Virus Flashcards
give an overview of the structural components of a virus
Capsid: The protein coat that surrounds the viral nucleic acid (either RNA or DNA). The capsid’s primary function is to protect the genetic material and facilitate its delivery into host cells.
Nucleocapsid: This term refers to the combination of the protein coat (capsid) and the viral nucleic acid. It represents the complete viral core structure.
Nucleic Acid: The viral genome, which can be composed of either RNA or DNA. This genetic material contains the instructions for replicating the virus within host cells.
Envelope: Many viruses have an optional outer lipid bilayer known as the envelope. The envelope is derived from the host cell membrane and can contain viral glycoproteins. It plays a crucial role in host recognition and cell entry.
Virion: The complete infectious viral particle, which includes the nucleocapsid, envelope (if present), and any additional factors or enzymes specific to the virus.
Optional components you mentioned, such as specific adhesins, DNA/RNA enzymes, and other factors, vary depending on the type of virus and its specific mechanisms of infection and replication.
The size of virions typically falls within the range of 50 to 250 nanometers, but this can vary widely among different viruses.
explain viruses and proteins
Helical Rod of Protein Encloses Genetic Material (RNA): This description appears to be related to the structure of certain viruses. Some viruses, like the Tobacco Mosaic Virus (TMV), have a helical structure. In these viruses, a protein coat forms a helical shape, and this protein coat encloses the genetic material, which in the case of TMV, is RNA. This genetic material contains the instructions for the virus to replicate itself once it infects a host cell.
TMV Causes Spots on Tobacco Leaves (and Leaves of Other Plants): The Tobacco Mosaic Virus (TMV) is a plant virus that is well-known for causing distinct mosaic-like patterns or spots on the leaves of tobacco plants and various other plant species. These symptoms can lead to stunted growth and reduced crop yield in affected plants.
Examples of Viruses: TMV, Ebola, Rabies:
Tobacco Mosaic Virus (TMV): As mentioned earlier, TMV is a plant virus that primarily affects members of the Solanaceae family, such as tobacco, tomatoes, and peppers.
Ebola Virus: The Ebola virus is a deadly virus that causes Ebola virus disease (EVD) in humans and nonhuman primates. It can lead to severe and often fatal illness, with symptoms that include fever, bleeding, and organ failure.
Rabies Virus: Rabies is a viral disease that affects mammals, including humans. It’s typically transmitted through the saliva of an infected animal, usually through a bite. If not treated promptly, rabies can be fatal.
explain the virus structure
Several Hundred Proteins: This suggests that the virus in question has a relatively complex structure, composed of hundreds of different proteins. Viruses are often composed of genetic material (DNA or RNA) enclosed by a protein coat, and the presence of many different proteins may indicate the complexity of this particular virus.
Membranes Actually Come from ER: This could imply that the virus utilizes the host cell’s endoplasmic reticulum (ER) to obtain its membrane. Some viruses manipulate host cell structures and processes to create their own viral envelopes or membranes.
Two Morphologies: Intracellular vs. Extracellular: This indicates that the virus can exist in two different forms or locations within a host organism. Intracellular viruses replicate and exist inside host cells, while extracellular viruses are typically found outside of host cells, such as in bodily fluids.
dsDNA Within Core - Very Tightly Packed: The virus contains double-stranded DNA (dsDNA) within its core. Double-stranded DNA is a common genetic material, and the fact that it’s described as “very tightly packed” suggests that the virus has a high DNA density, which may be important for its replication and stability.
Lateral Bodies - Unknown Function: “Lateral bodies” are structures within the virus, but their function is unknown. In virology, some viral structures or components may have undiscovered or poorly understood functions, and researchers continue to study and uncover the roles of various viral components.
explain the classification of viruses
International Committee on Taxonomy of Viruses (ICTV): The International Committee on Taxonomy of Viruses (ICTV) is responsible for classifying and naming viruses. It categorizes viruses based on their genetic and biological properties, with an emphasis on phylogeny, which refers to the evolutionary relationships between different organisms, including viruses. The hierarchical taxonomic classification of viruses by the ICTV includes the following ranks:
Order (-virales)
Family (-viridae)
Subfamily (-virinae)
Genus (-virus)
Species
Each virus is classified into one or more of these taxonomic ranks based on its characteristics and evolutionary relationships with other viruses.
Baltimore Classification - Based on Nucleic Acid: The Baltimore classification system, developed by Nobel laureate David Baltimore, categorizes viruses based on their genome type and replication strategy. It divides viruses into seven different classes (groups) based on the nature of their nucleic acid and the processes involved in replication. Here are the seven Baltimore classes: a) Double-stranded DNA (dsDNA) viruses: These viruses have a double-stranded DNA genome. b) Single-stranded DNA (ssDNA) viruses: These viruses have a single-stranded DNA genome. c) Double-stranded RNA (dsRNA) viruses: These viruses have a double-stranded RNA genome. d) Positive-sense single-stranded RNA (+ssRNA) viruses: The genome of these viruses can be directly used as messenger RNA (mRNA) by host cells. e) Negative-sense single-stranded RNA (-ssRNA) viruses: The genome of these viruses must be converted into mRNA before it can be used by host cells. f) Retroviruses: These viruses use reverse transcription to convert their RNA genome into DNA. g) Reverse-transcribing DNA (dsDNA-RT) viruses: These are retroviruses that have integrated their DNA into the host genome.
explain the key characteristics of viruses
Virion (Virus Particle) - No Metabolism: A virion is the complete, infectious virus particle. Virions lack the cellular machinery for metabolism. They do not carry out metabolic processes like respiration or energy production and cannot grow or divide on their own.
No ATP Synthesis, No Ribosomes, etc.: Viruses lack the cellular machinery to synthesize ATP (adenosine triphosphate), which is the energy currency of cells, and they do not possess ribosomes for protein synthesis. Instead, they rely on host cells to perform these functions.
Acellular: Viruses are considered acellular entities because they are not made up of cells. They are much simpler in structure, consisting primarily of genetic material (DNA or RNA) enclosed within a protein coat (capsid).
Protein Nanomachines Which Serve to Deliver Genetic Information to Target Cell: Viruses have evolved specialized protein structures that act as delivery systems to introduce their genetic material into a host cell. These structures often include viral proteins, such as capsids and viral envelopes.
Pirates of the Cell! Reprogram Host Cell + Hijack Cell Machinery and ATP → More Virions: Viruses are often described as “pirates” of the cell because they infect a host cell and take over its machinery to replicate themselves. They reprogram the host cell to produce more virions, utilizing the cell’s energy and resources.
Highly Evolved Parasites: Viruses are considered highly evolved parasites because they have evolved sophisticated mechanisms to exploit host cells for their reproduction. They have adapted to efficiently interact with and manipulate host cells.
Typically Have Extremely Economic Use of Genomic Material: Viruses tend to have compact genomes, which means they use their genetic material efficiently. They carry only the genes necessary for their replication and infection processes. This economical use of genomic material is a result of evolution and adaptation.
are viruses living?
Viruses exhibit some characteristics of living organisms but lack others, making their classification as living or non-living entities a topic of ongoing discussion. Here are some key points to consider:
Characteristics of Living Organisms:
Reproduction: Living organisms can reproduce independently. Viruses, however, cannot replicate on their own and require a host cell to reproduce.
Metabolism: Living organisms have metabolic processes, including energy production, growth, and responding to environmental stimuli. Viruses lack metabolic processes and do not generate energy.
Response to Environment: Living organisms can respond to their environment. Viruses do not exhibit this characteristic; they are inert outside of a host cell.
Cellular Structure: Living organisms are composed of cells, which are the basic structural and functional units of life. Viruses do not consist of cells; they are composed of genetic material (DNA or RNA) encased in a protein coat.
Characteristics of Non-Living Entities:
Inert Outside Host: Viruses are inert and non-functional outside of a host cell. They become active and replicate only when inside a suitable host cell.
Lack of Independent Life: Viruses do not have an independent life cycle or existence. They are completely dependent on host cells for replication.
The classification of viruses as living or non-living varies depending on the criteria used for defining life. Some scientists consider viruses as complex molecules or biological entities, while others view them as a bridge between living and non-living matter. In the end, it comes down to how one defines life.
Many biologists and virologists prefer to classify viruses as non-living entities due to their inability to perform the fundamental functions associated with living organisms. However, they acknowledge that viruses play a crucial role in biology, genetics, and disease, and studying them has provided valuable insights into various aspects of life and evolution.
explain how certain animal viruses, such as the influenza virus, adhere to specific targets on the surface of host cells
Animal Viruses Adhering to Specific Targets on Cell Surface Membrane: Animal viruses have evolved mechanisms to adhere to specific receptors on the surface of host cells. These interactions are often mediated by viral glycoproteins (GP spikes) on the virus’s outer surface.
Influenza Virus Adheres to Sialic Acid: The influenza virus is an example of an animal virus that adheres to target cells using a specific mechanism. Influenza viruses adhere to a class of sugar units called sialic acid. Sialic acid is found on glycolipids and glycoproteins on the surface of host cells, particularly in the respiratory tract.
Influenza Has HA (Haemagglutinin) GP Spikes: Influenza viruses have a glycoprotein called hemagglutinin (HA) on their surface. The HA glycoprotein is responsible for binding to specific sialic acid residues on host cells.
Different Sialic Acid Residues in Upper and Lower Respiratory Tracts: Sialic acid residues can vary in structure and distribution in different tissues of the respiratory tract. Influenza viruses often display specificity for particular sialic acid residues, which can influence the tissue tropism of the virus. For example, there may be differences in the types of sialic acids found in the upper respiratory tract compared to the lower respiratory tract.
explain the influenza pandemics caused by different strains of the influenza A virus
The examples you’ve provided are historical influenza pandemics caused by different strains of the influenza A virus. These pandemics had varying degrees of impact in terms of mortality and are illustrative of the significant public health challenges posed by the rapid mutations and emergence of new strains of the influenza virus.
1918 ‘Spanish Flu’ (H1N1):
The 1918 influenza pandemic, commonly referred to as the “Spanish Flu,” is one of the deadliest pandemics in history.
It was caused by an H1N1 strain of influenza A.
The pandemic occurred in several waves and resulted in the deaths of an estimated 20 to 100 million people worldwide.
The fatality rate was exceptionally high, with an estimated 2% of those infected succumbing to the disease.
This pandemic had a profound impact on global public health and remains a subject of extensive research and historical study.
1950s ‘Asian Flu’ (H2N2):
The 1957 influenza pandemic, often referred to as the “Asian Flu,” was caused by an H2N2 strain of influenza A.
It resulted in an estimated 1 to 1.5 million deaths worldwide.
The fatality rate for this pandemic was lower than that of the 1918 pandemic, with an estimated 0.13% of those infected dying from the disease.
Despite the lower overall mortality rate, the Asian Flu had a significant impact on public health.
These historical pandemics highlight the varying levels of severity and impact that different influenza strains can have on human populations. The emergence of new strains through antigenic shift and drift, coupled with the lack of preexisting immunity in the population, can lead to large-scale outbreaks and high mortality rates.
Efforts to prevent and mitigate the impact of influenza pandemics include the development and distribution of vaccines, ongoing surveillance of circulating strains, and research into antiviral treatments.
explain the general process of a virus infecting a host cell
Gaining Entry to Target Cell: Viruses need to enter a host cell to begin the infection process. This typically involves binding to specific receptors on the host cell’s surface and then penetrating or entering the cell.
Uncoating: Once inside the host cell, many viruses undergo a process called uncoating, where they shed their protein coat or envelope. This step exposes the viral genetic material (DNA or RNA) for replication.
Early Viral Gene Expression: After uncoating, the virus initiates the expression of its early genes. These genes often code for proteins that help the virus evade the host cell’s defenses and start taking control of the cell’s machinery.
Evading Cell Defenses: Viruses employ various strategies to evade the host cell’s immune defenses. They may inhibit the host cell’s antiviral responses and disrupt the host’s ability to recognize and combat the infection.
Reprogramming Host Cell: The virus reprograms the host cell, manipulating it to support viral replication. This often involves the expression of specific viral genes that control and modify host cell functions.
Late Viral Gene Expression: As the virus continues to replicate and assemble new viral particles, it may express late genes responsible for constructing new virions.
Viral Replication: During this stage, the virus replicates its genetic material and assembles new viral particles within the host cell.
Escape from Host Cell: Eventually, the newly assembled virions need to be released from the host cell. This can occur through processes like budding or cell lysis.
Adhesion to Target Cell: To continue the infection cycle, released virions need to adhere to and infect new target cells. This often involves viral proteins binding to receptors on the surface of the target cell.
As for the additional points you’ve listed:
Rapid, Reversible: The initial stages of viral infection, such as attachment and entry into the host cell, can be relatively rapid, and these processes can sometimes be reversed if the virus does not successfully enter the cell.
Stable Adhesion: Viruses that successfully enter the host cell establish stable adhesion through interactions between viral proteins and host cell receptors, ensuring efficient infection and subsequent stages of the viral life cycle.
explain what are the implications of such rapid mutations to host defences?
Reduced Immune Recognition: Rapid mutations can lead to changes in viral surface proteins, like hemagglutinin (HA). As a result, the virus may produce strains with altered antigenic properties, making it less recognizable to the immune system. This reduces the effectiveness of preexisting immunity, whether acquired through previous infections or vaccinations.
Seasonal Vaccine Updates: The need for frequent updates to influenza vaccines is a direct consequence of the rapid mutations of influenza viruses. The World Health Organization and health agencies worldwide continually monitor circulating strains and update vaccines to match the most prevalent and recently mutated strains.
Influenza Seasonal Variability: The rapid mutation rate contributes to the seasonal variability of the flu. Different influenza strains can dominate in different years, leading to variations in the severity of flu seasons.
Antigenic Drift: Antigenic drift, driven by these mutations, allows the virus to escape the immune system’s memory and cause recurrent infections in the same individuals. This is why people can get the flu multiple times in their lifetime.
Pandemic Potential: Influenza A’s ability to undergo rapid antigenic drift and mutation can lead to the emergence of entirely new strains (antigenic shift), which may have pandemic potential. When a completely novel strain emerges, the global population lacks preexisting immunity, increasing the risk of widespread infection.
Challenges for Vaccine Efficacy: The constantly changing nature of the virus makes it challenging to predict which strains will predominate in any given season. This can result in varying levels of vaccine efficacy, with some vaccines being more effective than others in a particular flu season.
Immunocompromised Individuals: Rapid mutations can pose a significant challenge for individuals with compromised immune systems, as they may have difficulty responding effectively to the continuously evolving virus.
Selective Pressure for Cross-Protection: The rapid mutations in influenza viruses exert selective pressure, favoring strains that can evade existing immunity.
explain antigenic drift.
Influenza B Infection:
Influenza B primarily infects humans.
It is relatively slow in mutating its genetic material.
As a result of its slower mutation rate, Influenza B tends to cause seasonal epidemics, but it is less likely to cause pandemics.
Influenza A Infection:
Influenza A can infect a wide variety of animals, including humans.
It has special abilities, such as rapid mutation and the potential to cause pandemics.
Influenza A viruses are known for their ability to infect a diverse range of host species, and they are responsible for most influenza pandemics throughout history.
Antigenic Drift:
Antigenic drift is a process by which influenza viruses, particularly Influenza A, undergo gradual genetic changes, leading to the creation of new viral strains.
These genetic changes, especially in the genes encoding surface proteins like hemagglutinin (HA) and neuraminidase (NA), result in changes in the viral antigens, which are recognized by the immune system.
These changes are often responsible for the need to update seasonal flu vaccines to provide protection against the most current strains.
Mutation of Influenza HA Antigen (HA1 - H1):
Influenza A’s antigenic drift, especially in the HA gene, can result in changes in the hemagglutinin glycoprotein.
These changes often occur near the receptor-binding site, which is involved in viral attachment to host cells.
The mutations can lead to differences in the antigenic sites A, B, and C on the HA protein, making the virus less recognizable to the immune system.
The Spanish Flu had a new mutant form of haemagglutinin, H1. How might this have affected virulence?
The emergence of a new mutant form of hemagglutinin (HA), specifically the H1 subtype, in the 1918 Spanish Flu (H1N1) had a profound impact on the virulence of the virus. Here’s how this mutation might have affected virulence:
Lack of Preexisting Immunity: Prior to 1918, humans had not been exposed to an H1 subtype of influenza A virus. As a result, there was little to no preexisting immunity to this particular strain among the population. This lack of immunity meant that a larger proportion of the population was susceptible to infection, contributing to the rapid spread of the virus.
Greater Host Susceptibility: The lack of prior exposure to the H1 subtype meant that people had limited immune defenses against the virus. This greater host susceptibility likely led to higher infection rates and more severe cases.
Increased Severity of Disease: The emergence of a new HA subtype could have led to a more severe disease because the immune system was less effective at recognizing and responding to the virus. This contributed to the high mortality rate associated with the Spanish Flu.
Antigenic Drift: The new H1 subtype may have undergone further mutations over time (antigenic drift), potentially altering the virus’s antigenic properties and making it more challenging for the immune system to recognize and combat.
Cross-Reactivity with Immune System: The new H1 HA might have had different antigenic sites and epitopes than those found in previously circulating influenza strains. This could have reduced the effectiveness of cross-reactivity, where the immune system responds to similar epitopes on different strains, further enhancing the virus’s ability to evade the immune response.
Increased Transmission: The new H1N1 strain may have had a higher transmission rate due to a lack of immunity in the population. This contributed to the rapid global spread of the virus.
Overall Virulence: The combination of these factors—lack of preexisting immunity, increased host susceptibility, and potential alterations in the virus’s antigenic properties—contributed to the overall virulence of the 1918 Spanish Flu. This pandemic had a significantly higher mortality rate than typical seasonal influenza outbreaks.
explain the various mechanisms by which viruses can gain entry into host cells
Pore-Mediated Penetration + Genome Injection:
Pore-Mediated Penetration: This mechanism involves the creation of pores in the host cell membrane through which the viral genome is injected. Some human rhinoviruses and bacteriophages, such as T4 and lambda, use this method. The creation of these pores often occurs upon attachment to the cell surface.
Endocytosis + Dissolution of Endosomal Membrane:
Endocytosis: In this process, the virus is engulfed by the host cell through endocytosis, forming an endosome.
Dissolution of Endosomal Membrane: The virus can then escape from the endosome by disrupting or dissolving the endosomal membrane. For example, adenoviruses use this mechanism to gain access to the host cell’s cytoplasm.
Membrane Fusion Proteins:
Envelope Fusion with Plasma Membrane: Certain viruses have envelope proteins that can fuse directly with the host cell’s plasma membrane. This fusion allows the virus to enter the cell without being taken up into an endosome. For example, Morbilliviruses (e.g., measles) and Rubulaviruses (e.g., mumps) employ this mechanism.
Endocytosis + Fusion with Endosomal Membrane: Some enveloped viruses enter host cells through endocytosis. The low pH environment of the endosome triggers conformational changes in viral envelope proteins, enabling them to fuse with the endosomal membrane. This process allows the virus to enter the host cell’s cytoplasm. Examples include Herpes Simplex Virus (HSV) and influenza viruses.
These entry mechanisms showcase the diversity of strategies used by viruses to access the interior of host cells. The choice of entry method can be influenced by the virus’s structure, surface proteins, and the host cell type, as well as the specific requirements for viral replication and infection.
what is clathrin?
Clathrin is a protein that plays a critical role in the process of clathrin-mediated endocytosis, a mechanism by which cells engulf molecules or particles from their external environment. Clathrin-mediated endocytosis is involved in the internalization of various substances, including receptors, nutrients, and pathogens, such as some viruses.
Here are some key points about clathrin:
Structural Protein: Clathrin is a structural protein that forms a lattice-like structure, known as a clathrin coat, on the inner surface of the plasma membrane of eukaryotic cells (cells with a defined nucleus). This clathrin coat is composed of triskelion-shaped molecules of clathrin.
Vesicle Formation: In clathrin-mediated endocytosis, clathrin assembles into a cage-like lattice structure around a region of the plasma membrane. This process induces the formation of a vesicle (membrane-bound sac) called a clathrin-coated vesicle.
Cargo Selection: Clathrin-coated vesicles are responsible for the selective uptake of specific cargo molecules from the extracellular environment. The selection of cargo is often mediated by receptor proteins on the cell surface, which bind to the cargo and then interact with clathrin to initiate vesicle formation.
Internalization: Once the clathrin-coated vesicle forms, it pinches off from the plasma membrane, bringing the cargo molecules into the cell’s interior. The vesicle then loses its clathrin coat, and the cargo is released into the cell’s cytoplasm.
Endocytosis and Recycling: Clathrin-mediated endocytosis is important for various cellular processes, including nutrient uptake, regulation of receptor levels on the cell surface, and the internalization of certain viruses and signaling molecules. It also plays a role in the recycling of membrane receptors.
explain the various mechanisms by which some viruses can infect neighboring cells without re-entering the extracellular fluid
You’ve described various mechanisms by which some viruses can infect neighboring cells without re-entering the extracellular fluid. These mechanisms are diverse and represent the ability of viruses to exploit cellular and host processes for their advantage. Let’s delve into each of these methods:
Poxviruses (Actin-Driven Rocket):
Poxviruses use a unique mechanism called actin-driven rocket-like movement to move within an infected cell. They induce the formation of actin tails that push the virus particles into neighboring cells through membrane protrusions, allowing for direct cell-to-cell transmission.
Nanotubes, Virological Synapses, or Bridges:
Some viruses, such as HIV-1 and influenza, can establish direct connections between infected cells and neighboring uninfected cells. These connections include nanotubes, virological synapses, or bridges. Through these structures, viruses can transfer viral particles or genetic material directly to adjacent cells, bypassing the extracellular environment.
Syncytia Formation:
Some viruses, particularly those that produce membrane fusion proteins, can induce the fusion of infected cells with neighboring uninfected cells. This creates a single, multinucleated cell known as a syncytium. Within the syncytium, viral particles and genetic material can spread between cells, avoiding exposure to the extracellular fluid.
Plasmodesmata in Plants:
In plant cells, viruses like Tobacco Mosaic Virus (TMV) can utilize plasmodesmata, which are channels that connect plant cells, to spread from cell to cell. Viral particles can move through these channels, allowing for the direct transmission of the virus between neighboring plant cells.
These mechanisms of cell-to-cell transmission are advantageous for viruses as they can evade certain aspects of the host’s immune response, such as antibodies and complement, which are typically present in the extracellular fluid. By directly infecting neighboring cells, viruses can maintain a local infection, propagate efficiently, and establish persistent or systemic infections in the host.
