Microbiology - MCQ Practice Questions
Microbiology sits behind a lot of applied biology, so the fundamentals here carry into medicine, food technology and biotechnology alike. Practice covers bacterial structure and growth, viruses, fungi and parasites, sterilisation and culture techniques, immunology, and microbial genetics. Technique based questions explain the purpose of each step, because that is usually what separates a memorised protocol from a usable one.
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Which of the following viruses is classified as a negative-sense single-stranded RNA virus?
Understanding:
We need to identify which of the given viruses has a negative-sense (antisense) single-stranded RNA genome.
Step 1: Classify each virus by genome type.
Poliovirus belongs to the family Picornaviridae and has a positive-sense single-stranded RNA genome (+ssRNA). It can directly serve as mRNA.
Step 2: Evaluate Influenza virus.
Influenza virus belongs to the family Orthomyxoviridae and possesses a negative-sense single-stranded RNA genome (−ssRNA). Its genome is complementary to mRNA and requires an RNA-dependent RNA polymerase (RdRp) carried within the virion to first transcribe it into positive-sense mRNA before translation can occur.
Step 3: Evaluate the remaining options.
Hepatitis A virus is a Picornavirus with +ssRNA. Dengue virus belongs to the family Flaviviridae and also has a +ssRNA genome.
Answer:
Influenza virus is the negative-sense single-stranded RNA virus among the given options.
Quick Tip:
A useful mnemonic — negative-sense RNA viruses (e.g., Orthomyxoviruses, Paramyxoviruses, Rhabdoviruses, Bunyaviruses) must carry their own RNA polymerase into the host cell since the host ribosomes cannot directly translate negative-sense RNA.
The Baltimore classification system groups viruses based on which of the following criteria?
Understanding:
We need to identify the basis of Baltimore's classification of viruses.
Step 1: Recall the principle behind Baltimore classification.
David Baltimore proposed this classification in 1971. It groups all viruses into seven classes (Groups I–VII) based on the nature of their nucleic acid genome (DNA or RNA, single-stranded or double-stranded, positive or negative sense) and the pathway used to generate messenger RNA (mRNA) from that genome.
Step 2: Evaluate why other options are incorrect.
Host range/tissue tropism and mode of transmission are epidemiological criteria, not used in Baltimore classification. Capsid morphology is the basis of a different classification approach (structural classification). Pathogenicity is a clinical criterion.
Step 3: Confirm the correct answer.
The central idea is that mRNA production is the common requirement for all viruses since ribosomes only translate mRNA. Baltimore defined each class by how the virus achieves this, making it a universally applicable system.
Answer:
Baltimore classification is based on the nature of the viral genome and the strategy used to produce mRNA.
Quick Tip:
Remember that Baltimore Group IV (+ssRNA) viruses use their genome directly as mRNA, whereas Group V (−ssRNA) must first transcribe it — this distinction is a favourite exam point.
Which of the following events occurs during the eclipse period of a viral replication cycle?
Understanding:
We need to identify what characterises the eclipse period in viral replication.
Step 1: Define the one-step growth curve phases.
When a synchronised viral infection is studied using a one-step growth experiment, three phases are observed: the latent period, the rise period, and the plateau. The latent period is further divided into the eclipse period and a post-eclipse accumulation phase.
Step 2: Characterise the eclipse period specifically.
The eclipse period begins immediately after viral entry and uncoating. During this time, the original infecting virion has been disassembled, new virions have not yet been assembled, and consequently no infectious virus can be detected either inside or outside the cell. The virus exists only as disassembled components (nucleic acid and proteins being synthesised separately).
Step 3: Distinguish from the latent period.
The latent period includes both the eclipse period and the time when newly assembled (but not yet released) virions are accumulating inside the cell. Infectious virus can be detected inside the cell in the late latent period but not during the eclipse.
Answer:
During the eclipse period, infectious virus cannot be detected inside or outside the host cell because the infecting virion has been uncoated and new virions have not yet assembled.
Quick Tip:
Eclipse period ⊂ Latent period. After the eclipse period ends, intracellular infectious virus can be detected, but extracellular virus remains undetectable until lysis or budding begins.
Interferons are antiviral proteins produced by virus-infected cells. Which of the following correctly describes the mechanism by which Type I interferons (IFN-α/β) protect uninfected neighbouring cells?
Understanding:
We need to identify the correct mechanism by which Type I interferons protect uninfected cells.
Step 1: Recall the nature of interferon action.
Type I interferons (IFN-α and IFN-β) are produced by virus-infected cells. They are secreted and bind to IFN receptors (IFNAR) on the surface of neighbouring uninfected cells. This binding triggers the JAK-STAT signalling pathway, leading to the upregulation of hundreds of Interferon-Stimulated Genes (ISGs).
Step 2: Identify the key antiviral proteins induced.
Two classic antiviral effectors induced by Type I IFN are:
These mechanisms create an antiviral state in uninfected cells before the virus reaches them.
Step 3: Eliminate incorrect options.
Interferons do not directly neutralise virions (that is the role of antibodies), do not immediately stimulate antibody production (that is adaptive immunity, which takes days), and do not activate complement directly.
Answer:
Type I interferons protect neighbouring cells by inducing antiviral proteins such as 2′-5′ oligoadenylate synthetase and PKR through the JAK-STAT pathway.
Quick Tip:
Interferons do not protect the cell that produces them — they warn neighbouring cells. This paracrine signalling is a key concept frequently tested in virology.
Which of the following viruses uses reverse transcriptase to replicate its genome and is classified under Baltimore Group VI?
Understanding:
We need to identify the Baltimore Group VI virus that uses reverse transcriptase.
Step 1: Review the relevant Baltimore groups.
Baltimore Group VI: ssRNA-RT viruses — these have a positive-sense ssRNA genome but replicate through a DNA intermediate using reverse transcriptase. Example: Retroviruses, including HIV.
Baltimore Group VII: dsDNA-RT viruses — these have a dsDNA genome and also use reverse transcriptase, but the template is DNA. Example: Hepadnaviruses (Hepatitis B virus) and Cauliflower Mosaic Virus.
Step 2: Classify each option.
Step 3: Confirm answer.
HIV is specifically a Group VI (ssRNA-RT) virus that uses reverse transcriptase to convert its RNA genome into dsDNA, which then integrates into the host chromosome as a provirus.
Answer:
HIV is the Baltimore Group VI virus that uses reverse transcriptase in its replication cycle.
Quick Tip:
The key distinction: Group VI (Retroviruses) starts as RNA and makes DNA; Group VII (Hepadnaviruses) starts as DNA and makes RNA via reverse transcriptase. Both use reverse transcriptase, but in opposite directions relative to their replication cycle.
The haemagglutinin (HA) protein of Influenza virus plays a critical role in viral entry. Which of the following correctly describes its function?
Understanding:
We need to identify the correct function of the haemagglutinin (HA) protein of Influenza virus.
Step 1: Recall the structure of Influenza surface proteins.
Influenza virus has two major surface glycoproteins: Haemagglutinin (HA) and Neuraminidase (NA). They have distinct and complementary roles.
Step 2: Define the role of HA.
HA performs two sequential functions in viral entry:
1. Receptor binding: HA binds to sialic acid (N-acetylneuraminic acid) residues present on glycoproteins and glycolipids on the surface of host respiratory epithelial cells.
2. Membrane fusion: After endocytosis, the acidic pH in the endosome triggers a conformational change in HA, exposing the fusion peptide. This mediates fusion of the viral envelope with the endosomal membrane, releasing the viral RNA segments into the cytoplasm.
Step 3: Identify the role described in each wrong option.
Answer:
Haemagglutinin binds sialic acid on host cell surfaces and mediates viral envelope–endosomal membrane fusion to release the viral genome.
Quick Tip:
Remember: HA = entry (binds in, fuses in); NA = exit (cleaves sialic acid so new virions can escape). Oseltamivir (Tamiflu) inhibits NA, preventing viral release.
Antigenic shift in Influenza A virus, which is responsible for pandemic influenza, occurs due to which of the following mechanisms?
Understanding:
We need to distinguish antigenic shift from antigenic drift and identify the mechanism of antigenic shift.
Step 1: Define antigenic drift.
Antigenic drift refers to the gradual accumulation of point mutations in the HA and NA genes due to the error-prone nature of viral RNA polymerase. This causes minor antigenic changes and is responsible for seasonal influenza epidemics. This corresponds to option A, which is incorrect for antigenic shift.
Step 2: Define antigenic shift.
Antigenic shift is an abrupt, major change in the HA and/or NA antigens of Influenza A virus. It occurs when two different strains of Influenza A (e.g., a human strain and an avian or swine strain) simultaneously infect the same host cell. Because the Influenza A genome is segmented (8 segments of −ssRNA), the genome segments from both strains can be packaged together in new virions in random combinations — a process called reassortment. This can produce a novel virus with a completely new HA or NA subtype to which the human population has little or no pre-existing immunity, potentially causing a pandemic.
Step 3: Evaluate the other options.
Influenza virus does not integrate into the host chromosome (that is a feature of retroviruses). Reassortment between Influenza A and Influenza B does not occur naturally due to incompatibility of their internal proteins.
Answer:
Antigenic shift results from the reassortment of genome segments between two different Influenza A strains co-infecting the same cell.
Quick Tip:
Antigenic DRIFT = small, gradual (like a boat drifting slowly) → epidemics. Antigenic SHIFT = sudden, large change (like a gear shift) → pandemics. Segmented genome = prerequisite for reassortment.
Which of the following correctly describes the role of the CD4 receptor and CCR5 co-receptor in HIV-1 entry into host cells?
Understanding:
We need to correctly describe the sequential roles of CD4 and CCR5 in HIV-1 entry.
Step 1: Describe the initial attachment.
The HIV-1 envelope glycoprotein complex consists of gp120 (surface unit) and gp41 (transmembrane unit). The first step of entry is the binding of gp120 to the CD4 receptor, which is expressed primarily on T helper lymphocytes, macrophages, and dendritic cells. This interaction is the primary, high-affinity attachment event.
Step 2: Describe co-receptor engagement.
Binding of gp120 to CD4 causes a conformational change in gp120, exposing the V3 loop region. This newly exposed region then binds to a chemokine co-receptor — either CCR5 (on macrophages and memory T cells) or CXCR4 (on naïve T cells). Engagement of the co-receptor causes a further conformational change.
Step 3: Describe membrane fusion.
The conformational changes triggered by co-receptor binding expose the hydrophobic fusion peptide at the N-terminus of gp41. This fusion peptide inserts into the host cell membrane, and gp41 undergoes a hairpin fold that brings the viral and cellular membranes together, resulting in fusion and release of the viral core into the cytoplasm.
Step 4: Confirm the correct answer.
CD4 is the primary receptor for gp120; CCR5 is the co-receptor whose engagement triggers gp41-mediated fusion. Individuals homozygous for the CCR5-Δ32 mutation are highly resistant to R5-tropic HIV infection.
Answer:
gp120 binds CD4 first, then CCR5 acts as co-receptor, triggering gp41-mediated membrane fusion.
Quick Tip:
Maraviroc, an antiretroviral drug, works by blocking CCR5, preventing HIV entry. This is only effective against R5-tropic (CCR5-using) strains, not X4-tropic strains.
A virologist performs a plaque assay using a serial dilution of a virus stock. A 10⁻⁶ dilution of the stock, when inoculated onto a cell monolayer, produces 45 plaques. What is the titre of the original virus stock in plaque-forming units per millilitre (PFU/mL), assuming 0.1 mL of the diluted sample was inoculated?
Understanding:
We need to calculate the titre of the original virus stock from plaque assay data.
Formula:
The titre of the original stock is calculated as:
Step 1: Substitute the known values.
Step 2: Verify units.
Dilution is dimensionless; volume is in mL; so the result is in PFU/mL. The calculation is consistent.
Answer:
The titre of the original virus stock is 4.5×108 PFU/mL.
Quick Tip:
A common error is forgetting to divide by the inoculation volume. Always account for the volume factor: inoculating 0.1 mL instead of 1 mL means the plaques observed represent only 101th of what would be seen per mL, so the titre is 10× higher than if you only used the dilution factor alone.
Which of the following best describes the concept of 'viral tropism'?
Understanding:
We need to correctly define the concept of viral tropism.
Step 1: Define viral tropism.
Viral tropism refers to the specificity of a virus for particular cell types, tissues, or host species. A virus is said to be tropic for the cell type it preferentially infects. This specificity is primarily governed by molecular interactions between viral surface proteins (e.g., attachment proteins such as haemagglutinin, gp120, or fibre proteins) and specific receptor molecules expressed on the target cell surface.
Step 2: Additional determinants of tropism.
While receptor compatibility is the primary determinant, other factors also influence tropism:
Step 3: Distinguish from the other options.
Answer:
Viral tropism describes the preference of a virus for infecting specific cell types or tissues, primarily determined by receptor compatibility.
Quick Tip:
Classic examples of tropism: HIV is lymphotropic and macrophage-tropic (CD4+ cells); Rabies virus is neurotropic (neurons); Hepatitis B virus is hepatotropic (hepatocytes). Receptor expression is the gatekeeper of tropism.