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Bio.203-19.Viruses
Molecular Biology Ch. 19 - Viruses
| Question | Answer |
|---|---|
| Virus | An infectious particle incapable of replicating outside of a cell, consisting of an RNA or DNA genome surrounded by a protein coat (capsid) and, for some viruses, a membranous envelope. |
| Why aren't viruses considered to be alive? | Because they cannot reproduce or carry out metabolic activities. |
| Size of the smallest viruses | 20nm; smaller than a ribosome. |
| The difference between genomes of living cells and viruses | The genes of living cells are made of double-stranded DNA. Viruses may have genes consisting of double stranded DNA, single stranded DNA, double stranded RNA, or double stranded RNA. Viruses are either DNA-viruses or RNA-viruses based on their genomes |
| The number of genes in the smallest vs largest viruses | The smallest viruses known only have four genes, while the largest have several hundred to a thousand. |
| Capsid | The protein shell enclosing the viral genome. |
| Capsid shape | Depending on the type of virus, the capsid may be rod-shaped, polyhedral, or a more complex shape |
| Capsids are built from a large number of protein subunits called __________ | Capsomeres |
| Capsid shape -- Describe helical (rod-shaped) capsids | They are rigid, rod-shaped capsids made from over a thousand molecules of a single type of protein arranged into a helix |
| Capsid shape -- Describe icosahedral viruses | E.g. adenoviruses (which infect the respiratory tracts of animals) have polyhedral capsids with 20 triangular facets--an icosahedron |
| Viral envelopes | A membrane, derived from membranes of the host cell, that cloaks the capsid, which in turn encloses the viral genome. |
| What are viral envelopes made of? | They contain host cell phospholipids, membrane proteins as well as glycoproteins/proteins of viral origin. |
| Review: What are glycoproteins? | Proteins with carbohydrates covalently attached to them |
| Other than the viral genome, are there any other proteins contained within the capsid? | Some viruses contain a few viral enzyme molecules such reverse transcriptase, integrase, etc. |
| Bacteriophages | A virus that infects bacteria; also called a phage |
| Structure of bacteriophages | Their capsids have elongated icosahedral heads enclosing their DNA. Attached to the head is a protein tail piece with fibers by which the phages attach to a bacterium. |
| Viruses are ________ parasites; in other words... | Viruses are obligate intracellular parasites; in other words, they can replicate only within a host cell. |
| Host range | Each particular virus can infect cells of only a limited number of host species, called the host range of the virus. |
| How do viruses identify the host cells? | By a "lock-and-key" fit between viral surface proteins and specific receptor molecules on the outside of cells. |
| Examples of host ranges for: West Nile virus, human cold virus, and HIV | West Nile: mosquitoes, birds, horses, and humans. Cold Virus: only human cells lining the upper respiratory tract. HIV: only certain white blood cells. |
| When does a viral infection begin? | When a virus binds to a host cell and the viral genome makes its way inside. |
| Naming scheme of the first 7 phages discovered | The first phages included seven that infected E. coli. They were named type 1 (T1), type 2 (T2), etc. |
| Examples of methods by which viruses insert their genome into host cells | T-even phages use their elaborate rail apparatus to inject DNA into the bacterium, other viruses are taken up by endocytosis, and others (enveloped viruses) fuse with the host cell’s plasma membrane. |
| Once the virus enters the cell, how does it replicate? | Many DNA viruses use DNA pol. of the host cell to synthesize new copies, using the viral DNA as the template. RNA viruses use virally coded RNA polymerases (uninfected hot cells don’t code for them). |
| After DNA pol synthesizes a copy of the viral DNA, how are viral proteins produced? | Host enzymes transcribe the viral genome into viral mRNA, which the host ribosomes use to make more capsid proteins |
| Once viral nucleic acid molecules and capsomeres are produced, how are they assembled into viruses? | They spontaneously self-assemble. This has been observed; researchers can separate the RNA and capsomeres of viruses and then reassemble them by simply mixing them together. |
| Research on phages led to the discovery that some double-stranded DNA viruses can replicate by two alternative mechanisms... | …the lytic cycle and the lysogenic cycle. |
| Lytic cycle | A type of phage replicative cycle resulting in the release of new phages by lysis (and death) of the host cell |
| Virulent phage | A phage that replicates only by a lytic cycle |
| Lytic cycle, step (1) | Attachment. The T4 phage uses its tail fibers to bind to specific receptor sites on the outer surface of an E. coli cell. |
| Lytic cycle, step (2) | The sheath of the tail contracts, injecting the phage DNA into the cell and leaving an empty capsid outside. The cell’s DNA is hydrolyzed. |
| Lytic cycle, step (3) | Synthesis of genomes/proteins. The phage DNA directs production of phage proteins and copies of the phage genome by host and viral enzymes, using components within the cell. |
| Lytic cycle, step (4) | Assembly. Three separate sets of proteins self-assemble to form phage heads, tails, and tail fibers. The phage genome is packaged inside the capsid as the head forms. |
| Lytic cycle, step (5) | Release. The phage directs production of an enzyme that damages the bacterial cell wall, allowing fluid to enter. The cell swells and finally bursts, releasing 100 to 200 phage particles. |
| Why haven’t all bacteria been exterminated by viruses? | 1. Natural selection favors bacterial mutants with receptors that are no longer recognized by a particular type of phage, 2. When phage DNA enters a bacterium, the DNA is often recognized as foreign and cut up by restriction enzymes. |
| Restriction enzymes | AKA Restriction endonuclease. It is a type of enzyme that recognizes and cuts DNA molecules foreign to a bacterium (e.g. phage genomes), thus protecting the cell (restricting viral proliferation). The enzyme cuts at specific nucleotide sequences |
| Restriction enzymes are so named because… | …they “restrict” the ability of the phage to infect the bacterium. |
| How are bacterial cells protected from restriction enzymes cutting up their own DNA | The bacterial cell’s own DNA is methylated in a way that prevents attack by its own restriction enzymes |
| Lysogenic cycle | A type of phage replicative cycle in which the viral genome becomes incorporated into the bacterial host chromosome as a prophage, is replicated along with the chromosome, and does not kill the host. |
| Prophage | A phage genome that has been inserted into a specific site on a bacterial chromosome |
| Temperate phages | Phages capable of using both lytic and lysogenic cycles to replicate within bacteria |
| Lysogenic cycle step (1) | The phage enters the cell and circulates its DNA. Certain factors determine whether the lytic cycle or lysogenic cycle is entered. In this case, the lysogenic cycle is induced. |
| Lysogenic cycle step (2) | Phage DNA integrates into the bacterial chromosome, becoming a prophage. |
| Lysogenic cycle step (3) | The bacterium reproduces normally, copying the prophage and transmitting it to daughter cells |
| Lysogenic cycle step (4) | Large populations of infected bacteria are produced through reproduction. Occasionally a prophage exits the bacterial chromosome, initiating a lytic cycle. |
| What kinds of proteins do prophrages express while in lysogeny | 1. Proteins that prevent transcription of other prophage genes. 2. Other genes that may alter the host’s phenotype. |
| Example of a prophage expressing a gene that effects the host’s phenotype | E. coli can be lethal if it contains certain prophages that express toxic materials. Other bacteria that are harmful due to prophages are botulism, diphtheria, and scarlet fever. |
| How are animal viruses classified and list their classifications | By the nature of their genome: I. Double-Stranded DNA (dsDNA), II. ssDNA, III. dsRNA, IV. ssRNA Serving as mRNA, V. ssRNA as a template for mRNA synthesis, VI. ssRNA as a template for DNA synthesis |
| How are some ways animal viruses differ from Bacteriophages | Whereas few bacteriophages have an envelope or RNA genome, many animal viruses have both. |
| How do animal viruses use viral envelopes to their advantage? | The viruses use the envelopes to enter the host cell. Protruding from the outer surface of the envelope are viral glycoproteins that bind to specific receptor molecules on the surface of a host cell. |
| How are the various components of the viral membrane synthesized? | Ribosomes bound to the ER of the host cell make the protein parts of the envelope glycoproteins; cellular enzymes in the ER and golgi apparatus then add the sugars. |
| When the enveloped virus leaves the animal cell, does the cell die (like the lytic cycle in bacteriophages)? | No. First the glycoproteins are sent to the host cell surface. Then the new viral capsids are wrapped a membrane (derived from the host cell) as they bud from the cell, much like exocytosis. This cycle does not result in the death of the host cell. |
| Do all enveloped viruses obtain their envelopes from the plasma membrane of their host cells? | No. Herpesviruses, for example, are temporarily cloaked in membranes derived from the nuclear envelope of the host; they then shed this membrane in the cytoplasm and acquire a new envelope made from membrane of the Golgi apparatus. |
| Why does the herpesvirus express itself as recurrent flare-ups? | The herpesvirus replicates within the host cell nucleus. Copies of the viral DNA can remain behind as mini-chromosomes in the nuclei of certain nerve cells. They remain latent until physical/emotional stress triggers a new round of virus production. |
| The replicative cycle of an enveloped class V RNA virus, step (1) | Glycoproteins on the viral envelope bind to specific receptor molecules on the host cell, promoting viral entry into the cell. |
| The replicative cycle of an enveloped class V RNA virus, step (2) | The capsid and viral genome enter the cell. Digestion of the capsid by cellular enzymes releases the viral genome. |
| The replicative cycle of an enveloped class V RNA virus, step (3) | The viral genome functions as a template for synthesis of complementary RNA strands by a viral RNA polymerase. |
| The replicative cycle of an enveloped class V RNA virus, step (4) | New copies of viral genome RNA are made using complementary RNA strands as templates |
| The replicative cycle of an enveloped class V RNA virus, step (5) | Complementary RNA strands also function as mRNA, which is translated into both capsid proteins (in the cytosol) and glycoproteins (in the ER and Golgi apparatus) |
| The replicative cycle of an enveloped class V RNA virus, step (6) | Vesicles transport envelope glycoproteins to the plasma membrane. A capsid assembles around each viral genome molecule. |
| The replicative cycle of an enveloped class V RNA virus, step (7) | Each new virus buds from the cell, its envelope studded with viral glycoproteins embedded in membrane derived from the host cell. |
| The RNA animal viruses with the most complicated replicative cycles are | Retroviruses |
| What is a retrovirus | An RNA virus that replicates by transcribing its RNA into DNA and then inserting the DNA into a cellular chromosome; an important class of cancer-causing viruses |
| Retroviruses are equipped with an enzyme called | Reverse transcriptase |
| Function of reverse transcriptase | An enzyme encoded by certain viruses that uses RNA as a template for DNA synthesis. Hence the prefix “retro-“ referring to the fact that the flow of genetic information in retroviruses is reversed (RNA -> DNA instead of DNA -> RNA). |
| HIV virus | Human immunodeficiency virus. The infectious agent that causes AIDS. HIV is a retrovirus. |
| AIDS | Acquired immunodeficiency syndrome. The symptoms and signs present during the late stages of HIV infection, defined by a specified reduction in the number of T cells and the appearance of characteristic secondary infections. |
| How many strands of RNA and how many reverse transcriptase enzymes are contained within the envelope and capsid of retroviruses? | Two molecules of RNA and two reverse transcriptase enzymes |
| The replicative cycle of HIV step (1) | The envelope glycoproteins enable the virus to bind to specific receptors on certain white blood cells |
| The replicative cycle of HIV step (2) | The virus fuses with the cell’s plasma membrane. The capsid proteins are hydrolyzed by the host cell, releasing the viral proteins and RNA. |
| The replicative cycle of HIV step (3) | Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. |
| The replicative cycle of HIV step (4) | Reverse transcriptase catalyzes the synthesis of a second DNA strand complementary to the first. |
| The replicative cycle of HIV step (5) | The double-stranded DNA is incorporated as a provirus into the cell’s DNA |
| The replicative cycle of HIV step (6) | Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral protein. |
| The replicative cycle of HIV step (7) | The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). |
| The replicative cycle of HIV step (8) | Vesicles transport the glycoproteins to the cell’s plasma membrane. Capsids are assembled around viral genomes and reverse transcriptase molecules. New viruses then bud off from the host cell. |
| Provirus | A viral genome that is permanently inserted into the host genome. (In contrast a prophage leaves the host’s genome at the start of the lytic cycle). The provirus can then begin expressing proteins and RNA. |
| Hypothesis for the origin of viruses | Viruses originated from naked bits of cellular nucleic acids. Candidates for the original sources of viral genomes include plasmids and transposons. They are both mobile genetic elements. |
| How much damage a virus causes depends partly on… | …the ability of the infected tissue to regenerate by cell division. (E.g. people usually recover from colds because the epithelium of the respiratory tract can efficiently repair itself). |
| The temporary symptoms, such as fevers and aches, associated with viral infections originate from… | … the body’s own efforts at defending itself against infection rather than from cell death caused by the virus. |
| Vaccine | A harmless variant or derivative of a pathogen that stimulates a host’s immune system to mount defenses against the pathogen. |
| How do most antiviral drugs work? | They resemble nucleosides and as a result interfere with nucleic acid synthesis, e.g. acyclovir. |
| Acyclovir | Antiviral medication that impedes herpesvirus replication by inhibiting the viral polymerase that synthesizes viral DNA |
| Azidothymidine (AZT) | Curbs HIV replication by interfering with the synthesis of DNA by reverse transcriptase |
| HIV treatment “cocktails” | A combination of two nucleoside mimics and a protease inhibitor, which interferes with an enzyme required for assembly of the virus |
| Emerging viruses | Viruses that suddenly become apparent |
| First case of HIV | Discovered in the Belgian Congo in 1959 |
| First case of Ebola | Discovered initially in 1976 in central Africa |
| Epidemic | A general outbreak of a disease |
| Pandemic | A global epidemic |
| The spread of the H1N1 virus (swine flu) | Epidemic appeared in Mexico and the US in 2009, the viral disease then spread rapidly, prompting the WHO to declare a pandemic in June 2009. By November 2009 the disease reached 207 countries, infecting 600k people, killing 8k. |
| What method was used in South Korean airports to screen for H1N1-infected individuals? | Thermal scans to detect passengers with a fever |
| Three processes that contribute to the emergence of viral diseases: (1) | The mutation of existing viruses. RNA viruses tend to have an unusually high rate of mutation because errors in replicating their RNA genomes are not corrected by proofreading. These mutations can lead to new strains (genetic varieties). |
| Three processes that contribute to the emergence of viral diseases: (2) | The dissemination of a viral disease from a small, isolated human population. For instance, AIDS went unnamed and unnoticed for decades before it began to spread. |
| Three processes that contribute to the emergence of viral diseases: (3) | The spread of existing viruses from other animals. Scientists estimate that about three-quarters of new human diseases originate this way. |
| Three types of influenza virus | Types B and C, which infect only humans, and have never caused an epidemic, and type A, which infects a wide range of animals, including birds, pigs, horses, and humans. |
| The worst influenza pandemic in history | The “Spanish flu” pandemic of 1918-1919, which killed about 40 million people, including many WWI soldiers. |
| How are influenza A strains named? E.g. the H1N1 strain | The name identifies which forms of the two viral surface proteins are present: hemagglutinin (H) and neuraminidase (N). There are 16 different types of H and 9 types of N. |
| What are the functions of hemagglutinin and neuraminidase? | H is a protein that helps the flu virus attach to host cells; and N is an enzyme that helps release new virus particles from infected cells. |
| Relationship between the Spanish flu and Swine flu. Age group of those most likely to die from swine flu? | Both are of the strain H1N1. Young people had a higher mortality rate when exposed to swine flu because they were less likely to have been exposed to the virus and thus develop immunity. |
| How does a previously harmless strain of influenza become dangerous to humans? | They virus is mutated as it passes from one host species to another. When animal, such as a pig or bird, is infected with more than one strain of the virus, the different strains can undergo genetic recombination. |
| What are the risks of viral genetic recombinations? | Coupled with mutation, reassortments can lead to the emergence of a viral strain that is capable of infecting humans. If the recombinant virus recombines with viruses that circulate widely among humans, it can result in a pandemic. |
| Danger of the avian flu | The avian flu (H5N1) has a very high mortality rate, >50%. Host range of H5N1 is expanding, increasing likelihood of contact with each other, which can result in new strains. A pandemic caused by the H5N1 strain can rival the Spanish flu. |
| Structure of plant viruses | Most plant viruses have an RNA genome. Many have a helical capsid, while others have an icosahedral capsid. |
| Viral diseases of plants spread by what two major routes? | Horizontal transmission and vertical transmission |
| Horizontal transmission | A plant is infected from an external source of the virus. A plant is more susceptible to horizontal transmission if it has an open injury, caused by weather hazards, insects, etc. |
| Vertical transmission | A plant inherits a viral infection from a parent. It can occur in asexual propagation (e.g. through cuttings) or in sexual reproduction via infected seeds. |
| Once a virus enters a plant cell and begins replicating, viral genomes and associated proteins can spread throughout the plant by means of… | … plasmodesmata, the cytoplasmic connections that penetrate the walls between adjacent plant cells. |
| The passage of viral macromolecules from cell to cell is facilitated by | Virally encoded proteins that cause enlargement of the plasmodesmata |
| Viroid | A plant pathogen consisting of a molecule of naked, circular RNA a few hundred nucleotides long. These are smaller and simpler than viruses. |
| What effects do viroids have on infected plants? | While viroids don’t code for proteins, they can replicate in host plant cells, apparently using plant enzymes. They seem to cause errors in the regulatory systems that control plant growth; the typical signs being abnormal development and stunted growth. |
| Prion | An infectious agent that is a misfolded version of a normal cellular protein. Prions appear to increase in number by converting correctly folded versions of the protein to more prions. |
| Conditions caused by prions | They appear to cause a number of degenerative brain diseases in various animal species including scrapie in sheep, mad cow disease, and Creutzfeldt-Jacob disease. |
| How are prions transmitted? | In food, as may occur when people eat prion-laden beef from cattle with mad-cow disease. Another prion disease, kuru, which spread in New Guinea during the 1960s, was transmitted through ritual cannibalism. |
| How quickly do prions begin to affect the host? | Very slowly; with an incubation period of at least ten years before symptoms begin to develop. |
| How are prion diseases cured? | There are no known cures. Prions are virtually indestructible; e.g. they are not destroyed or deactivated by heating to normal cooking temperatures. |
| How can a protein, which cannot replicate itself, be a transmissible pathogen? | A prion is a misfolded form of a protein normally present in the brain cells. When the prion gets in contact with a cell, the prion somehow converts normal proteins into prions. Over time this has obviously detrimental phenotypic effects. |
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