Question 1

Medical virology and epidemiology: West Nile virus causes disease in humans and is transmitted from an infected bird to a person by a mosquito vector. This pattern represents which type of disease transmission?

Accepted Answer

Introduction / Context: West Nile virus is a classic example of an arbovirus, a term derived from arthropod-borne virus. Understanding vector-mediated transmission is central to infection control, outbreak investigation, and public health messaging. Given Data / Assumptions: Reservoir: birds can carry West Nile virus. Vector: mosquitoes acquire virus by feeding on viremic birds. Humans are infected when bitten by a competent infected mosquito. No direct person-to-person spread via casual contact or fomites is implied. Concept / Approach: Transmission categories include endogenous (from a patient’s own flora), fomite borne (via contaminated objects), nosocomial (healthcare-associated), and vector-borne (via arthropods such as mosquitoes or ticks). When a mosquito transmits a pathogen from an animal reservoir to humans, the correct category is arthropod borne. Step-by-Step Solution: Identify the vector in the scenario: mosquito. Recognize mosquitoes as arthropods. Match vector involvement to the transmission category: arthropod borne disease. Exclude endogenous, fomite borne, and nosocomial, which do not fit the described chain. Verification / Alternative check: Many arboviruses share this pattern (dengue, Zika, chikungunya). The unifying feature is obligatory transmission by an arthropod vector. Why Other Options Are Wrong: Endogenous infection: Originates from a patient’s own microbiota, not via mosquitoes. Fomite borne disease: Involves contaminated objects, not blood-feeding arthropods. Nosocomial infection: Acquired in healthcare settings, not from wildlife via mosquitoes. Zoonosis without a vector: Omits the mosquito step that is essential here. Common Pitfalls: Confusing general zoonoses with vector-borne zoonoses; overlooking that arthropod involvement specifically defines the category. Final Answer: arthropod borne disease.

Question 2

Viral cytopathic effects: Intracytoplasmic inclusion bodies may be seen in cells infected with which of the following viruses?

Accepted Answer

Introduction / Context: In diagnostic virology, inclusion bodies are hallmark cytopathic effects that help point to viral families. Distinguishing intracytoplasmic from intranuclear inclusions guides presumptive identification on histology or cytology. Given Data / Assumptions: Rabies virus produces Negri bodies (cytoplasmic). Vaccinia virus (a poxvirus) replicates in cytoplasm and forms cytoplasmic inclusions. Fowlpox virus, another poxvirus, also forms cytoplasmic inclusions. Concept / Approach: Poxviruses replicate in the host cell cytoplasm and typically generate prominent cytoplasmic inclusion bodies. Rabies virus likewise leads to cytoplasmic Negri bodies in neurons. Therefore, multiple listed viruses share intracytoplasmic inclusion formation. Step-by-Step Solution: Match each virus to typical inclusion location. Rabies: Negri bodies in cytoplasm. Vaccinia/Fowlpox: cytoplasmic inclusions due to cytoplasmic replication. Therefore, select the comprehensive choice “all of these”. Verification / Alternative check: Histopathology texts repeatedly cite these inclusions for quick recognition and teaching slides often feature them. Why Other Options Are Wrong: Single-virus answers omit other correct examples; “none” is contradicted by well-known inclusions. Common Pitfalls: Confusing intracytoplasmic inclusions of poxviruses with intranuclear inclusions typical of herpesviruses and adenoviruses. Final Answer: all of these.

Question 3

Viral envelopes: Which lipid class predominates in the membranes that form the viral envelope derived from host cells?

Accepted Answer

Introduction / Context: Enveloped viruses bud through host membranes, acquiring a lipid bilayer. Knowing its composition helps explain sensitivity to detergents, desiccation, and disinfectants. Given Data / Assumptions: Viral envelopes are derived from host plasma membrane or internal membranes. Typical eukaryotic membranes are composed mainly of phospholipids and cholesterol, with smaller fractions of glycolipids. Neutral fats (triacylglycerols) are storage lipids, not main bilayer components. Concept / Approach: The bilayer’s structural backbone is phospholipids, which form amphipathic sheets. Cholesterol modulates fluidity but is not listed among options. Therefore, the predominant lipid class is phospholipids. Step-by-Step Solution: Identify the source of the envelope: host membrane. Recall membrane composition: mostly phospholipids with cholesterol. Exclude storage and minor lipid classes. Choose “phospholipids”. Verification / Alternative check: Basic cell biology consistently places phospholipids as the principal bilayer constituents across cell and viral envelopes. Why Other Options Are Wrong: Glycolipids: Present but minor compared with phospholipids. Neutral fat: Not a bilayer structural lipid. All of these: Overstates contributions of non-structural lipids. Ceramides only: Too narrow; sphingolipids are not exclusive. Common Pitfalls: Equating storage lipids with membrane structure, or assuming all lipid classes contribute equally. Final Answer: phospholipids.

Question 4

Interferons and cell sources: Which type of interferon is primarily produced by T lymphocytes in response to immune activation?

Accepted Answer

Introduction / Context: Interferons are cytokines with antiviral, immunomodulatory, and antiproliferative actions. Recognizing which cells produce which interferon subtype is important in immunology. Given Data / Assumptions: Type I interferons include interferon-α and interferon-β, produced by many cells including plasmacytoid dendritic cells and fibroblasts. Type II interferon is interferon-γ, produced mainly by activated T lymphocytes and NK cells. Interferon-γ has potent macrophage-activating and Th1-skewing effects. Concept / Approach: Match interferon subtype to its predominant cellular source. T cells are classically linked to interferon-γ production during cell-mediated responses. Step-by-Step Solution: Identify T lymphocyte-associated interferon: interferon-γ. Exclude interferon-α/β (type I, broad cellular sources). Select option “γ”. Note that NK cells also produce interferon-γ, reinforcing its immune role. Verification / Alternative check: Clinical assays measuring interferon-γ release (e.g., TB IGRA tests) demonstrate T cell-derived IFN-γ responses. Why Other Options Are Wrong: α and β are type I interferons not specific to T cells; combining γ with β is inaccurate for source specificity; λ is a distinct family with mucosal roles. Common Pitfalls: Assuming all interferons are produced by the same cell types; mixing type I and type II categories. Final Answer: γ.

Question 5

Viral replication sequence: Identify the correct chronological order of events in a typical productive viral replication cycle.

Accepted Answer

Introduction / Context: Although the details vary among DNA and RNA viruses, the core sequence of a lytic replication cycle follows a consistent logic from host recognition to progeny exit. Given Data / Assumptions: Attachment (adsorption) precedes entry. Penetration and uncoating allow genome access to host machinery. Biosynthesis of nucleic acids and proteins precedes assembly (maturation). Release occurs last, by lysis or budding. Concept / Approach: Think causally: you cannot synthesize viral components prior to entry, and you cannot release before assembly. Therefore the sequence is attachment → penetration (and uncoating) → biosynthesis → maturation (assembly) → release. Step-by-Step Solution: Start with attachment to host receptors. Proceed to penetration and uncoating to free the genome. Perform biosynthesis of viral RNA/DNA and proteins. Assemble capsids and package genomes (maturation). Exit the cell via lysis or budding (release). Verification / Alternative check: Textbook schematics for bacteriophages and animal viruses present this same order, differing mainly in entry and release mechanisms. Why Other Options Are Wrong: Sequences that put release or maturation before biosynthesis violate causality; sporulation is a bacterial process, not viral. Common Pitfalls: Forgetting uncoating is part of the early entry phase and mixing up assembly with synthesis. Final Answer: Attachment, penetration, biosynthesis, maturation, release.

Question 6

Viral cytopathic effects: Intranuclear inclusion bodies are characteristically observed in cells infected with which viruses?

Accepted Answer

Introduction / Context: Recognizing intranuclear versus intracytoplasmic inclusions helps narrow the differential diagnosis in viral infections. Different DNA viruses leave distinctive histologic footprints. Given Data / Assumptions: Parvoviruses can produce intranuclear inclusions. Herpesviruses produce Cowdry-type intranuclear inclusions. Adenoviruses classically cause smudgy intranuclear inclusions. Concept / Approach: Most DNA viruses replicate in the nucleus and may form intranuclear inclusions, with poxviruses being a notable exception (cytoplasmic replication). The listed viruses are well-known for nuclear inclusions. Step-by-Step Solution: List each virus family and typical inclusion location. Confirm nuclear inclusions for parvo, herpes, adeno. Select the aggregate correct option “all of these”. Verification / Alternative check: Histopathologic atlases describe these hallmark nuclear changes for teaching and diagnosis. Why Other Options Are Wrong: Any single-virus choice omits other true examples; “none” contradicts established findings. Common Pitfalls: Confusing poxvirus cytoplasmic inclusions with the nuclear inclusions of most other DNA viruses. Final Answer: all of these.

Question 7

Virus classification criteria: Which characteristic would not be used to classify viruses into families or genera?

Accepted Answer

Introduction / Context: Viruses lack many cellular structures. Their classification relies on properties of the virion and genome rather than traits found in cellular organisms. Given Data / Assumptions: Viruses do not possess cell walls. Key viral classification features include nucleic acid type (DNA/RNA, single or double stranded), capsid symmetry (icosahedral/helical), presence or absence of an envelope, and genome segmentation. Host range and replication strategy may also inform taxonomy. Concept / Approach: Evaluate each option for relevance to viral taxonomy. Cell wall structure is irrelevant because virions lack cell walls altogether. Step-by-Step Solution: Identify structural and genomic properties used in current classification. Confirm that “type of cell wall structure” is inapplicable. Select option “Type of cell wall structure”. Verification / Alternative check: Taxonomies from virology references consistently enumerate nucleic acid, symmetry, and envelope as core criteria. Why Other Options Are Wrong: Type of nucleic acid: Foundational criterion. Envelope: Major structural feature with epidemiologic implications. Symmetry: Distinguishes capsid architecture. Genome segmentation: Critical for reassortment potential. Common Pitfalls: Projecting bacterial classification criteria (e.g., cell wall type) onto viruses. Final Answer: Type of cell wall structure.

Question 8

Host dependence: Which microbes are most strictly dependent on a living plant or animal host for replication and survival?

Accepted Answer

Introduction / Context: Obligate intracellular dependence separates viruses from cellular life. This concept underlies antiviral strategies that target steps unique to virus-host interactions. Given Data / Assumptions: Viruses lack ribosomes and metabolic machinery for independent replication. Many bacteria, fungi, and algae can live and reproduce in the environment. Some parasites are obligate intracellular, but viruses are universally dependent. Concept / Approach: Identify the class of microbes that cannot replicate without commandeering host cell processes. Only viruses fit this requirement universally. Step-by-Step Solution: Assess each group’s autonomy. Confirm that viruses lack translation and energy generation systems. Select “viruses”. Verification / Alternative check: Culture techniques: viruses require living cells; bacteria and fungi can be grown on artificial media. Why Other Options Are Wrong: Bacteria, fungi, algae, and many protozoa can grow independently under suitable conditions. Common Pitfalls: Confusing obligate intracellular bacteria (e.g., Chlamydia) with the universal dependence characteristic of all viruses. Final Answer: viruses.

Question 9

ELISA design (direct antigen detection): If you perform a direct ELISA to detect polio virus antigen in a specimen, what should be coated onto the plastic microtiter wells as the capture layer?

Accepted Answer

Introduction / Context: Enzyme-linked immunosorbent assays (ELISA) rely on specific antigen-antibody interactions. Proper plate coating is essential to capture the target and achieve specificity and sensitivity. Given Data / Assumptions: Goal: detect polio virus antigen present in the test sample. Direct antigen-detection ELISA uses an immobilized capture antibody. Signal is generated by an enzyme-labeled antibody or detection reagent binding the captured antigen. Concept / Approach: For direct detection of antigen, wells are coated with a specific capture antibody that binds the target antigen from the sample. Patient serum is not a capture reagent in this design. Antigen-coated plates are used for antibody detection assays, not antigen detection. Step-by-Step Solution: Define the assay objective: detect viral antigen. Choose a capture layer specific to that antigen: anti-polio antibody. Apply specimen; antigen binds to immobilized antibody. Add enzyme-conjugated detection antibody to generate measurable signal. Verification / Alternative check: Compare against indirect ELISA (antibody detection) where antigen is coated and patient antibodies are probed. Here, the setup is the reverse because the target is antigen. Why Other Options Are Wrong: Patient serum: Contains unknowns; not a defined capture reagent. Polio capsid protein: Used to detect anti-polio antibodies, not to capture antigen. Colored substrate: Added after enzyme binding, not as a coating. Blocking protein only: Used to prevent nonspecific binding, not to capture target. Common Pitfalls: Confusing antigen-capture ELISA with antibody-detection formats; misplacing blocking and detection steps. Final Answer: Anti-polio antibody.

Question 10

Oncology terminology: What is the correct term for uncontrolled, autonomous proliferation of cells forming a neoplasm?

Accepted Answer

Introduction / Context: Precise terminology in pathology is critical. Several similar-sounding words describe different growth and differentiation abnormalities. This question focuses on the term that specifically denotes uncontrolled and autonomous proliferation. Given Data / Assumptions: The process in question is uncontrolled and autonomous, not a physiologic or regulated response. The proliferating mass is a neoplasm (tumor), which may be benign or malignant. Differentiation status and spread are related but distinct concepts. Concept / Approach: Neoplasia is defined as new, uncontrolled growth that persists even after the initiating stimulus is removed. Hyperplasia is an increase in cell number due to a stimulus and is often reversible. Dysplasia denotes disordered growth. Anaplasia describes loss of differentiation, typically in malignant tumors. Metastasis refers to spread to distant sites. Step-by-Step Solution: Identify the key qualifiers: uncontrolled and autonomous growth. Map terms: neoplasia fits those qualifiers; hyperplasia is controlled; anaplasia relates to differentiation; metastasis refers to spread. Select “Neoplasia”. Verification / Alternative check: Standard pathology texts use neoplasia as the umbrella process for tumor formation, with malignancy determined by additional behaviors such as invasion and metastasis. Why Other Options Are Wrong: Hyperplasia: Stimulus-driven and potentially reversible, not autonomous. Anaplasia: Loss of mature features, not the act of proliferation itself. Metastasis: Movement of tumor cells to distant sites, not primary growth. Dysplasia: Disordered maturation and architecture, may precede neoplasia but is not synonymous with it. Common Pitfalls: Using hyperplasia or dysplasia as synonyms for cancer; conflating differentiation status with proliferation control. Final Answer: Neoplasia.

Question 11

Viral structure and assembly: what is the role of matrix (M) proteins? In medical virology, which statement best describes where viral matrix proteins are located and what they primarily do in enveloped viruses?

Accepted Answer

Introduction / Context: Matrix proteins (often abbreviated as M, MA, or tegument-like layers depending on the family) are key structural components of many enveloped viruses. This question tests your understanding of where matrix proteins are located and their central role during virion assembly and stability. Given Data / Assumptions: Enveloped viruses possess a lipid bilayer derived from host membranes. Inside the envelope lies the nucleocapsid (genome plus capsid proteins). Matrix proteins frequently occupy the space between the envelope and the nucleocapsid. The options contrast surface spikes, naked virion composition, and nucleocore roles. Concept / Approach: Matrix proteins form a proteinaceous layer on the inner face of the viral envelope. They connect the cytoplasmic tails of envelope glycoproteins to the nucleocapsid. This scaffolding function stabilizes virion shape, orchestrates budding at host membranes, and can recruit host factors needed for assembly. Step-by-Step Solution: Identify matrix proteins as perenvelope scaffolds in enveloped viruses.Recall that spikes (for example, hemagglutinin, gp120) are transmembrane glycoproteins exposed externally—not matrix proteins.Recognize that naked viruses lack an envelope, so a matrix layer is not their defining feature.Select the choice stating matrix proteins anchor the envelope to the nucleocapsid. Verification / Alternative check: Examples include the M1 protein of influenza, the M protein of paramyxoviruses, and the MA (matrix) domain of retroviral Gag. All localize under the envelope and coordinate assembly and budding from host membranes. Why Other Options Are Wrong: Surface spikes: those are distinct envelope glycoproteins, not matrix proteins. Mainly on naked viruses: incorrect; matrix associates with envelopes. Part of nucleoprotein core as the capsid: capsid proteins differ from matrix proteins. Integrate into host chromosomes in all RNA viruses: integration is a retroviral reverse-transcription event, not a matrix function. Common Pitfalls: Confusing matrix proteins with envelope glycoprotein spikes or with capsid proteins. Keep the three layers conceptually distinct: envelope (lipid), matrix (inner scaffold), and nucleocapsid (core). Final Answer: They form an inner layer that anchors and links the envelope to the nucleocapsid in enveloped viruses.

Question 12

Clinical virology diagnostics: for which central nervous system infections is fluorescence microscopy useful? Select the best option summarizing where immunofluorescence or fluorescence microscopy can aid in diagnosis.

Accepted Answer

Introduction / Context: Fluorescence microscopy, especially immunofluorescence (IF), is a rapid antigen-detection technique in clinical virology. This question checks whether you recognize its applicability to several central nervous system infections where speed can be lifesaving or supportive for diagnosis. Given Data / Assumptions: IF detects viral antigens in tissue imprints or clinical specimens using labeled antibodies. Rabies diagnosis classically uses direct fluorescent antibody testing on brain tissue. Herpes simplex virus (HSV) antigens in lesions or cerebrospinal fluid cells can be detected in some laboratories (though PCR is now standard). SSPE is a chronic, measles-associated condition; IF may demonstrate measles antigens in brain tissue in specialized settings. Concept / Approach: While molecular assays (PCR) dominate modern diagnostics, fluorescence microscopy remains accepted or historically important in all three entities listed. It is definitive for rabies, supportive for HSV, and demonstrable in SSPE neuropathology. Therefore, the most inclusive correct answer is “All of these.” Step-by-Step Solution: Link rabies to direct fluorescent antibody (DFA) testing of brain smears.Acknowledge HSV antigen detection by IF in certain clinical specimens.Recognize measles antigen demonstration by IF in SSPE brain tissue sections.Choose the option encompassing all three uses. Verification / Alternative check: Public health references cite DFA as a frontline test for rabies. Hospital virology labs historically employed IF panels for HSV antigens; neuropathology texts note IF detection of measles antigens in SSPE. Why Other Options Are Wrong: Each single-condition option is incomplete, as the method applies across all listed diseases. “None of these” contradicts well-established rabies DFA testing. Common Pitfalls: Assuming PCR has entirely replaced antigen detection. PCR is now common, but the question focuses on usefulness of fluorescence microscopy, which remains valid in indicated scenarios. Final Answer: All of these.

Question 13

Plant virology: through which transient pores do many plant viruses penetrate host cells? Choose the classical term used for the transient surface pores implicated in viral entry into plant cells.

Accepted Answer

Introduction / Context: Unlike animal viruses that bind receptors on a plasma membrane, many plant viruses rely on breaches or specialized transient pathways to cross the rigid cell wall. Historical plant virology literature uses distinct terms for structures involved in entry versus cell-to-cell spread. This question targets that terminology. Given Data / Assumptions: Plant cell walls limit direct viral entry; vectors (insects, tools) and transient pores can facilitate penetration. Once inside, viruses often move cell-to-cell via intercellular channels. The options list several “-desmata” terms historically used in plant anatomy and virology. Concept / Approach: “Ectodesmata” refers to transient pores or channels across the cell wall surface through which materials (and, in classical descriptions, viruses) can penetrate into a plant cell. By contrast, “plasmodesmata” are permanent intercellular channels that permit direct cytoplasmic continuity, crucial for cell-to-cell spread after entry, not initial penetration. The other terms are not standard for entry. Step-by-Step Solution: Differentiate initial penetration from intercellular movement.Recall the classical term “ectodesmata” for transient entry pores.Recognize plasmodesmata are used mainly for cell-to-cell transport post-entry.Select “Ectodesmata.” Verification / Alternative check: Older plant pathology texts describe ectodesmata in the context of nutrient and virus passage through the wall; modern literature emphasizes mechanical/vector-mediated entry and movement proteins dilating plasmodesmata for spread, consistent with entry versus spread distinction. Why Other Options Are Wrong: Plasmodesmata: primarily for cell-to-cell movement, not initial penetration. Endodesmata, cytodesmata, protodesmata: not accepted standard terms for viral entry pores in plant cells. Common Pitfalls: Equating plasmodesmata with entry structures. They are critical for systemic movement, but the question asks specifically about entry pores, historically termed ectodesmata. Final Answer: Ectodesmata.

Question 14

Capsid symmetry identification: which common human viruses are typically icosahedral? Choose the most accurate statement about capsid symmetry for polioviruses and adenoviruses.

Accepted Answer

Introduction / Context: Recognizing capsid symmetry is a core skill in general virology. Many non-enveloped viruses possess icosahedral capsids that confer robustness and efficient genome packaging. This question asks you to match two familiar human viruses with their typical symmetry class. Given Data / Assumptions: Poliovirus is a non-enveloped, positive-sense RNA virus (Picornaviridae). Adenovirus is a non-enveloped, double-stranded DNA virus (Adenoviridae). Icosahedral symmetry is common among non-enveloped human viruses. Concept / Approach: Polioviruses have small, T=3 icosahedral capsids composed of VP1–VP4 proteins. Adenoviruses have larger icosahedral capsids with characteristic fiber projections at the vertices. Despite differences in size and composition, both share icosahedral symmetry. Step-by-Step Solution: Recall poliovirus as a classic icosahedral picornavirus.Recall adenovirus particle with icosahedral geometry and vertex fibers.Select the statement affirming that both are icosahedral. Verification / Alternative check: Electron micrographs and structural studies consistently show icosahedral geometry for both viruses, confirming the match. Why Other Options Are Wrong: Claims that one or both are helical or lack defined symmetry contradict standard structural virology. Helical symmetry is typical of many enveloped RNA viruses (for example, orthomyxoviruses), not these two. Common Pitfalls: Confusing adenoviral vertex fibers with a non-icosahedral structure. The fibers decorate, but do not change, the underlying icosahedral symmetry. Final Answer: Both polioviruses and adenoviruses generally exhibit icosahedral capsid symmetry.

Question 15

Why must negative-sense single-stranded RNA viruses carry a pre-formed polymerase? Select the best mechanistic reason these viruses package an RNA-dependent RNA polymerase in the virion.

Accepted Answer

Introduction / Context: Genome polarity determines early events in viral replication. Negative-sense single-stranded RNA (ssRNA) genomes are the reverse complement of mRNA and cannot be translated directly. This question probes why these viruses must bring their own polymerase activity when entering a mammalian cell. Given Data / Assumptions: Host ribosomes translate positive-sense mRNA, not negative-sense templates. Cytoplasmic host cells generally lack an RNA-dependent RNA polymerase. Virion-associated polymerase is needed immediately upon uncoating. Concept / Approach: The essential step is converting the negative-sense genome into positive-sense transcripts (mRNAs). Because host cells do not supply an enzyme that reads RNA templates to make RNA products, the virus packages an RNA-dependent RNA polymerase (replicase) to transcribe the incoming genome into mRNAs. Step-by-Step Solution: Note genome polarity: negative-sense cannot be read by ribosomes.Identify needed enzyme: RNA-dependent RNA polymerase to make positive-sense mRNAs.Recognize why packaging is required: host lacks this activity.Select the option stating the need to produce positive-sense RNA for translation. Verification / Alternative check: Paramyxoviruses, orthomyxoviruses, rhabdoviruses, and filoviruses all deliver an RdRP with the genome to initiate primary transcription to mRNAs. Why Other Options Are Wrong: They describe unrelated processes (poly(A) clipping, host polymerase modification, direct translation of negative RNA, or obligatory integration—none match negative-sense RNA virus biology). Common Pitfalls: Confusing positive-sense RNA viruses (which can translate immediately) with negative-sense viruses that must first transcribe mRNA. Final Answer: Because they must synthesize a complementary positive-sense RNA that serves as mRNA for translation.

Question 16

Sexual (genital) transmission of human viruses: which set is correct? Identify the most inclusive correct option regarding viruses transmitted through the genital route.

Accepted Answer

Introduction / Context: Several clinically important viruses spread efficiently via sexual contact and genital secretions. Recognizing these pathogens is essential for counseling, prevention, and vaccination strategies. This question asks for the most inclusive correct statement. Given Data / Assumptions: HPV includes high-risk oncogenic types (for example, 16, 18) and low-risk wart-associated types (for example, 6, 11). HSV-2 commonly causes genital herpes; HSV-1 can also be genital via oral-genital contact. HBV is present in blood and bodily fluids, including semen and vaginal secretions. Concept / Approach: All three listed viruses can be transmitted sexually. Prevention includes barrier methods, vaccination where available (HBV, HPV), and risk-reduction counseling. Therefore, the comprehensive answer is “All of these.” Step-by-Step Solution: Confirm each virus has a recognized genital transmission route.Note that HPV and HBV have effective vaccines, reducing incidence and sequelae.Recognize HSV-2 lacks a vaccine; management relies on antivirals and prevention.Select the inclusive option. Verification / Alternative check: Public health guidelines list sexual transmission for HPV, HSV-2, and HBV, and recommend vaccination for eligible populations (HPV, HBV). Why Other Options Are Wrong: Any single-virus option is incomplete; “None” is incorrect given well-documented sexual transmission of these viruses. Common Pitfalls: Assuming HBV is only blood-borne. Sexual contact is a major transmission route for HBV globally. Final Answer: All of these.

Question 17

DNA topology: which enzyme introduces negative supercoils into bacterial double-stranded DNA? Select the enzyme whose action leads to supercoiling of dsDNA in bacteria.

Accepted Answer

Introduction / Context: DNA topology is controlled by topoisomerases that relieve or introduce supercoils. In bacteria, negative supercoiling aids in genome compaction and replication. This question probes recognition of the specific enzyme responsible. Given Data / Assumptions: Bacterial chromosomes are circular and highly compacted. Topoisomerases alter linking number by introducing transient breaks. Nomenclature in the options contrasts real versus fictitious enzyme names. Concept / Approach: DNA gyrase (topoisomerase II) introduces negative supercoils using ATP and can relax positive supercoils ahead of replication forks. It is the target of quinolone and fluoroquinolone antibiotics (for example, ciprofloxacin), which inhibit DNA replication by trapping gyrase–DNA complexes. Step-by-Step Solution: Recall that “gyrase” is the canonical bacterial enzyme adding negative supercoils.Recognize “pyrase” and “RNA gyrase/pyrase” are not standard enzymes in DNA topology.Select DNA gyrase as the correct choice. Verification / Alternative check: Genetics and microbiology texts describe gyrase subunits GyrA and GyrB and their inhibition by quinolones; this confirms its role in supercoiling. Why Other Options Are Wrong: They are either fictitious or not relevant to introducing negative supercoils (helicase unwinds DNA but does not change linking number directly). Common Pitfalls: Confusing gyrase (Type II) with Topo I. Topo I relieves negative supercoils; gyrase introduces them. Final Answer: DNA gyrase (a type II topoisomerase).

Question 18

Respiratory transmission: which viruses spread primarily via the respiratory route? Choose the most inclusive correct option from the list below.

Accepted Answer

Introduction / Context: Transmission route is a cornerstone of infection prevention and control. Many clinically important viruses spread via respiratory droplets, aerosols, or contact with contaminated secretions. This question checks your recognition of common respiratory pathogens across different families. Given Data / Assumptions: Rhinoviruses cause the majority of common colds. Human coronaviruses include several common cold strains and notable respiratory pathogens. Measles virus is among the most contagious respiratory viruses, spreading via aerosols. Concept / Approach: All three listed viruses are transmitted by the respiratory route. Although exact dynamics (droplets, aerosols, fomites) vary, infection control measures emphasize respiratory hygiene, vaccination where available (measles), and environmental controls. Step-by-Step Solution: Confirm each virus spreads via respiratory secretions.Note overlapping clinical syndromes (upper respiratory infections, rash illnesses for measles).Select the inclusive option. Verification / Alternative check: Epidemiology references consistently list respiratory transmission for rhinoviruses, coronaviruses, and measles virus. Why Other Options Are Wrong: Single-pathogen choices are incomplete; “None” is clearly incorrect. Common Pitfalls: Assuming coronaviruses are exclusively severe pathogens; several endemic human coronaviruses routinely cause mild respiratory disease via the same route. Final Answer: All of these.

Question 19

Plant virus spread between adjacent cells: which channels mediate direct virion transfer? Identify the primary intercellular structures responsible for cell-to-cell transfer of plant viruses.

Accepted Answer

Introduction / Context: After a plant virus gains entry into a cell, it must move to neighboring cells to establish a local infection and, eventually, systemic spread. Plant cells are connected by specialized channels that enable this movement, often assisted by viral movement proteins. Given Data / Assumptions: Rigid cell walls prevent direct budding or endocytosis-based spread typical of animal viruses. Intercellular connectivity exists via microscopic channels. Some terms in the options are nonstandard or incorrect in modern plant biology. Concept / Approach: Plasmodesmata are cytoplasmic channels crossing plant cell walls, connecting adjacent cells. Plant viruses encode movement proteins that modify plasmodesmatal size exclusion limits to allow passage of viral ribonucleoprotein complexes or even whole virions, depending on the virus family. Step-by-Step Solution: Recall that plasmodesmata provide symplastic continuity.Recognize viral movement proteins target plasmodesmata to increase permeability.Select “Plasmodesmata” as the correct choice for direct intercellular transfer. Verification / Alternative check: Classic studies on Tobacco mosaic virus and many potyviruses demonstrate movement through plasmodesmata via dedicated movement proteins and tubule formation in some cases. Why Other Options Are Wrong: “Cytodesmata” and “protodesmata” are not standard modern terms for these channels; “None” is wrong because plasmodesmata are well-established structures; “Tight junctions” occur in animal epithelia, not plants. Common Pitfalls: Confusing initial entry structures with intercellular movement routes. Entry may be via wounding or vectors; spread is mainly via plasmodesmata. Final Answer: Plasmodesmata.

Question 20

Cytopathic effect (CPE): what is the term for virus-induced deterioration of host cell structure? Choose the correct term used in cell culture virology for visible structural changes caused by viral replication.

Accepted Answer

Introduction / Context: When viruses replicate in cultured cells, they often produce characteristic morphological changes observable under the microscope. Recognizing and naming these changes is fundamental in diagnostic and research virology. Given Data / Assumptions: Virus replication can cause rounding, shrinkage, syncytia, inclusion bodies, and lysis. These changes can be virus- and cell line-specific. The question asks for the standard term describing this overall deterioration. Concept / Approach: “Cytopathic effect” (CPE) is the umbrella term for structural alterations in host cells due to viral invasion. CPE patterns (for example, ballooning, syncytium formation, focal degeneration) are used to suggest etiologic agents prior to confirmatory tests. Step-by-Step Solution: Recall definition: CPE = morphological cell damage from viral replication.Map examples: HSV causes multinucleated giant cells; paramyxoviruses cause syncytia; adenovirus causes rounding and clustering.Choose “Cytopathic effect” as the correct term. Verification / Alternative check: Cell culture manuals and diagnostic algorithms begin with CPE observation before antigen detection, PCR, or sequencing, confirming the terminology. Why Other Options Are Wrong: Aneuploidy: abnormal chromosome number, not a general term for virus-induced morphology. Protopathic effect: not the accepted term in virology for culture changes. Cytotonic effect: used in toxin pharmacology for nonlethal morphological changes; not the standard virology term. None of these: incorrect because CPE is correct and widely used. Common Pitfalls: Assuming all viruses cause identical CPE. Patterns vary; hence, CPE guides, but does not by itself prove, a specific diagnosis. Final Answer: Cytopathic effect.

Viruses From Animal and Plants Questions