these / RT inhibition: Do not address tumor formation. Common Pitfalls: Equating transformation with mere infection; oncogenesis involves stable genetic or regulatory changes leading to unregulated growth. Final Answer: The oncogene theory explains how viruses transform normal cells into tumor cells.

Question 3

Temperate phage immunity: The prophage-encoded repressor renders the host cell resistant to lysis initiated by which source?

Accepted Answer

Introduction: Temperate phages can integrate into the host genome as prophages under lysogeny. A key feature is “superinfection immunity,” where a prophage-encoded repressor protects the lysogen from subsequent infection by the same or closely related phages that attempt to enter the lytic program. Given Data / Assumptions: A temperate phage encodes a repressor protein. We must identify what lytic trigger the repressor blocks. Induction of the resident prophage is a distinct process regulated by repressor stability. Concept / Approach: The repressor binds operator sites of lytic promoters, preventing expression of lytic genes. This blocks incoming phages of the same immunity group from initiating lytic growth, thereby conferring immunity to superinfection. However, under stress (e.g., DNA damage), repressor cleavage can induce the prophage, allowing it to enter the lytic cycle; this is not “blocked” by the repressor. Step-by-Step Solution: Recognize that superinfection immunity targets external lytic attempts by related phages. Differentiate induction of the resident prophage (repressor inactivation) from blocking of superinfecting phages (repressor active). Choose resistance to lytic infection by other related phages as the correct outcome. Verification / Alternative check: Lambda phage immunity system (cI repressor) exemplifies how lysogens resist superinfection by lambda-like phages while remaining inducible under SOS conditions. Why Other Options Are Wrong: The resident prophage: Induction occurs when repressor is inactivated; immunity does not prevent this. Both (a) and (b): Incorrect because (a) is not blocked under induction. None / Environmental lysozyme: Do not represent the genetic immunity mechanism. Common Pitfalls: Confusing superinfection immunity with resistance to prophage induction; they are mechanistically distinct. Final Answer: The repressor protects against lytic infection by superinfecting related phages.

Question 4

Reverse transcriptase is most useful in which virological situation?

Accepted Answer

Introduction: Reverse transcriptase (RT) is a hallmark enzyme of retroviruses and other reverse-transcribing viruses. It synthesizes complementary DNA (cDNA) from an RNA template, enabling integration into the host genome and persistent infection. Given Data / Assumptions: RT activity converts RNA to DNA (RNA-dependent DNA polymerase). Retroviruses (e.g., HIV) require RT to form proviral DNA. Other listed scenarios do not inherently require RT. Concept / Approach: Retroviral replication cycles depend on RT to generate a DNA form that can integrate via integrase. Non-retroviral processes like spike formation, host starvation, or DNA virus mRNA synthesis do not require RT. Step-by-Step Solution: Identify the process that needs RNA-to-DNA conversion. Match it to retroviral biology (formation of provirus). Select the option specifying RNA → DNA conversion. Verification / Alternative check: Antiretroviral therapies target RT (e.g., NRTIs/NNRTIs), confirming its essential role in retrovirus replication. Why Other Options Are Wrong: No host cells present: Viruses cannot replicate without cells; RT is irrelevant alone. Nutrient scarcity: Host physiology issue, not an RT-dependent step. Spike formation: Involves protein synthesis and trafficking, not reverse transcription. DNA virus mRNA synthesis: Uses host RNA polymerase II or viral DNA-dependent RNA polymerase, not RT. Common Pitfalls: Assuming RT is a general viral enzyme; it is specific to reverse-transcribing viruses. Final Answer: An RNA virus converting its RNA to DNA (proviral DNA formation) requires reverse transcriptase.

Question 5

Capsid architecture: In the simplest icosahedral capsid, the capsomere located at each of the 12 vertices and surrounded by five neighbors is called what?

Accepted Answer

Introduction: Many viruses adopt icosahedral symmetry to build robust capsids from repeating subunits. Understanding the naming of architectural elements such as pentons and hexons is crucial in structural virology. Given Data / Assumptions: An icosahedron has 12 vertices. At each vertex lies a capsomere surrounded by five others. We must identify the correct term for this vertex capsomere. Concept / Approach: In icosahedral capsids, capsomeres at fivefold axes (vertices) are called pentons. Capsomeres at sixfold positions are termed hexons. This naming reflects local symmetry and packing rather than the entire particle’s symmetry number. Step-by-Step Solution: Recall that an icosahedron has 12 fivefold vertices. Associate fivefold positions with penton capsomeres. Select “penton” for the vertex capsomere surrounded by five neighbors. Verification / Alternative check: Classic adenovirus models and other icosahedral maps distinguish penton base (at vertices) from hexon facets; this convention is standard across textbooks. Why Other Options Are Wrong: Polyhedra / Icosahedral unit: Generic terms, not the specific capsomere name. Helical turn: Applies to helical symmetry, not icosahedral. Portal complex: A specialized vertex in some tailed phages, not a general vertex capsomere term. Common Pitfalls: Confusing overall particle symmetry with local capsomere terminology; “penton” specifically denotes fivefold vertex units. Final Answer: The vertex capsomere is a penton.

Question 6

Identify the false statement about viruses (select the option that is NOT true).

Accepted Answer

Introduction: A core property of viruses is their absolute dependence on living cells for replication. Distinguishing true foundational statements from false ones helps prevent conceptual errors in virology. Given Data / Assumptions: We must choose the statement that is NOT true. Options include basic facts and one misleading claim. Concept / Approach: Viruses require host cell machinery to replicate; they cannot grow on inert media like bacteria or fungi can. Although we can culture viruses using cell lines, embryonated eggs, or live hosts, “pure culture in test tubes” without living cells is not possible. Step-by-Step Solution: Review each statement against virology fundamentals. Identify dependence on living cells as the key discriminant. Select the statement wrongly claiming growth in pure, cell-free media. Verification / Alternative check: Standard lab methods (cell culture, plaque assays) all rely on viable host cells; no routine cell-free “pure culture” growth exists for intact viruses. Why Other Options Are Wrong (i.e., true statements): Obligate intracellular parasites: True for all viruses. DNA or RNA as genetic material: True; they never have both. Arising from fragments of cellular chromosomes: A plausible hypothesis; not proven but not a categorical falsehood. Integration into host genome: True for many, e.g., retroviruses and some DNA viruses. Common Pitfalls: Confusing “cell culture” (which uses living cells) with “pure culture” in nutrient broth; only the former supports viral replication. Final Answer: The false statement is “Viruses have been successfully grown in pure cultures in test tubes.”

Question 7

Because a lysogen resists lysis by superinfecting phage, the prophage repressor is also called the:

Accepted Answer

Introduction: Temperate phages provide their hosts with “immunity” to further infection by the same or closely related phages. The protein responsible for this phenotype has a conventional name that reflects its function. Given Data / Assumptions: Lysogens resist lytic development by superinfecting related phages. This resistance is mediated by a prophage-encoded repressor. Concept / Approach: The repressor binds operator regions of lytic promoters in incoming phage DNA, preventing expression of lytic genes. Hence it confers “immunity” to superinfection, and is aptly termed an “immunity repressor.” Lambda phage cI is a paradigmatic example. Step-by-Step Solution: Identify the phenotype: superinfection immunity. Match phenotype to the responsible protein: the phage repressor. Recall conventional term: immunity repressor. Verification / Alternative check: Genetic studies of lambda and related phages consistently use “immunity” terminology to describe repressor-governed resistance to superinfection. Why Other Options Are Wrong: Immunity operon / Operon repressor: Misleading phrasing; the standard term is immunity repressor (a protein), not an operon name. None / Superinfection lysozyme: Lysozyme is unrelated; “none” does not fit the well-established term. Common Pitfalls: Confusing repressor-mediated immunity with nonspecific resistance; immunity is sequence- and immunity-group–specific. Final Answer: The repressor is called the immunity repressor.

Question 8

Viruses lack most metabolic machinery; they cannot generate energy or synthesize what key macromolecule on their own?

Accepted Answer

Introduction: Unlike cells, viruses are metabolically inert outside a host. They depend on the host’s systems for both energy and biosynthesis. A classic teaching point is the inability of viruses to make their own proteins without hijacking host ribosomes. Given Data / Assumptions: Viruses lack ribosomes and translation factors. They require host cell machinery to synthesize viral proteins. Options include various molecules and an overbroad “all of these.” Concept / Approach: Protein synthesis requires ribosomes, tRNAs, initiation/elongation/termination factors, and aminoacyl-tRNA synthetases. Viruses do not encode complete translation systems; therefore, they cannot synthesize proteins independently. While they also lack metabolic pathways for carbohydrate or alcohol synthesis, the most precise, universally emphasized limitation is protein synthesis. Step-by-Step Solution: Identify the universally cited deficit: absence of ribosomes. Relate this to protein synthesis dependency on the host. Choose “protein” as the key macromolecule viruses cannot synthesize alone. Verification / Alternative check: Laboratory cultivation always requires living cells because viral gene expression and protein production occur on host translational machinery. Why Other Options Are Wrong: Carbohydrate / Alcohol / Cholesterol: While viruses do not conduct these metabolic syntheses, exam convention highlights protein synthesis as the defining limitation. All of these: Overbroad and less precise than the canonical teaching point. Common Pitfalls: Assuming “all of these” is always safest; targeted knowledge about ribosome absence makes “protein” the best answer. Final Answer: Viruses cannot synthesize protein without host machinery.

Question 9

Baltimore/Bradley perspective: Group E bacteriophages are characterized by which type of nucleic acid?

Accepted Answer

Introduction: Historic bacteriophage classifications (e.g., Bradley groups) and broader genome-type schemes highlight that some coliphages, such as MS2 and related male-specific phages, possess RNA genomes. Recognizing which group corresponds to RNA phages is a common exam objective. Given Data / Assumptions: The question refers to “Group E phages,” a classic morphology/genome grouping. Representative members include small icosahedral phages like MS2. We must select the correct nucleic acid type. Concept / Approach: Group E phages (male-specific, leviviruses) have positive-sense single-stranded RNA genomes. They infect bacteria via F pili and are distinct from the large dsDNA tailed phages. Their compact genomes encode maturation, coat, lysis, and replicase proteins. Step-by-Step Solution: Recall examples: MS2, f2, Qβ-like phages. Associate these with +ssRNA genomes and small icosahedral capsids. Select “single-stranded RNA.” Verification / Alternative check: Classic literature and modern databases list MS2 as a positive-sense ssRNA phage, aligning with Group E designation in older schemes. Why Other Options Are Wrong: Single-/Double-stranded DNA: Describe many tailed phages, not Group E RNA phages. Double-stranded RNA / Segmented dsDNA: Not characteristic of MS2-like coliphages. Common Pitfalls: Confusing Baltimore numbering (I–VII) with older lettered phage groups; cross-checking exemplars like MS2 prevents errors. Final Answer: Group E phages possess single-stranded RNA genomes.

Question 10

Oncogenic transformation in virology: Which of the following human viruses are known to transform infected cells (in vitro or in vivo), indicating oncogenic potential or immortalization ability?

Accepted Answer

Introduction: Some human viruses possess oncogenic properties, meaning they can drive cellular transformation, immortalization, or dysregulated proliferation either in experimental systems or within the human host. This question examines recognition of three classic oncogenic viruses—HBV, HTLV-1, and EBV—that are well documented to transform infected cells and contribute to cancer pathogenesis. Given Data / Assumptions: Hepatitis B virus (HBV) is etiologically linked with hepatocellular carcinoma. Human T-cell lymphotropic virus type 1 (HTLV-1) is associated with adult T-cell leukemia/lymphoma. Epstein–Barr virus (EBV) is associated with Burkitt lymphoma, nasopharyngeal carcinoma, and other lymphoproliferative disorders. Concept / Approach: Cellular transformation by viruses typically involves viral proteins that alter host cell cycle regulation, apoptosis, or genomic stability. For HBV, the HBx protein and chronic inflammatory microenvironment are key. HTLV-1 uses Tax and HBZ to dysregulate signaling and proliferation in T cells. EBV employs latent proteins (e.g., LMP1, EBNA2) to drive B-cell activation and survival. If each listed virus has credible evidence of transformation/oncogenicity, then a combined option is correct. Step-by-Step Solution: Step 1: Evaluate HBV: chronic infection and HBx contribute to oncogenesis in the liver.Step 2: Evaluate HTLV-1: Tax/HBZ promote T-cell proliferation leading to adult T-cell leukemia/lymphoma.Step 3: Evaluate EBV: latent genes transform B cells; multiple EBV-associated cancers are documented.Step 4: Integrate: all three are transforming/oncogenic; therefore select the comprehensive option. Verification / Alternative check: Oncovirology references consistently list HBV, HTLV-1, and EBV among definitive human oncogenic viruses, with mechanistic and epidemiological support. Multiple in vitro systems also show immortalization/transformation of target cells by these agents under defined conditions. Why Other Options Are Wrong: HBV only: ignores HTLV-1 and EBV. HTLV-1 only: ignores HBV and EBV. EBV only: ignores HBV and HTLV-1. HPV only: although HPV is oncogenic, the question lists three others that are also transforming. Common Pitfalls: Confusing “transforming in vitro” with “causing cancer” in vivo; both are relevant but not identical. Another pitfall is assuming only DNA tumor viruses transform; HTLV-1 is an RNA retrovirus with clear oncogenicity. Final Answer: All of these.

Question 11

Virus architecture vocabulary: The capsomeres of an icosahedral capsid are themselves built from repeating protein subunits called what?

Accepted Answer

Introduction: Virus particles are highly ordered assemblies. Understanding the hierarchy of structural units—from proteins to capsomeres to the full capsid—is fundamental in virology, structural biology, and vaccine design. This question tests the correct term for the basic protein subunits that polymerize to form capsomeres in many icosahedral viruses. Given Data / Assumptions: Capsid: the protective protein shell around the viral genome. Capsomere: a morphological unit visible by electron microscopy that builds the capsid, often arranged with icosahedral symmetry. We seek the name of the protein subunits that assemble into each capsomere. Concept / Approach: The standard terminology in classical virology is: protomer (basic structural protein subunit) → several protomers associate to form a capsomere → capsomeres assemble into the capsid. While terms like procapsid and scaffolding proteins exist, they refer to intermediates or helper factors during assembly, not the basic repeating subunit of the capsomere itself. Step-by-Step Solution: Step 1: Recall the hierarchy: protomer → capsomere → capsid.Step 2: Distinguish from “procapsid,” a precursor shell that later matures, often aided by scaffolding proteins.Step 3: Exclude invented or incorrect terms such as “caproproteins” or vague phrases that lack acceptance in virology texts.Step 4: Identify “protomers” as the correct unit building capsomeres. Verification / Alternative check: Standard microbiology and virology references define protomers as the fundamental polypeptide units forming capsomeres. Electron microscopy and cryo-EM studies support this modular assembly model for many icosahedral viruses. Why Other Options Are Wrong: Caproproteins: non-standard term; not used in virology literature. Procapsid scaffolds: refer to assembly intermediates or helper proteins, not the basic repeating subunits. None of these: incorrect because “protomers” is correct. Peptidomer units: fabricated term without consensus usage. Common Pitfalls: Confusing morphological units (capsomeres) with molecular subunits (protomers); assuming “procapsid” is a subunit rather than a pre-assembled shell. Final Answer: Protomers.

Question 12

Temperate bacteriophages: Which temperate phage lacks site specificity for chromosomal insertion and can integrate multiple copies into a single bacterial chromosome?

Accepted Answer

Introduction: Temperate bacteriophages can integrate their genomes into the host chromosome. While some use site-specific recombination, others employ transposition-like mechanisms. This question tests knowledge of a phage renowned for random integration (lack of strict site specificity) and potential for multiple insertions—features that have made it a valuable genetic tool. Given Data / Assumptions: Some phages integrate at defined attachment sites (e.g., lambda at attB/attP). Other phages transpose into the genome with less sequence constraint. We are asked to pick the phage that integrates with low site specificity and can insert multiple copies. Concept / Approach: Lambda (λ) is the model of site-specific integration via integrase at att sites. In contrast, Phage Mu (Mutator) integrates using a transposition mechanism with broad target preference, leading to diverse insertion sites and possible multicopy lysogens. Therefore, Mu matches the described behavior. Step-by-Step Solution: Step 1: Recall λ phage: site-specific recombination at attB in the host and attP on the phage.Step 2: Recall Mu phage: transposition-based integration with low sequence specificity.Step 3: Note that Mu can integrate multiple times, creating genomic rearrangements and mutations.Step 4: Conclude Mu is the correct choice. Verification / Alternative check: Genetics literature documents Mu as a transposable phage causing insertional mutagenesis across the chromosome. Laboratory use of Mu for mutagenesis underscores its lack of strict site specificity. Why Other Options Are Wrong: Lambda enzyme integrase: an enzyme, not a phage; moreover lambda integrates site-specifically. Lambda DNA: relies on att sites; not random. Phage Mn: not a standard, recognized temperate phage in classical literature. P1 phage: establishes plasmid-like lysogeny; not characterized by random multicopy chromosomal insertions in the sense of Mu. Common Pitfalls: Assuming all temperate phages integrate similarly; confusing site-specific recombination with transposition. Final Answer: Phage Mu (Mutator phage).

Question 13

Human oncogenic viruses: Which virus listed has not been convincingly associated with human cancer in epidemiologic and mechanistic studies?

Accepted Answer

Introduction: Numerous human viruses have established or strongly suspected links to cancer. Differentiating those with robust causal evidence from those without is critical in oncology, public health, and vaccination policy. This question asks which listed virus has not been convincingly associated with human cancer. Given Data / Assumptions: HBV and HCV are definitively linked with hepatocellular carcinoma. EBV is linked to multiple malignancies including Burkitt lymphoma and nasopharyngeal carcinoma. HSV-2 has been historically debated but lacks conclusive causal evidence comparable to HBV/HCV/EBV. Varicella–Zoster virus primarily causes varicella (chickenpox) and zoster (shingles). Concept / Approach: Pick the virus without a solid, widely accepted causal association with human cancer. VZV is not recognized as an oncogenic human virus. The others (HBV, HCV, EBV) are established carcinogenic agents; HSV-2 is not definitively causal, but VZV is clearly the best answer as “not associated.” Step-by-Step Solution: Step 1: Identify well-established oncogenic viruses among options (HBV, HCV, EBV).Step 2: Evaluate HSV-2: not confirmed as a human carcinogen at the level of the above; however it is still more plausible historically than VZV.Step 3: Recognize VZV causes lytic skin/nerve disease and latency in sensory ganglia, not cancer.Step 4: Select VZV as the virus not associated with human cancer. Verification / Alternative check: Oncovirology overviews and IARC classifications list HBV, HCV, EBV as carcinogenic agents. There is no comparable classification for VZV as a human carcinogen. Why Other Options Are Wrong: HCV: strong association with liver cancer via chronic inflammation and direct effects. HBV: linked to hepatocellular carcinoma; HBV vaccination is a cancer prevention strategy. HSV-2: debated historically; not the best “not associated” choice compared to VZV. EBV: established links to several malignancies. Common Pitfalls: Assuming that all herpesviruses have similar oncogenicity; conflating latency with oncogenic transformation. Final Answer: Varicella–Zoster virus (VZV).

Question 14

Viral envelopes and cellular origin: The envelope of which virus family is derived primarily from the host cell nuclear membrane during maturation?

Accepted Answer

Introduction: Enveloped viruses acquire their membranes from host cell compartments during budding or envelopment. Identifying the cellular origin of the viral envelope helps understand replication sites, antiviral targets, and cytopathic effects. This question focuses on the unique nuclear envelopment of herpesviruses. Given Data / Assumptions: Different virus families bud through distinct membranes (plasma membrane, ER, Golgi, or nuclear envelope). Herpesviruses replicate their DNA in the nucleus. Primary envelopment of herpesviruses occurs at the inner nuclear membrane with subsequent maturation steps. Concept / Approach: Map each family to its typical budding site. Retroviruses and paramyxoviruses usually bud at the plasma membrane. Orthomyxoviruses (e.g., influenza) also bud at the plasma membrane after nuclear genome replication. Herpesviruses obtain an initial envelope from the inner nuclear membrane before complex de/envelopment steps via ER/Golgi compartments. Step-by-Step Solution: Step 1: Identify herpesvirus replication in host nucleus.Step 2: Recall primary envelopment at the inner nuclear membrane, forming perinuclear enveloped particles.Step 3: Understand de-envelopment/re-envelopment through ER/Golgi leading to the mature virion.Step 4: Conclude herpesviruses derive their envelope from nuclear/ER-Golgi membranes, uniquely beginning at the nucleus. Verification / Alternative check: Electron microscopy studies of HSV show capsids bud through the inner nuclear membrane; though subsequent membrane exchanges occur, nuclear origin is the hallmark distinguishing feature in exam contexts. Why Other Options Are Wrong: Paramyxoviruses: bud from the plasma membrane. Retroviruses: assemble and bud at the plasma membrane. Orthomyxoviruses: genome replication in nucleus but budding at plasma membrane. Poxviruses: replicate in cytoplasm; complex assembly from intracellular membranes, not nuclear origin. Common Pitfalls: Confusing genome replication site with envelope origin; assuming nuclear replication always implies nuclear budding for all families. Final Answer: Herpesviruses.

Question 15

History of vaccination: Edward Jenner initiated protective inoculation of humans using material taken from which type of lesions?

Accepted Answer

Introduction: Edward Jenner’s pioneering work in the late 18th century established the concept of vaccination. He observed that exposure to cowpox could protect against smallpox, a devastating human disease. This question tests historical knowledge of the source material Jenner used for his inoculations. Given Data / Assumptions: Jenner noted milkmaids exposed to cowpox were resistant to smallpox. He transferred material from cowpox lesions to humans to induce protection. Terminology can be confusing (smallpox vs. chickenpox vs. cowpox); only cowpox is correct in Jenner’s original experiments. Concept / Approach: Differentiate among pox and pox-like diseases. Smallpox (Variola) was the deadly human disease. Cowpox is a related orthopoxvirus producing milder disease in humans. Varicella (chickenpox) is a herpesvirus, unrelated to orthopoxviruses, and was not used by Jenner. Avianpox affects birds, not the historical source for Jenner’s inoculum. Step-by-Step Solution: Step 1: Recall Jenner’s observation of milkmaids’ immunity.Step 2: Identify cowpox as the immunizing agent he used.Step 3: Exclude smallpox/chickenpox as sources; they are etiologically distinct.Step 4: Provide the historically accurate answer: cowpox. Verification / Alternative check: Historical accounts of Jenner’s 1796 experiment with James Phipps document inoculation using cowpox material, followed later by challenge with smallpox, demonstrating protection. Why Other Options Are Wrong: Smallpox lesions: too dangerous; not Jenner’s inoculum source. Avianpox: a bird pathogen; not used by Jenner. Chickenpox: unrelated herpesvirus; not the historical vaccine source. Monkeypox: recognized much later; not part of Jenner’s work. Common Pitfalls: Confusing chickenpox (varicella) with smallpox/cowpox due to similar names; assuming “pox” diseases are interchangeable. Final Answer: Cowpox lesions (Vaccinia-like).

Question 16

Measles virus cytopathic effect: In cell culture, infection with measles virus most characteristically leads to which observable effect?

Accepted Answer

Introduction: Paramyxoviruses, including measles virus (Morbillivirus), express fusion proteins that can mediate cell–cell fusion. Recognizing the hallmark cytopathic effect (CPE) of measles infection in culture is important for laboratory diagnosis and understanding pathogenesis. Given Data / Assumptions: Measles virus is an enveloped, negative-sense RNA virus of the Paramyxoviridae family. Viral fusion (F) protein on infected cell membranes can cause neighboring cells to fuse. Characteristic CPE includes formation of multinucleated giant cells (syncytia). Concept / Approach: Different viruses produce distinct CPEs: some cause rounding and lysis, others produce inclusion bodies, and some drive syncytium formation through fusion proteins. For measles, the most striking and testable feature is syncytium formation and, in tissues, Warthin–Finkeldey giant cells in lymphoid organs. Step-by-Step Solution: Step 1: Identify the virus family (Paramyxoviridae) and the presence of a fusion protein.Step 2: Understand that fusion of adjacent cell membranes yields multinucleated cells.Step 3: Recall that measles infection often shows cytoplasmic and sometimes nuclear inclusions, but the cardinal culture finding is syncytia.Step 4: Choose the option explicitly naming syncytium formation. Verification / Alternative check: Virology lab manuals describe syncytium formation as a rapid, recognizable CPE for measles and other paramyxoviruses (e.g., RSV). Histopathology texts note Warthin–Finkeldey giant cells in vivo, aligning with the in vitro fusion phenotype. Why Other Options Are Wrong: Nuclear pyknosis: non-specific cell injury; not the distinctive hallmark. Neoplastic transformation: measles is not an oncogenic virus. Only rounding/aggregation: too generic; does not capture the fusion-driven giant cells. Intranuclear inclusions only: measles has cytoplasmic inclusions; the signature is syncytia rather than inclusions alone. Common Pitfalls: Confusing generic CPE (rounding, detachment) with the specific fusion-driven syncytia of paramyxoviruses. Final Answer: Syncytium (multinucleated giant cell) formation.

Question 17

Virucidal agents in practice: Which disinfectant(s) are effective against viruses when used at appropriate concentrations and contact times?

Accepted Answer

Introduction: Choosing an appropriate disinfectant for viral contamination requires understanding virucidal spectra, concentration, and contact time. Many commonly available agents inactivate enveloped viruses readily and can also act against numerous non-enveloped viruses under proper conditions. This question checks familiarity with three well-known virucidal agents used in laboratories and healthcare settings. Given Data / Assumptions: Hydrogen peroxide is an oxidizing agent with broad microbicidal activity. Hypochlorite solutions (bleach) are widely used surface disinfectants with strong virucidal action. Formaldehyde has historical use for high-level disinfection and fumigation, though modern practice emphasizes safety and alternatives. Concept / Approach: Evaluate each listed agent for documented virucidal efficacy. Oxidizing agents (peroxides, chlorine) denature proteins, disrupt membranes, and can damage nucleic acids. Aldehydes (e.g., formaldehyde, glutaraldehyde) crosslink proteins and nucleic acids, inactivating viruses with adequate exposure. When all options have recognized virucidal activity, the composite answer is appropriate. Step-by-Step Solution: Step 1: Hydrogen peroxide: effective against enveloped viruses and many non-enveloped viruses; vaporized forms are used for room decontamination.Step 2: Hypochlorite: rapidly virucidal at recommended dilutions; commonly used for blood/body fluid spills.Step 3: Formaldehyde: historically used for surface/room decontamination; potent but with occupational safety concerns.Step 4: Conclude that all three agents exhibit virucidal activity under proper use conditions. Verification / Alternative check: Infection control guidelines and disinfectant efficacy standards list chlorine compounds, peroxides, and aldehydes as effective against a broad range of viruses, with caveats about concentration, organic load, and contact time. Why Other Options Are Wrong: Single-agent choices (A–C) are incomplete because multiple agents are effective. Quaternary ammonium compounds only: quats have variable activity against non-enveloped viruses; not superior to the listed broad virucidal agents. Common Pitfalls: Ignoring the critical roles of concentration and contact time; assuming one disinfectant works for every situation regardless of organic load or material compatibility. Final Answer: All of these.

Question 18

Virology basics — In virus architecture, what exactly constitutes the nucleocapsid (state the two parts clearly)?

Accepted Answer

Introduction / Context: The term nucleocapsid is foundational in virology and appears in diagnostic reports, vaccine papers, and antiviral targets. It precisely refers to the viral nucleic acid packaged together with its protective protein coat, the capsid. Understanding this term avoids confusion with other layers such as envelopes and spike glycoproteins. Given Data / Assumptions: Nucleocapsid = nucleic acid + capsid (protein shell). Some but not all viruses also possess a lipid envelope with spikes. Capsomeres are the repeating protein subunits that assemble to form a capsid; they are not an alternative to the whole capsid. Concept / Approach: Disentangle the hierarchical structure: capsomeres assemble into a capsid; the capsid encloses the genome; genome + capsid = nucleocapsid. If present, an envelope (with spikes) surrounds the nucleocapsid but is not part of it by definition. Step-by-Step Solution: Identify the two indispensable components: genome (RNA or DNA) and capsid.Exclude envelope and spikes because many nonenveloped viruses still have a nucleocapsid.Recognize that “capsomere and genome” is incomplete because capsomeres are subunits; the assembled structure is the capsid. Verification / Alternative check: Electron microscopy and structural biology textbooks consistently define nucleocapsid as genome + capsid. Enveloped viruses have an added lipid bilayer, but the core concept remains the same across families. Why Other Options Are Wrong: Capsid and spikes: spikes are envelope proteins, not part of the nucleocapsid. Envelope and capsid: the envelope is optional and external. Capsomere and genome: capsomere is a subunit, not the assembled capsid. Common Pitfalls: Equating the presence of spikes with the definition of the core particle; assuming envelopes are universal. Many clinically significant viruses are nonenveloped and still have a nucleocapsid. Final Answer: Genome and capsid

Question 19

Comparative genomics — Across sequence comparisons, where would you expect greater similarity: among viruses themselves or between viruses and their specific hosts?

Accepted Answer

Introduction / Context: This question probes evolutionary relationships and sequence homology expectations in host–virus systems. Despite viral diversity, many viruses evolve from and adapt to specific host cellular environments, often sharing motifs with host factors they hijack. Given Data / Assumptions: Viruses are highly diverse across families and genome types (DNA/RNA, ss/ds, segmented/nonsegmented). Host genomes are far larger but contain proteins and motifs that viruses target or mimic. We are comparing overall similarity trends, not cherry-picked genes. Concept / Approach: Because of extreme viral diversity, inter-virus similarity across unrelated families is typically low. Conversely, specific viral proteins (or sequence motifs) may resemble host proteins, interaction domains, or regulatory sequences due to convergent evolution, mimicry, or gene capture. Hence, measured similarity can be higher between a virus and its host than between two unrelated viruses. Step-by-Step Solution: Note low baseline similarity among distant viral families.Recognize virus–host mimicry and co-evolution leading to shared motifs.Infer that the expected higher similarity is between viruses and their specific hosts rather than among unrelated viruses. Verification / Alternative check: Comparative analyses often reveal host-derived sequences in large DNA viruses and host-like interaction motifs in many RNA viruses, elevating virus–host similarity relative to cross-family virus–virus comparisons. Why Other Options Are Wrong: Among different viruses: too diverse to be generally more similar. Among different hosts: question focuses on virus–host versus inter-virus similarity. Among hosts vs viruses: misframes the comparison. Common Pitfalls: Assuming “all viruses are similar” because of shared small size; in reality, genome strategies differ profoundly across lineages. Final Answer: Between viruses and their hosts than among different viruses

Question 20

Virus classification — The primary basis for separating viruses into major groups is:

Accepted Answer

Introduction / Context: Modern virology relies on genome type and replication strategy to classify viruses at high levels. This echoes the Baltimore classification and underpins diagnostics and antiviral development. Given Data / Assumptions: Possible criteria include host range, capsid symmetry, and particle size. However, genome and replication mode dictate core biology. Concept / Approach: At the broadest grouping, genome properties (DNA vs RNA; ss vs ds; positive-sense vs negative-sense; reverse-transcribing) and how genomes are expressed/replicated dominate classification because they determine essential enzymes, replication sites, and susceptibilities to drugs. Step-by-Step Solution: Identify primary discriminator: nucleic acid and replication strategy.Down-rank morphology/size; useful but secondary.Note that host range is informative for ecology, not for top-level taxonomy. Verification / Alternative check: Reference frameworks consistently group viruses into DNA/RNA and Baltimore classes I–VII, before fine-graining by morphology and host range. Why Other Options Are Wrong: Host nature: many unrelated viruses infect the same host group. Capsid symmetry: shared across disparate families. Diameter: overlaps widely and is not diagnostic. Common Pitfalls: Overemphasizing EM morphology; two morphologically similar viruses can have radically different replication strategies. Final Answer: Nucleic acid characteristics (DNA/RNA, sense, strandedness, replication strategy)

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