Virus Infection and Hosts Quiz

PDF page 867: Viruses differ from other organisms in their method of replication. Viruses replicate within a living host cell, producing changes in the cell that often result in the death of the infected cell. Thus, viruses are considered intracellular parasites. Viral replication involves several steps: attachment, penetration, replication, assembly, and release. Viruses are host-specific because they only can attach to and infect cells of certain organisms. Cells that a virus may use to replicate are called permissive. The virus attacks the host cell by first attaching to a specific receptor site on the membrane of the host cell. Next, the viral nucleic acid, either DNA or RNA, enters the host cell, either naked, leaving the protein capsid behind, or with the capsid. If the capsid enters the cell, an additional uncoating step is needed. Viral nucleic acid then becomes available for replication and transcription. The last stage of viral replication is the release of the new virions produced by the host that are able to infect other cells. Depending on the type of virus, the replication cycle facilitates the transfer of genetic information through the lytic and lysogenic cycles. Bacteriophages, such as T4 are viruses that infect bacterial cells, can enter both the lytic and lysogenic cycles. Animal viruses cause a variety of infections, for example, hepatitis C, herpes, HPV, colds, and flu. Occasionally, viruses can “hide” and remain latent (dormant) in cells such as nerve or liver cells for months, or even years; for example, the varicellazoster virus that causes chickenpox in children can reactivate in adults to cause the painful condition known as “shingles.” Oncogenic viruses in animals can cause cancer by interfering with the regulation of the host cell cycle. Plant viruses can cause considerable economic damage caused by poor crop quality and quantity globally.

PDF page 867: Viruses differ from other organisms in their method of replication. Viruses replicate within a living host cell, producing changes in the cell that often result in the death of the infected cell. Thus, viruses are considered intracellular parasites. Viral replication involves several steps: attachment, penetration, replication, assembly, and release. Viruses are host-specific because they only can attach to and infect cells of certain organisms. Cells that a virus may use to replicate are called permissive. The virus attacks the host cell by first attaching to a specific receptor site on the membrane of the host cell. Next, the viral nucleic acid, either DNA or RNA, enters the host cell, either naked, leaving the protein capsid behind, or with the capsid. If the capsid enters the cell, an additional uncoating step is needed. Viral nucleic acid then becomes available for replication and transcription. The last stage of viral replication is the release of the new virions produced by the host that are able to infect other cells. Depending on the type of virus, the replication cycle facilitates the transfer of genetic information through the lytic and lysogenic cycles. Bacteriophages, such as T4 are viruses that infect bacterial cells, can enter both the lytic and lysogenic cycles. Animal viruses cause a variety of infections, for example, hepatitis C, herpes, HPV, colds, and flu. Occasionally, viruses can “hide” and remain latent (dormant) in cells such as nerve or liver cells for months, or even years; for example, the varicellazoster virus that causes chickenpox in children can reactivate in adults to cause the painful condition known as “shingles.” Oncogenic viruses in animals can cause cancer by interfering with the regulation of the host cell cycle. Plant viruses can cause considerable economic damage caused by poor crop quality and quantity globally.

PDF page 870: Bacteriophages are viruses that infect bacteria (Figure 21.9). When infection of a cell by a bacteriophage results in the production of new virions, the infection is said to be productive. If the virions are released by bursting the cell, the virus replicates by means of a lytic cycle (Figure 21.10). An example of a lytic bacteriophage is T4, which infects Escherichia coli found in the human intestinal tract. Sometimes, however, a virus can remain within the cell without being released. For example, when a temperate bacteriophage infects a bacterial cell, it replicates by means of a lysogenic cycle (Figure 21.10), and the viral genome is incorporated into the genome of the host cell. When the phage DNA is incorporated into the host cell genome, it is called a prophage. An example of a lysogenic bacteriophage is the λ (lambda) virus, which also infects

PDF page 870: Bacteriophages are viruses that infect bacteria (Figure 21.9). When infection of a cell by a bacteriophage results in the production of new virions, the infection is said to be productive. If the virions are released by bursting the cell, the virus replicates by means of a lytic cycle (Figure 21.10). An example of a lytic bacteriophage is T4, which infects Escherichia coli found in the human intestinal tract. Sometimes, however, a virus can remain within the cell without being released. For example, when a temperate bacteriophage infects a bacterial cell, it replicates by means of a lysogenic cycle (Figure 21.10), and the viral genome is incorporated into the genome of the host cell. When the phage DNA is incorporated into the host cell genome, it is called a prophage. An example of a lysogenic bacteriophage is the λ (lambda) virus, which also infects

PDF page 867: A virus must use cell processes to replicate. The viral replication cycle can produce dramatic biochemical and structural changes in the host cell, which may cause cell damage. These changes, called cytopathic (causing cell damage) effects, can change cell functions or even destroy the cell. Some infected cells, such as those infected by the common cold virus known as rhinovirus, die through lysis (bursting) or apoptosis (programmed cell death), releasing all progeny virions at once. The symptoms of viral diseases result from the immune response to the virus, which attempts to control and eliminate

PDF page 868: the virus from the body, and from cell damage caused by the virus. Many animal viruses leave the infected cells of the immune system by a process known as budding, where virions leave the cell individually. During the budding process, the cell does not undergo lysis and is not immediately killed. However, the damage to the cells that the virus infects may make it impossible for the cells to function normally, even though the cells remain alive for a period of time. Most productive viral infections follow similar steps in the virus replication cycle: attachment, penetration, uncoating, replication, assembly, and release (Figure 21.8). Attachment A virus attaches to a specific receptor site on the host cell membrane through attachment proteins in the capsid or via glycoproteins embedded in the viral envelope. The specificity of this interaction determines the host—and the cells within the host—that can be infected by a particular virus. This can be illustrated by thinking of several keys and several locks, where each key will fit only one specific lock.

PDF page 868: Entry The nucleic acid of bacteriophages enters the host cell naked, leaving the capsid outside the cell. Plant and animal viruses can enter through endocytosis, in which the cell membrane surrounds and engulfs the entire virus. Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane. Once inside the cell, the viral capsid is degraded, and the viral nucleic acid is released, which then becomes available for replication and transcription. Replication and Assembly The replication mechanism depends on the viral genome. DNA viruses usually use host cell proteins and enzymes to make additional DNA that is transcribed to messenger RNA (mRNA), which is then used to direct protein synthesis. RNA viruses usually use the RNA core as a template for synthesis of viral genomic RNA and mRNA. The viral mRNA directs the host cell to synthesize viral enzymes and capsid proteins, and assemble new virions. Of course, there are exceptions to this pattern. If a host cell does not provide the enzymes necessary for viral replication, viral genes supply the information to direct synthesis of the missing proteins. Retroviruses have an RNA genome that must be reverse transcribed into DNA, which then is incorporated into the host cell genome. They are within group VI of the Baltimore classification scheme. To convert RNA into DNA, retroviruses must contain genes that encode the virus-specific enzyme reverse transcriptase that transcribes an RNA template to DNA. Reverse transcription never occurs in uninfected host cells—the needed enzyme reverse transcriptase is only derived from the expression of viral genes within the infected host cells. The fact that some retroviruses produces some of its own enzymes not found in the host has allowed researchers to develop drugs that inhibit these enzymes. These drugs inhibit replication by reducing the activity of the enzyme without affecting the host’s metabolism. This approach has led to the development of a variety of drugs used to treat these viruses and has been effective at reducing the number of infectious virions (copies of viral RNA) in the blood to non-detectable levels in people affected with the virus. Egress The last stage of viral replication is the release of the new virions produced in the host organism, where they are able to

PDF page 868: Entry The nucleic acid of bacteriophages enters the host cell naked, leaving the capsid outside the cell. Plant and animal viruses can enter through endocytosis, in which the cell membrane surrounds and engulfs the entire virus. Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane. Once inside the cell, the viral capsid is degraded, and the viral nucleic acid is released, which then becomes available for replication and transcription. Replication and Assembly The replication mechanism depends on the viral genome. DNA viruses usually use host cell proteins and enzymes to make additional DNA that is transcribed to messenger RNA (mRNA), which is then used to direct protein synthesis. RNA viruses usually use the RNA core as a template for synthesis of viral genomic RNA and mRNA. The viral mRNA directs the host cell to synthesize viral enzymes and capsid proteins, and assemble new virions. Of course, there are exceptions to this pattern. If a host cell does not provide the enzymes necessary for viral replication, viral genes supply the information to direct synthesis of the missing proteins. Retroviruses have an RNA genome that must be reverse transcribed into DNA, which then is incorporated into the host cell genome. They are within group VI of the Baltimore classification scheme. To convert RNA into DNA, retroviruses must contain genes that encode the virus-specific enzyme reverse transcriptase that transcribes an RNA template to DNA. Reverse transcription never occurs in uninfected host cells—the needed enzyme reverse transcriptase is only derived from the expression of viral genes within the infected host cells. The fact that some retroviruses produces some of its own enzymes not found in the host has allowed researchers to develop drugs that inhibit these enzymes. These drugs inhibit replication by reducing the activity of the enzyme without affecting the host’s metabolism. This approach has led to the development of a variety of drugs used to treat these viruses and has been effective at reducing the number of infectious virions (copies of viral RNA) in the blood to non-detectable levels in people affected with the virus. Egress The last stage of viral replication is the release of the new virions produced in the host organism, where they are able to

PDF page 868: Entry The nucleic acid of bacteriophages enters the host cell naked, leaving the capsid outside the cell. Plant and animal viruses can enter through endocytosis, in which the cell membrane surrounds and engulfs the entire virus. Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane. Once inside the cell, the viral capsid is degraded, and the viral nucleic acid is released, which then becomes available for replication and transcription. Replication and Assembly The replication mechanism depends on the viral genome. DNA viruses usually use host cell proteins and enzymes to make additional DNA that is transcribed to messenger RNA (mRNA), which is then used to direct protein synthesis. RNA viruses usually use the RNA core as a template for synthesis of viral genomic RNA and mRNA. The viral mRNA directs the host cell to synthesize viral enzymes and capsid proteins, and assemble new virions. Of course, there are exceptions to this pattern. If a host cell does not provide the enzymes necessary for viral replication, viral genes supply the information to direct synthesis of the missing proteins. Retroviruses have an RNA genome that must be reverse transcribed into DNA, which then is incorporated into the host cell genome. They are within group VI of the Baltimore classification scheme. To convert RNA into DNA, retroviruses must contain genes that encode the virus-specific enzyme reverse transcriptase that transcribes an RNA template to DNA. Reverse transcription never occurs in uninfected host cells—the needed enzyme reverse transcriptase is only derived from the expression of viral genes within the infected host cells. The fact that some retroviruses produces some of its own enzymes not found in the host has allowed researchers to develop drugs that inhibit these enzymes. These drugs inhibit replication by reducing the activity of the enzyme without affecting the host’s metabolism. This approach has led to the development of a variety of drugs used to treat these viruses and has been effective at reducing the number of infectious virions (copies of viral RNA) in the blood to non-detectable levels in people affected with the virus. Egress The last stage of viral replication is the release of the new virions produced in the host organism, where they are able to

PDF page 872: viruses also have two ways of entering cells after binding to their receptors: receptor-mediated endocytosis, or fusion. Many enveloped viruses enter the cell by receptor-mediated endocytosis in a fashion similar to some non-enveloped viruses. On the other hand, fusion only occurs with enveloped virions. These viruses, which include HIV among others, use special fusion proteins in their envelopes to cause the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the cell cytoplasm. After making their proteins and copying their genomes, animal viruses complete the assembly of new virions and exit the cell Enveloped animal viruses may bud from the cell membrane as they assemble themselves, taking a piece of the cell’s plasma membrane in the process. On the other hand, non-enveloped viral progeny, such as rhinoviruses, accumulate in infected cells until there is a signal for lysis or apoptosis, and all virions are released together. As you will learn in the next module, animal viruses are associated with a variety of human diseases. Some of them follow the classic pattern of acute disease, where symptoms get increasingly worse for a short period followed by the elimination of the virus from the body by the immune system and eventual recovery from the infection. Examples of acute viral diseases are the common cold and influenza. Other viruses cause long-term chronic infections, such as the virus causing hepatitis C, whereas others, like herpes simplex virus, only cause intermittent symptoms. Still other viruses, such as human herpesviruses 6 and 7, which in some cases can cause the minor childhood disease roseola, often successfully cause productive infections without causing any symptoms at all in the host, and thus we say these patients have an asymptomatic infection. In hepatitis C infections, the virus grows and reproduces in liver cells, causing low levels of liver damage. The damage is so low that infected individuals are often unaware that they are infected, and many infections are detected only by routine blood work on patients with risk factors. On the other hand, since many of the symptoms of viral diseases are caused by immune responses, a lack of symptoms is an indication of a weak immune response to the virus. This allows for the virus to escape elimination by the immune system and persist in individuals for years, all the while producing low levels of progeny virions in what is known as a chronic viral disease. As already discussed, herpes simplex virus can remain in a state of latency in nervous tissue for months, even years. As the virus “hides” in the tissue and makes few if any viral proteins, there is nothing for the immune response to act against, and immunity to the virus slowly declines. Under certain conditions, including various types of physical and psychological stress, the latent herpes simplex virus may be reactivated and undergo a lytic replication cycle in the skin, causing the lesions associated with the disease. Once virions are produced in the skin and viral proteins are synthesized, the immune response is again stimulated and resolves the skin lesions in a few days by destroying viruses in the skin. As a result of this type of replicative cycle, appearances of cold sores outbreaks only occur intermittently, even though the viruses remain in the nervous tissue for life. Latent infections are common with other herpesviruses as well, including the varicella-zoster virus that causes chickenpox. After having a chickenpox infection in childhood, the varicella-zoster virus can remain latent for many years and reactivate in adults to cause the painful condition known as “shingles” (Figure 21.11ab).

PDF page 872: viruses also have two ways of entering cells after binding to their receptors: receptor-mediated endocytosis, or fusion. Many enveloped viruses enter the cell by receptor-mediated endocytosis in a fashion similar to some non-enveloped viruses. On the other hand, fusion only occurs with enveloped virions. These viruses, which include HIV among others, use special fusion proteins in their envelopes to cause the envelope to fuse with the plasma membrane of the cell, thus releasing the genome and capsid of the virus into the cell cytoplasm. After making their proteins and copying their genomes, animal viruses complete the assembly of new virions and exit the cell Enveloped animal viruses may bud from the cell membrane as they assemble themselves, taking a piece of the cell’s plasma membrane in the process. On the other hand, non-enveloped viral progeny, such as rhinoviruses, accumulate in infected cells until there is a signal for lysis or apoptosis, and all virions are released together. As you will learn in the next module, animal viruses are associated with a variety of human diseases. Some of them follow the classic pattern of acute disease, where symptoms get increasingly worse for a short period followed by the elimination of the virus from the body by the immune system and eventual recovery from the infection. Examples of acute viral diseases are the common cold and influenza. Other viruses cause long-term chronic infections, such as the virus causing hepatitis C, whereas others, like herpes simplex virus, only cause intermittent symptoms. Still other viruses, such as human herpesviruses 6 and 7, which in some cases can cause the minor childhood disease roseola, often successfully cause productive infections without causing any symptoms at all in the host, and thus we say these patients have an asymptomatic infection. In hepatitis C infections, the virus grows and reproduces in liver cells, causing low levels of liver damage. The damage is so low that infected individuals are often unaware that they are infected, and many infections are detected only by routine blood work on patients with risk factors. On the other hand, since many of the symptoms of viral diseases are caused by immune responses, a lack of symptoms is an indication of a weak immune response to the virus. This allows for the virus to escape elimination by the immune system and persist in individuals for years, all the while producing low levels of progeny virions in what is known as a chronic viral disease. As already discussed, herpes simplex virus can remain in a state of latency in nervous tissue for months, even years. As the virus “hides” in the tissue and makes few if any viral proteins, there is nothing for the immune response to act against, and immunity to the virus slowly declines. Under certain conditions, including various types of physical and psychological stress, the latent herpes simplex virus may be reactivated and undergo a lytic replication cycle in the skin, causing the lesions associated with the disease. Once virions are produced in the skin and viral proteins are synthesized, the immune response is again stimulated and resolves the skin lesions in a few days by destroying viruses in the skin. As a result of this type of replicative cycle, appearances of cold sores outbreaks only occur intermittently, even though the viruses remain in the nervous tissue for life. Latent infections are common with other herpesviruses as well, including the varicella-zoster virus that causes chickenpox. After having a chickenpox infection in childhood, the varicella-zoster virus can remain latent for many years and reactivate in adults to cause the painful condition known as “shingles” (Figure 21.11ab).

PDF page 872: transmission electron micrograph. Its double-stranded DNA genome becomes incorporated in the host DNA and can reactivate after latency in the form of (b) shingles, often exhibiting a rash. (credit a: modification of work by Dr. Erskine Palmer, B. G. Martin, CDC; credit b: modification of work by “rosmary”/Flickr; scale-bar data from Matt Russell)

PDF page 872: Some animal-infecting viruses, including the hepatitis C virus discussed above, are known as oncogenic viruses: They have the ability to cause cancer. These viruses interfere with the normal regulation of the host cell cycle either by either introducing genes that stimulate unregulated cell growth (oncogenes) or by interfering with the expression of genes that