Supplemental Lecture (98/04/18 update) by Stephen T. Abedon (firstname.lastname@example.org)
- Chapter title: Virus Growth
- A list of vocabulary words is found toward the end of this document
- Progeny producing machines
- What is a virus infected cell? It is a virus progeny producing machine!
- Small size/r strategists:
- Viruses may be distinguished from cellular life by their very small sizes.
- Small size is consistent with the typical virus reproductive strategy; one in which progeny are produced in abundance which are:
- particularly cheap
- Viruses can be, essentially, the ultimate r strategists.
- In some viruses nearly all of the virus genes are devoted to progeny production---the co-opting of resources into new, progeny viruses. As many progeny as possible, as fast as possible.
- Viruses don't have to make new cells in order to replicate.
- Large size/K strategists:
- Many viruses nevertheless display strong adherence to a K-selected reproductive strategy.
- Such adherence is usually at the expense of the expression of those aspects of their life cycle that one would consider most virus-like, i.e., the acellular, extracellular state.
- In other words, the more time a virus spends in the cellular state (infecting a cell), the more genes that virus must devote to tasks not directly tied to resource acquisition and progeny production.
- Viruses make new viruses while infecting cells.
- No increase in mass component:
- Unlike cellular microorganisms, virus growth cannot be distinguished into increase in mass and increase in number aspects.
- Instead, viruses are assembled from component parts into mature or nearly mature virions.
During typical virus replication and maturation, a single infected cell can make many hundreds or even thousands of new (progeny) virions.
Note how this high virus fecundity contrasts with the merely doubling per generation achieved by most cellular organisms during cell replication.
This high viral fecundity, however, is conceptually indestinguishable from a plant or animal which:
In any of these cases what is being exhibited is simply a high biotic potential.
Dramatic exponential growth:
- simply has large litters
- produces large numbers of eggs
- releases large numbers of seeds
- produces large numbers of progeny
Note how the ability to produce more than two progeny per generation changes calculations of exponential growth:
For binary fission P in this equation is equal to 2.
For a virus which produced 100 progeny virus particles per infection, P is equal to 100.
That is, 1, 2, 4, 8, 16, 32, . . . for a bacterial cell vs. 1, 100, 10,000, 1,000,000, 100,000,000, 10,000,000,000 for a virus over the same number of generations.
For example, starting with 3 individuals and going 4 generations (with 100 virus produced per generation) gives you 3 x 108 individuals (i.e., 3 x 1004).
Short generation times:
- Nt = NoPt
- where No is the initial organismal number, P is the number of progeny produced per individual per generation, t is in generations, and Nt is the number of organisms at time t.
Many viruses can produce these large numbers of progeny in the same amount of time it takes the host cell to divide (if, for example, it were not infected).
Among human viruses, viral multiplication cycles range in length from 4 to 36 hours.
Consequently, virus numbers can rapidly overwhelm host numbers if not kept in check by some mechanism.
For some viruses, this intense ability to propagate is tempered somewhat be a tendency toward producing defective progeny (e.g., HIV).
Consequently, the number of progeny produced by an average infection may differ when considered in terms of total numbers of progeny relative to total numbers of infectious progeny.
The life cycle of a virus typically involves, in order, the following steps:
Search for a host
- search for host
- genome replication
Alternatively, this host search aspect of the virus life cycle is analogous to spores or seeds which lie in a dormant state until environmental conditions come to favor growth.
- Reproductive inactivity:
- One major difference between virus and cell generation times is that incorporated into the amount of time it takes a given virus to produce its progeny is the amount of time it takes the virus to find a host cell.
- That amount of time can be long or short depending upon the environment and the concentration of host cells.
- Minimally, a virus' host search may be considered analogous to any other required step in development necessary to the achievement of reproductive maturity.
- However, it is a step which is variable in length depending upon environmental factors such as host density.
- Conceptually similar to delays between resource acquisition:
- This host search component of the virus life cycle is also equivalent to an organism which is able to replicate if and only if it finds food.
- Much (and a variable portion) of an organism's life could be spent in search of the food needed for replication (if food supplies are limiting and the distribution of food patchy---e.g., mosquitoes in search of a blood meal).
- Viral entry (a.k.a, penetration) is a post-adsorption step in which a virus genome is delivered into the cytoplasm of adsorbed cells.
- Replication of virus genomes:
- For viruses, replication consists just of the replication of the viral genome.
- That is, unlike in cellular replication, the "replication" of everything else (i.e., non-genomic parts) is considered instead under the heading maturation.
- Replication as transcription:
- In some cases replication and transcription may be synonymous.
- Retroviruses, in particular, produce progeny RNA genomes from DNA genomes which themselves are integrated into a host chromosome.
- For RNA viruses which remain RNA, the virus produces both mRNA and new RNA genomes using an RNA-dependent RNA polymerase.
- Genome packaging:
- Viral maturation are the steps associated with packaging the viral genome into its capsid and/or envelope.
- Maturation additionally includes various steps associated with converting progeny virus into intracellular particles ready for release.
Lytic infection [lytic cycle]
- Release is the movement from the intracellular to extracellular state.
- Modes of release vary though may be categorically divided into:
- methods involving movement across an intact host cytoplasmic membrane
- methods involving the destruction of the host cytoplasmic membrane
Continuous [chronic] infection
- Dissemination requires host cell destruction:
- A virus that requires that its host cell be destroyed (and virus replication within that host stopped) in order for progeny virions to be released and allowed to disseminate to new cells is called a lytic virus.
- Often the reason a virus must undergo a lytic infection is that the host's plasma membrane serves as a barrier to the extracellular dissemination of these virus progeny. Removal of this barrier results in cell death.
- Many viruses have less drastic means by which progeny are disseminated, ones that do not require plasma membrane destruction. Such viruses often produce chronic infections.
- Many bacteriophage as well as nonenveloped viruses undergo lytic infections.
- Lytic cycle/developmental cycle:
- A virion that has infected a cell and is undergoing a lytic infection is said to have entered a lytic cycle.
- Some bacteriophage obligately enter a lytic cycle upon infection while others can delay the initiation of the lytic cycle.
- The lytic cycle is thus basically a developmental program.
- A virus destined to chronically infect will, upon infection, begin to produce and release progeny virus.
- Dissemination achieved without host cell destruction:
- Chronically infecting viruses can release progeny without killing their host.
- Though not outright killing the host cell, nevertheless the effect of these chronic infections is not always sufficiently benevolent that the infected cell is able to live as long or reproduce as fast as an equivalent uninfected cell.
To release virions located in the bacterial or eucaryotic cell cytoplasm without disrupting the bacterial or eucaryotic cell membrane, the virus must be budded (extruded or exocytosed) through the membrane and other portions of the cell envelope (if present).
It is in the process of budding that the envelope (of enveloped viruses) is formed over the capsid.
Some bacteriophage as well as enveloped viruses undergo these "not-lytic" infections.
Latent [lysogenic, temperate] infection
Host phenotypic modification:
- No dissemination/no host cell destruction:
- Lysogeny is a method employed by many viruses whereby productive infections (i.e., ones in which progeny are made) are delayed.
- This is done presumably in order that virus progeny may be made in the future rather than immediately.
- Waiting for another day:
- A virus which is destined to infect latently will not take steps to injure its host and instead will enter a state whereby the replication of its host and its own genome are intimately tied.
- No progeny bacteriophage are produced until a later time.
- Latent infections may serve to protect progeny, or to keep progeny from being produced when host cell numbers are low or otherwise not easily obtained (i.e., when host searches are likely to be long and fruitless).
- Latent infection may be a strategy that assures that some viruses produce progeny immediately (in case that should be advantageous) and some virus tie their fortunes to that of the infected cell (in case that should be advantageous or should production of progeny in the future instead of the present offer some advantage). This is an example of a coin flipping strategy.
In bacteria the presence of a latent infecting bacteriophage can impart new properties on the cell.
In some cases these new properties can lead to increased bacteria pathogenicity.
Clostridium botulinum whose exotoxin, which is what is responsible for the disease botulism, is actually coded by the gene of a lysogenic virus.
example: host viral resistance
For many animal viruses latency allows a virus to remain infecting without causing disease and allow resumption or initiation of disease in the future.
Example: herpes viruses:
Various Herpes viruses are able to enter a latent state from which they can emerge later to cause disease.
The shingles (zoster) stage of the chicken pox virus (varicella-zoster virus) or the episodic lesion caused by the various oral and genital herpes viruses.
General animal virus life cycle
Infection is established when:
- Acquisition and infection:
- The life cycle of an animal virus generally is one consisting of acellular host acquisition and cellular progeny production during infection.
- Typically, various sub-steps and events occur including:
- entrance into the animal
- infection of cells
- exponential growth
- trophic limitation on growth
- host immune response
- achievement of sterilizing immunity
- infection latency
- dissemination to new hosts
- Entrance into animal:
- Initiation of infection usually follows entrance into the animal of one or a few infectious virus particles.
- Entrance typically occurs through a well defined portal of entry.
- Often this portal of entry is different from what you might expect.
- For example:
- many skin rash causing viruses (e.g., chicken pox virus) have a respiratory portal of entry
- hepatitis B virus first enters the blood then finds its way to the liver
- a virus particle attaches to a host cell (adsorption)
- the virus particle is endocytosed by or fuses with the cytoplasmic membrane of the host
- the uncoated virus genome is deposited in the host cell's cytoplasm (entry)
- some degree of take over of host metablism subsequently occurs (either immediately or with some characteristic delay)
- progeny viruses are produced intracellularly using diverted host metabolic machinery
- progeny viruses are released into the extracellular environment
Viremia follows infection.
Viremia basically is a state in which virus particles are found in the blood in relatively high concentrations (or, if not the blood, then in other locations within the body).
Significant viremia is an indication that the progeny of viral infections of some fraction of individual cells within a body are attempting to initiate new infections in other body cells.
Because of the initiation of new infections, in the early stages of virus replication within multicelled organisms the total amount of virus can increase exponentially.
Often virus replication is at least somewhat limited, however, due to many virus being capable of infecting only certain classes of cells termed target cells.
High concentrations of virus particles as well as the infection of individual cells alerts the immune system to the existence of an invading pathogen.
It takes time for the immune system to fully react.virus replication.
Full reaction of the body's immune system acts to destroy all virus (of that type) found in the body.
In some cases the immune system is not capable of destroying all of the virus in the body.
In these cases:
Certain viruses are capable of remaining in the body, hidden from the host immune system (e.g., herpesvirus).
Dissemination to new hosts:
- virus replication may be brought under only partial control (e.g., HIV, etc.)
- the infection may be in some way self limiting
- the infection can lead to the death of the individual.
The major evolutionary "goal" of a virus infection is the production of progeny virus which may disseminate and find new hosts.
This is achieved through various portals of exit, the one employed generally typical of the virus infecting.
General bacteriophage life cycle
Growth of viruses
- Diffusion limited adsorption:
- In the extracellular environment, progeny viruses are considered free viruses and remain, ideally, biochemically inert until collision to a new host occurs and infection ensues.
- Since bacteriophage infect free living cells (bacteria), a portal of entry generally is not needed other than some means of arriving in the same environment.
- In fact, random contact following diffusion is probably the most common method by which bacteriophage establish the first steps of virus infection:
- contact with the host
- virus genome entry
- Once the genome has entered the host cell, details become even more dependent on what type of virus is infecting.
- Note that entry does not occur via endocytosis, as it typically does in animal viruses.
- Types of bacteriophage infections:
- Generally, bacteriophage infections may be assigned to the following categories:
- These categories are all conceptually similar to strategies of infection exhibited by animal viruses.
- Because of their nature as obligate intracellular parasites, viruses cannot be grown in standard culture media but instead must be grown on living cells or in multicelled organisms.
- Various methods by which host cells may be maintained to support virus growth include growth:
- in solid medium (plaquing)
- in liquid culture
- in tissue culture
- in host organisms
- in embryonated eggs
Growth in liquid culture
- A plaque is the virus equivalent of a colony seen upon microorganism growth on or in a solid medium or substrate.
- A plaque is literally a hole in a solid medium culture otherwise containing so many cells that individual colonies are not distinguishable and the background is turbid. The hole is due to virus inflicted cell death or less severe cytopathic effects.
- Plaque assays can be very quantitative and therefore very powerful experimentally.
- One way of doing the plaque assay is to mix cells and virus using the pour plate or, even better, the soft agar overlay method.
Growth in tissue culture
- Viruses may be grown in liquid medium by mixing together host cells and virus.
- Note that not all host cells are capable of growth in liquid culture thus decreasing the utility of this method.
Growth in host organisms
- Cells from plants and animals may be grown in vitro often in flasks on a plastic substrate.
- These cells may be infected by viruses often quite readily.
- This allows for the study of virus replication under well controlled, often more convenient, and maybe even less expensive circumstances.
Growth in embryonated eggs
- Viruses that normally infect animals, plants, or bacteria can be grown simply by infecting living hosts.
- Plants and especially animals can be very expensive to maintain.
- Suitable animal "models" for human virus diseases do not always exist (e.g., AIDS) thus limiting the utility of whole organismal infection methods.
- Fertilized and growing eggs such as those from chickens make excellent, relatively inexpensive in situ growth chambers for many animal viruses.
- Animal virus life cycle
- Bacteriophage life cycle
- Chronic infection
- Continuous infection
- Genome replication
- Growth in embryonated eggs
- Growth in host organisms
- Growth in liquid culture
- Growth in tissue culture
- Growth of viruses
- Latent infection
- Lysogenic infection
- Lytic cycle
- Lytic infection
- Plaque assay
- Progeny producing machines
- Search for a host
- Temperate infection
- Virus fecundity
- Virus growth
- Virus replication
Practice question answers
- True or False, infecting lytic viruses undergo intracellular binary fission (circle True or False)? [PEEK]
- Which is likely to be directly interfered with by an antibody (circle only one correct answer)? [PEEK]
- viral lysis
- viral replication
- viral adsorption
- viral host range
- all of the above
- none of the above
- A virus produces 100 progeny virus per infection, the progeny viruses are released en mass by lysis, and it takes on average three minutes for each progeny virus to find and infect a new cell. If you started with 1 free virus, had an unlimited number of cells to infect, and just after two hours you had 10,000,000,000 resulting, individual, progeny viruses, how long does it take for an infected cell to produce 100 progeny virus (i.e., time(adsorption to lysis); note: it should be possible to do this without a calculator)? [PEEK]
- Give me an example of a kind of viral protein. [PEEK]
- A lytic virus produces 250 progeny per round of lytic cycle (adsorption through lysis). That same virus lives in an environment in which it takes an average of 10 minutes to find a new host following lysis. Starting with a single free virus, how many free virus would you expect to exist following a total of five rounds of replication, the final round terminated with lysis? Assume that there are no limits on virus growth (i.e., the potential host cell population is large and the culture well mixed). [PEEK]
- What is a plaque? [PEEK]
- A bacteriophage capable of infecting lysogenically has on average a burst size of 150 following entrance into its lytic cycle (burst size is the number of phage produced per lytically infected cell). You have a culture containing one million host bacteria. You add an excess of phage (say about 10 million---This assures that a sufficiently large fraction of cells are infected and therefore that uninfected cells can be ignored). Only a single phage is able to infect any given bacteria (i.e., late arrivers are excluded---this makes calculations much easier and in many cases even approximates the truth). On average only a randomly selected 5% of the phage are able to initiate a latent infection (i.e., 95% produce lytic infections). The lytically infected bacteria go through a fairly rapid period of infection and lyse their hosts. Following the lysis of those bacteria which have been lytically infected by this phage, you separate cells from free virus by simple repeated centrifugations. Thus, at this point you hold in your hand only those bacteria which have been latently infected (i.e., no free phage are left to complicate experimental interpretations). You resuspend these bacteria in a large volume of media (i.e., an excess). Brief application of UV radiation is known to efficiently convert lysogenic infections into lytic ones (i.e., it does not directly kill the cells or the phage, but reactivates the latently infecting phage). You UV irradiate your culture two hours after the initiation of phage latent infection. After this induced lysis of all of the cells present in the culture, you determine bacteriophage number as 6 x 107. Assuming that no lysis occurred after resuspension in media and prior to UV irradiation, that 150 phage are produced per infected cell following UV radiation, and that latent infection does not affect the rate at which a cell replicates, what is the doubling time of the bacterial host? Hint: to answer this question you first have to figure out what both the initial and final infected cell concentration are (i.e., just following establishment of lysogeny and just prior to UV irradiation, respectively). You can do this calculation based on your knowledge of what the initial number of cells was and what fraction was lytically infected, and then calculate the final number of cells based on your knowledge of final bacteriophage count and the expected bacteriophage burst size. [PEEK]
- Why can't viruses be cultured as easily as many other microorganisms (e.g., many bacteria)?[PEEK]
- Name the five steps which define a viral replicative cycle. [PEEK]
- Matching: [PEEK]
- latent infection
- continuous infection
- lytic infection
- _____ infects but does not produce progeny virus through remains capable of doing so.
- _____ infects, produces progeny, and releases those progeny without killing host cell.
- _____ progeny release requires removal of host plasma membrane.
- A virus produces about 500 virus particles per generation. Starting with one virus infected cell, after 3 generations (first generation ends in lysis of the originally infected cell), if only half of all progeny ultimately successfully find new cells to infect, how many virus would you expect to have been produced? Caution: the virus counted in the last generation (essentially free virus) is different (both qualitatively and numerically, i.e., in the last generation you should count all virus produced rather than only those viruses which are likely to successfully infect cells) from that counted in previous generations (successfully infecting virus). [PEEK]
- A virus produces 300 progeny per generation. Starting with one virus and going through three generations (and ignoring all complications), how many virus progeny, in total would you expect? [PEEK]
- A virus produces 300 progeny per generation. Starting with 15 virus and going through three generations (and ignoring all complications), how many virus progeny, in total would you expect? [PEEK]
- A virus produces 400 progeny per generation. Starting with 4 x 102 virus and going through 4 generations (and ignoring all complications), how many virus progeny, in total would you expect? [PEEK]
- A virus produces 400 progeny per generation. Starting with 4 x 102 virus and going through 4 generations (and ignoring all complications). Assuming that this is all happening within an animal which has been exposed to a typically low concentration of viruses thus resulting in the infection described here, how many generations do you suppose have actually been described? [PEEK]
- A bacterial cell replicates by binary fission. By contrast, many viruses replicate by manufacturing progeny, releasing, for example, 50 progeny as free virus particles, and thereby kill the host cell (i.e., go through a lytic infection cycle). Assume that generation times are equal for both cell and virus, that environments are unlimited (i.e., there are no limits on the replication of either the cell or the virus), and that all viruses instantaneously find new cells to infect (this eliminates from our calculations the complication of the search phase of the virus life cycle). Start with two environments, one containing only one cell and the other containing one virus (plus an unlimited number of potential host cells). At the end of 10 rounds of replication, what will be the ratio of viruses (in the latter environment) to cells (in the former environment)? (assume a 50 progeny virus burst size) [PEEK]
- The reason viruses are able to increase their numbers so rapidly as compared to cells has everything to do with the fact that viruses don't have to waste their time making new cells in order to replicate. Instead they let others make cells, then conveniently take over these cells. If a lytic virus can make 100 progeny virus per round of replication, how many rounds of replication would it take for one virus to produce enough descendants to take over one billion susceptible, uninfected cells? [PEEK]
- Describe two features which are common to lambda bacteriophage and human immunodeficiency virus (HIV) and which distinguish these organisms from various other viruses. (note: the features you describe need not be completely independent of one another) [PEEK]
- Describe one common morphological feature of the free virion particles of those animal viruses which chronically infect. [PEEK]
- What are the two major evolutionary "goals" of an animal virus? [PEEK]
- Other than differences in overall fecundity (i.e., number of progeny produced per generation), describe two differences between bacterial exponential growth and viral exponential growth (e.g., growth other than as latent infections). [PEEK]
- The search phase of viral replication typically ends upon interaction with what host-associated, typically membrane-bound structure? (note: membrane, cell envelope, and cell wall are all not correct answers) [PEEK]
- True or False, a latent viral infection can be distinguished from a not latent viral infection in terms of whether the host plasma membrane remains intact upon progeny virus dissemination? [PEEK]
- The process by which progeny genomes, virus proteins, and other cell components are turned into virion particles is called viral __________. [PEEK]
- Describe how the structure of an enveloped virus might change as it moves from within an infected cell to the extracellular environment. [PEEK]
- A hypothetical lytic virus produces on average 250 virus particles per infection. If you started with 25 viruses, how many virus particles would be present following 500 generations of virus growth? [PEEK]
- What is achieved following successful immune system action against a non-latently infecting animal virus? [PEEK]
- Enveloped animal viruses __________. (choose best answer) [PEEK]
- generally have lytic infective cycles.
- always latently infect.
- destroy the host plasma membrane upon progeny virus release.
- employ capsid proteins to attach to the viral receptor.
- always chronically infect.
- are always DNA viruses.
- Given a lytic virus, distinguish latent period from eclipse period. [PEEK]
- Why do administrators of flu shots persistently query whether recipients are allergic to eggs? [PEEK]
- A __________ is the virus equivalent of a bacterial colony. It is a transparent region in an otherwise opaque cellular growth corresponding to an absence of living or healthy cells. [PEEK]
- A __________ cycle is one means by which a prophage may subsequently produce and then release mature virion progeny? [PEEK]
- What may be achieved by employing liquid culture, tissue culture, or embryonated eggs? [PEEK]
- Start with a single virus which is adsorbed to a cell. Ten hours later you have 10,000,000,000 viruses. Assume the simplest possible case (synchronized latent periods, viruses lyse host cells to release progeny, all progeny find new cells instantly, there is a gross excess of cells, the environment is well mixed, etc.). Given that a single virus produces 100 progeny per latent period, how long is this virus' latent period? [PEEK]
- An r-selected individual is very good at filling up virgin environments with its own kind. I noted that viruses which tend to spend most of their time in the acellular (i.e., not cellular) state may be considered to be a paradigm of r-selectedness. Describe 2 characteristics of viruses which would result in their being typically r-selected organisms, that is, which are similar to characteristics seen in other, non-viral r-selected organisms. [PEEK]
- false, only cells undergo binary fission.
- iii, adsorption
- 2 hours = 120 minutes. 10,000,000,000 = 1010 progeny virus = 1005. Consequently you know that you have gone through five rounds of replication in 120 minutes: 120 / 5 = 24. Thus, each round must have taken 24 minutes. However, the time between infections devoted to finding a host you were told was three minutes. 24 - 3 = 21. Each infection, from adsorption through progeny release took 21 minutes.
- I was looking for capsomer but a number of answers would have been acceptable such as capsid protein, reverse transcriptase, polymerase, and envelope protein.
- 1 x 250 x 250 x 250 x 250 x 250 = 1 x 2505 = approximately 1012. The business about the 10 minutes to find a new host is irrelevant in this example since I told you specifically how many rounds of replication the virus went through: You didn't have to calculate this from anything and it's all you need to answer the question.
- A region in agar, generally infused with numerous cells (or plastic surface containing numerous cells), which contains non-opaque "holes" corresponding to regions in which viral replication has occurred. The presence of high concentrations of virus leads to localized cell lysis hence an absence of turbidity/opacity. High concentrations of virus occurs as a consequence of virus replication using the cells present as hosts. Holes are localized due to the inhibition of diffusion imparted by the agar.
- The idea here is that only a certain fraction of bacteria are initially infected latently. These continue to divide while their brethren lyse. Allowing some well defined period of growth, these infected bacteria are induced to produce 150 progeny phage each. Dividing 6 x 107 by 150 gives you the final (latently infected) cell number: 400,000. Multiplying the initial, uninfected cell number, 106, by 0.05 (5% / 100%) gives the initial latently infected cell number: 50,000. Dividing final cell number by initial cell number (both latently infected) gives the relative increase in cell number over the two hour period: 8. This is equal to 23 so you know that three generations occurred within this two hour period. This means that each generation was one-third of two hours or 40 minutes long. This is also the doubling time of the culture.
- Viruses are obligate intracellular parasites; they require the presence of another living thing to grow.
- adsorption, entry, replication, maturation, release. Note that this list could also have the word expression (as in gene expression) after entry and before maturation: adsorption, entry, (expression), replication, (expression), maturation, release.
- (1) i, (2) ii, (3) iii.
- 500*(500/2)2 or 31,250,000; the first 500 refers to the last generation's free phage while the two 250s (i.e., 500/2) refer to the successfully infecting virus produced by the first two generations.
- 3003 = 27,000,000 = 2.7 x 107. Why? Note that the 3 in the exponent is the number of generations while the 300 is the number of progeny produced per generation.
- 15 * 3003 = 405,000,000 = 4.05 x 108. Why? Note that the 3 in the exponent is the number of generations, while the 300 is the number of progeny produced per generation, and the 15 is the number of virus particles you started with.
- 4 x 102 * 4004 = 1.024 x 1013. Why? Note that the 4 in the exponent is the number of generations, while the 400 is the number of progeny produced per generation, and the 4 x 102 is the number of virus particles you started with.
- 5. Why? Note that the starting virus number is the same as the number of viruses at the end of one round of replication. Therefore, if this were an animal system and we assume that the animal was exposed to only a small number of viruses, or at least only a small number managed to actually initiate the infectio by replicating, then the 400 we started with (i.e., 4 x 102) probably came on the scene as a consequence of one virus going through one round of infection.
- For the virus the total number of progeny after 10 rounds of replication is 50 x 50 x 50 x 50 x 50 x 50 x 50 x 50 x 50 x 50 = 5010 = 9.7 x 1016. Divide this number by the number of cells present after 10 rounds of replication which is 2 x 2 x 2 x 2 x 2 x 2 x 2 x 2 x 2 x 2 = 210 = 1024. 9.7 x 1016 / 1024 = 9.5 x 1013 times as many virus as cells after 10 rounds of replication. More simply, the answer is 5010/210 = 2510.
- The question basically breaks down to what integer value of x is necessary for the following inequality to hold true: 100x 109. Note that 100x = 102x 109. Taking the log of both sides gives 2x 9 so x 9/2 = 4.5. Therefore x must be equal to 5. To check your answer, note that 1004 = 108 while 1005 = 1010. The non-algebraic means of answer this question, of course, is to note that 1001, 1002, 1003, and 1004 are not greater than one billion, while 1005 is.
- Both are capable of latent infections, both integrate into their host's genome, both also express superinfection exclusion which prevents subsequently virus from adsorbing or infecting.
- They have envelopes.
- production of progeny and the dissemination of those progeny to new host cells.
- (i) viruses have a cell search phase; (ii) viruses have a ramp up period prior to when intracellular progeny are actually produced (I'm loath to call this a difference, but I would accept it as a correct answer to the question); (iii) viruses do not have to produce new, replication competent cells in order to reproduce; (iv) some viruses have to destroy their cells in order to disseminate their progeny; (v) viruses mature while bacteria divide.
- receptor molecule.
- false, how progeny virion particles are disseminated has nothing to do with whether a virus is going through a latent or not latent infection.
- acquisition of the envelope.
- 25 x 250500. Note that this number is far greater than the estimated number of particles in the entire universe (according to Sir Author Stanley Eddington, there are only about 1080 particles in the entire universe; Rotman, B., 1997. The truth about counting. The Sciences November/December 34-39).
- sterilizing immunity.
- always chronically infect.
- The latent period is the interval starting with adsorption (i.e., infection of a cell) and ending with host cell lysis. The eclipse period starts with adsorption and ends with the appearance of the progeny phage in the host cell cytoplasm.
- Because the influenza vaccine is grown in embryonated eggs.
- the growth of viruses
- two hours
- Ability to produce (i) large numbers of (ii) cheap progeny.
- Black, J.G. (1996). Microbiology. Principles and Applications. Third Edition. Prentice Hall. Upper Saddle River, New Jersey. pp. 280-290.
- Raven, P.H., Johnson, G.B. (1995). Biology (updated version). Third Edition. Wm. C. Brown publishers, Dubuque, Iowa. pp. 573-588.
- Talaro, K., Talaro, A. (1996). Foundations in Microbiology. Second Edition. Wm. C. Brown Publishers. pp. 160-188, 741-766, 767-813.
- Tortora, G.J., Funke, B.R., Case, C.L. (1995). Microbiology. An Introduction. Fifth Edition. The Benjamin/Cummings Publishing, Co., Inc., Redwood City, CA, pp. 332-363.