- A newly discovered pathogen contains a single-stranded RNA genome, a protein capsid, and the enzyme reverse transcriptase, but lacks an envelope. How would its replication strategy most likely differ from that of HIV?
Answer: It would form a DNA provirus that integrates into the host genome, but new virions would exit the cell via lysis.
The presence of reverse transcriptase indicates it is a retrovirus, meaning it will create a DNA copy of its genome that integrates into the host chromosome (a provirus), just like HIV. However, HIV has an envelope and exits by budding. A non-enveloped (naked) virus cannot bud from the cell membrane and must exit by causing the host cell to rupture (lysis).
- How does the establishment of a latent provirus by HIV in a host T-helper cell help the virus evade the host immune system?
Answer: In its integrated and transcriptionally inactive state, no viral antigens are presented on the cell surface, rendering the cell invisible to cytotoxic T-cells.
The adaptive immune system, specifically cytotoxic T-lymphocytes (CTLs), recognizes and kills infected cells by detecting viral protein fragments (antigens) displayed on the cell's surface by MHC class I molecules. If the provirus is latent, viral genes are not being transcribed or translated, so no viral proteins are made. Without viral proteins, there are no antigens to display, and the CTLs cannot identify the cell as infected.
- The bacterium Vibrio cholerae only produces the potent cholera toxin when it is infected by the CTXφ phage, which introduces the toxin-coding genes. What is this phenomenon an example of?
Answer: Lysogenic conversion, where the prophage confers a new phenotype upon the host.
Lysogenic conversion is the process by which the phenotype of a host bacterium is altered by the presence of a prophage. In this case, the integrated phage genome contains the genes for the cholera toxin. The bacterium expresses these viral genes, gaining the new pathogenic trait.
- A single lytic bacteriophage infects one bacterium in a liquid culture containing 10⁷ bacteria. The latent period for this phage is 30 minutes, and the burst size is 200 virions. Assuming no secondary infections occur before the first lysis event, what is the composition of the culture 35 minutes after the initial infection?
Answer: 200 phages and (10⁷ – 1) intact bacteria.
At t=0, 1 phage infects 1 bacterium. For the next 30 minutes (the latent period), the virus replicates inside. At t=30 minutes, the host cell lyses, releasing 200 new virions. At t=35 minutes, these 200 virions are now free in the medium. The original host cell has been destroyed, so there are (10⁷ – 1) intact bacteria remaining. Secondary infections have not yet had time to complete.
- The latency of herpesviruses in human neurons is functionally analogous to the lysogenic cycle of a bacteriophage. Which statement identifies a key difference between the state of the viral genome in these two processes?
Answer: The phage prophage integrates into the host chromosome, while the latent herpesvirus genome often exists as a separate episome.
A defining feature of a bacteriophage prophage is its physical integration into the circular bacterial chromosome. In contrast, many latent animal viruses, including herpesviruses, maintain their DNA genome in the host nucleus as a non-integrated, circular piece of DNA called an episome. This is a significant structural difference in their latent states.
- A scientist engineers a temperate bacteriophage to contain a gene for green fluorescent protein (GFP) within its genome. A bacterial culture is infected. After several generations of bacterial division, the culture is exposed to UV light, an inducer of the lytic cycle. What would be observed?
Answer: A subpopulation of bacteria would fluoresce green, and these fluorescent cells would subsequently lyse.
During the initial growth, some phages will establish lysogeny, creating a subpopulation of bacteria that carry the prophage and pass it to their descendants. If the GFP gene is expressed, this subpopulation will fluoresce. The UV light then specifically induces these lysogens to enter the lytic cycle, leading to their lysis. Uninfected bacteria would neither fluoresce nor lyse.
- From an evolutionary fitness perspective, what is the primary advantage for a temperate phage to maintain a lysogenic life cycle in a stable, nutrient-rich environment?
Answer: It ensures the phage's genome is propagated vertically to daughter cells without destroying the successful host lineage.
In a stable environment where the host is thriving, the most successful strategy for the virus is to 'go along for the ride.' By integrating as a prophage, the virus's genome is replicated and passed to all daughter cells as the host population grows. This vertical transmission is highly efficient and preserves the host, which is the virus's essential resource. Killing a successful host via the lytic cycle would be counterproductive.
- A temperate bacteriophage infects a bacterial population. If environmental conditions are favourable for continued bacterial growth and replication, what outcome is most advantageous for the long-term propagation of the phage genome?
Answer: Integration as a prophage to replicate passively as the host population expands exponentially.
In favourable conditions for the host, the host population will grow rapidly. The most advantageous long-term strategy for the phage is to enter the lysogenic cycle, integrating its genome as a prophage. This allows the viral genome to be replicated along with the host's DNA every time the bacterium divides, vastly increasing the number of infected cells without destroying the host population. The lytic cycle (A) is a better strategy when host cells are stressed or dying.
- The envelope of the influenza virus is derived from the host cell's plasma membrane during budding. Which statement correctly explains a consequence of this structural feature?
Answer: The virus becomes a target for the immune system due to viral glycoproteins like hemagglutinin being inserted into the envelope.
Although the lipid bilayer is from the host, the virus embeds its own unique glycoproteins (antigens) into the envelope. These proteins are essential for binding to and entering new host cells, and they are the primary targets that the host's adaptive immune system recognizes. Distractor A is incorrect because of these viral proteins. Distractor B is incorrect; enveloped viruses are generally less stable in the environment. Distractor C is too broad; while true for influenza, the presence of an envelope does not universally preclude infection of other kingdoms.
- The high mutation rate of RNA viruses like influenza and HIV is a major challenge for vaccine development. What is the primary molecular mechanism responsible for this rapid evolution?
Answer: The viral RNA polymerases and reverse transcriptases involved in genome replication lack proofreading capacity.
During DNA replication, DNA polymerases have a 3' to 5' exonuclease activity that allows them to proofread and correct mismatched nucleotides, ensuring high fidelity. The RNA-dependent polymerases used by RNA viruses do not have this proofreading function. Consequently, errors made during replication are not corrected, leading to a much higher mutation rate.
- Bacteriophage T4 specifically infects certain strains of Escherichia coli and is completely unable to infect human cells. What is the primary molecular basis for this stringent host specificity?
Answer: The phage's tail fibres must bind to specific lipopolysaccharide and protein receptors on the E. coli outer membrane.
The first step of viral infection, attachment, is highly specific. Viral surface proteins (in this case, tail fibres) must recognize and bind to specific receptor molecules on the host cell surface. If the host cell lacks the correct receptor, the virus cannot attach and therefore cannot infect. Human cells do not have the specific receptors required by T4.
- During the lytic cycle of a bacteriophage, hundreds of new virions are synthesized. What are the sources of the nucleotides for the viral genomes and the ATP required for biosynthesis?
Answer: Nucleotides are recycled from the degraded host chromosome, and ATP is supplied by the host's cellular respiration.
Viruses are obligate intracellular parasites, meaning they lack their own metabolic machinery. They hijack the host cell's resources. Many phages produce enzymes that degrade the host's chromosome, providing a ready supply of nucleotides for viral DNA replication. All ATP is generated by the host cell's metabolic pathways, such as glycolysis and cellular respiration.
- HIV is a retrovirus. A patient is treated with a drug that acts as a non-competitive inhibitor of integrase. How would this drug specifically disrupt the HIV life cycle?
Answer: It would block the insertion of the viral DNA copy into the host cell's chromosomal DNA.
The HIV life cycle involves reverse transcription (RNA to DNA), followed by the integration of this viral DNA into the host chromosome, which is catalyzed by the viral enzyme integrase. A drug that inhibits integrase would allow the viral DNA to be made but would prevent it from becoming a provirus, effectively halting the replication cycle at that step.
- A lysogenic bacterium carrying a prophage is exposed to high levels of UV radiation, a mutagen that activates the host's DNA repair (SOS) system. What is the most likely immediate consequence for the virus?
Answer: The prophage is induced, excises from the host chromosome, and enters the lytic cycle.
The host's SOS response is a danger signal indicating the host cell may be dying. Many temperate phages have evolved to detect this signal (often via cleavage of a repressor protein). In response, the prophage excises itself from the host chromosome and initiates the lytic cycle to replicate and escape the doomed host cell.
- Prions, the infectious agents that cause diseases like BSE (mad cow disease), are fundamentally different from viruses. Which feature of prions is the most critical distinction from all known viruses?
Answer: Prions are infectious particles composed solely of protein and contain no nucleic acid genome.
The central dogma of molecular biology is based on information flowing from nucleic acids. All viruses, by definition, have a nucleic acid genome (DNA or RNA) that directs their replication. Prions are unique because they are infectious proteins that propagate by causing normally folded proteins to misfold. They completely lack a nucleic acid genome.
- An antiviral drug is developed to treat infections caused by an enveloped RNA virus. To achieve high specificity and minimize cytotoxic effects on the human host cells, which viral process should the drug ideally target?
Answer: Blocking the activity of RNA-dependent RNA polymerase used for viral genome replication.
Human cells do not possess RNA-dependent RNA polymerase; they use DNA-dependent polymerases. This enzyme is unique to the virus, making it an excellent target for a specific drug that will not harm host cells. Targeting host ribosomes (A), the plasma membrane (B), or mitochondria (D) would cause severe side effects as these are essential for the host cell's survival.
- An enveloped virus relies on the host cell's endomembrane system to produce its components. Which pathway correctly identifies the host organelles involved in synthesizing and transporting viral envelope glycoproteins?
Answer: Synthesis on rough endoplasmic reticulum ribosomes, processing in the Golgi apparatus, and transport to the plasma membrane.
Viral glycoproteins, like any protein destined for a cell membrane or for secretion, follow the eukaryotic cell's standard secretory pathway. They are synthesized by ribosomes on the rough ER, translocated into the ER lumen for folding and glycosylation, transported to the Golgi apparatus for further processing and sorting, and finally moved to the plasma membrane in transport vesicles.
- Viruses are often described as existing at the boundary between living and non-living entities. Which viral characteristic provides the strongest evidence for the argument that viruses are non-living?
Answer: Outside a host cell, virions are metabolically inert and can be crystallized like a chemical compound.
One of the fundamental definitions of life is the ability to carry out metabolic processes. The fact that a virus particle (virion) has no metabolism of its own—it does not respire, synthesize molecules, or respond to stimuli—and can be purified and crystallized like a simple chemical (e.g., NaCl) strongly supports the view of it as a non-living complex of macromolecules. Dependence on a host (D) is a feature, but the complete lack of independent metabolism (B) is the more fundamental argument for being non-living.
- A pig is simultaneously infected with a human influenza virus and an avian influenza virus. Both viruses have segmented RNA genomes. What process accounts for the generation of a novel, potentially pandemic strain of influenza in this scenario?
Answer: The two different viral genomes are packaged into new virions via genetic reassortment.
When two different strains of a segmented virus like influenza co-infect the same cell, the RNA segments from both parent viruses are replicated. During the assembly of new virions, these segments can be mixed up and packaged in new combinations. This process, called genetic reassortment or antigenic shift, can create a new virus with a novel combination of surface proteins, potentially allowing an avian virus to infect humans.
- Which statement accurately contrasts the mechanism of genome entry by a T4 bacteriophage with that of an enveloped virus like HIV?
Answer: The T4 phage injects its DNA, leaving its capsid outside, while HIV's envelope fuses with the host membrane, releasing the capsid inside.
These represent two different fundamental strategies. Bacteriophages act like a hypodermic syringe, binding to the surface and injecting their genetic material into the host, leaving the protein coat outside. Enveloped animal viruses like HIV fuse their lipid envelope with the host's lipid plasma membrane, a process which releases the entire viral capsid into the host's cytoplasm.
