Might virus cause transformation host cell

This may be achieved by virus-induced apoptosis or by a decrease in cellular protein synthesis. Reoviruses and some herpesviruses may be exceptions in that they cause a decrease in cell DNA synthesis before a substantial decline in cellular protein synthesis occurs. Direct degradation of host DNA is seen in vaccinia virus infections due to a virion-associated DNase. Chromosome damage may be caused directly by the virus particle or indirectly by events occurring during synthesis of new viral macromolecules RNA, DNA, protein.

The chromosome damage Fig. When the cell survives, the virus genome may persist within the cell, possibly leading to continued instability of cellular genomic material or to altered expression of cellular genes e. Virus-induced genomic instability appears to be associated with accumulation of mutations and related to the process of cell immortalization and oncogenic transformation.

Chromosomal aberrations resulting from cytomegalovirus infection of human peripheral blood lymphocytes. The biologic consequences of virus infection results from the aforementioned biochemical, physiological, structural, morphological and genetic changes. In productive infections virus-induced biological modifications of the cell may be closely related to the efficiency of virus replication or to the recognition of these cells by the immune system. For cells that are persistently infected, the cellular changes caused by the virus could lead to disease e.

The wide variety of these effects of virus infection points to the complex interaction between the viruses and their host cell.

Although most of the events that damage or modify the host cell during lytic infection are difficult to separate from viral replication, the effects are not always linked directly to the production of progeny virions.

For example, changes in cell size, shape, and physiologic parameters may occur before progeny virions or even many virus proteins, are produced. These alterations in cell structure and function may be important aspects of the pathogenesis of a number of viral infections see Ch. For example, through their cellular effects many viruses e. Cytocidal viral infections e.

Rubella virus infections are associated with demyelination without neural degeneration. The long-term effects of persistent virus infections see below may also be related to such progressive diseases as atherosclerosis and demyelination in multiple sclerosis.

In a persistent infection the virus is not eliminated from all of the host tissues after initial infection or the acute phase of disease.

The several types of persistent infection [chronic, slow, latent, and transforming Table ; see Chs. In chronic infections, a limited number of cells in the target organs are infected.

These infected cells may demonstrate a cytopathic effect, synthesize virus macromolecules, and release infectious virus. The spread of infection is limited by host factors such as humoral and cell-mediated immune responses, interferons and other nonspecific inhibitors. Slow infections induced by conventional e. In latent infections, infectious virus is seldom detected between clinical episodes of disease.

Few cells are infected, and virus expression and replication are extensively restricted. Common features of latent infection are their ability to reactivate in response to various environmental stimuli e. In transforming persistent infections, infectious virus RNA tumor viruses may or may not be released, but as a result of heritable genetic changes to cellular genes, acquisition of a viral oncogene, or the effect of integrated viral sequences, the cells undergo alterations that result in malignant phenotypes.

Autoimmune injury and other forms of cell damage may occur during persistent infections. Budding virions and viral peptides associated with the cell membrane change the antigenic characteristics of the cell so that the immune system may recognize it as foreign see Chs.

The cell then may be attacked by the humoral and cellular immune systems of the host and may die, even if it was infected by a noncytocidal virus. The immune response also may cause formation of circulating antigen-antibody complexes involving viral antigens. These complexes may deposit e. The long-term association of the virus with specific target cells may lead to altered function or responses; this type of mechanism is thought to be responsible for the progressive neurologic disease associated with slow virus infections such as kuru, Creutzfeldt-Jakob disease, or subacute sclerosing panencephalitis see Ch.

The term oncogenic transformation refers to the process through which control of cell proliferation is genetically modified, so that the cell becomes cancerous see Ch.

In the context of virus-cell interactions, the cells can also undergo various types of heritable changes, that result in biochemical, antigenic, morphologic, and physiologic alterations, called non-oncogenic transformation.

DNA viruses induce transformation only under conditions that restrict virus replication and permit survival of infected cells e. Under such conditions, immediate early e. In contrast, because RNA tumor virus replication is usually noncytocidal, they can cause oncogenic transformation in permissive cells or in their natural hosts, and viral products may be produced whether or not virus is released.

For specific details see Chapter Current data indicate that transformation of a cell involves at least two components: first, the cell gains the capacity for unlimited cell division immortalization , and second, the immortalized cells acquire the ability to produce a tumor in an appropriate host.

Some viral genes that can immortalize cells include, for example, T antigens Fig. In these cases, the viral proteins may interact and inactivate one or more cellular tumor suppresser proteins e. During the perturbed cell cycling, accumulation of mutations may occur either spontaneously or as an effect of other agents virus, chemical, radiation in cellular oncogenes e.

In vivo , the history of malignancies also suggests a multiple process of cellular evolution, involving cumulative genetic changes, selection of rare cells that have the ability to invade, metastasize, and avoid immune surveillance. The number of mutations supporting an oncogenic transformation is estimated to range from six to more. Virus infections may contribute both to immortalization and to the accumulation of mutations in growth related cellular genes during oncogenic processes.

The characteristics of oncogenically transformed cells are summarized in Table Intranuclear transforming T antigen specified by simian virus 40 in transformed human cells. Turn recording back on. National Center for Biotechnology Information , U.

Show details Baron S, editor. Search term. General Concepts Definitions Cells that support viral replication are called permissive. Cytocidal Infections Infection by cytocidal viruses is usually associated with changes in cell morphology, in cell physiology and sequential biosynthetic events. Persistent Infections Some viruses evolved the ability to remain in specific cells for long periods of time. Introduction In most cases, the disturbances of bodily function that are manifested as the signs and symptoms of viral disease result from the direct effects of viruses on cells.

Cytocidal Infections Morphologic and Structural Effects Infection of permissive cells with virus leads to productive infection and often results in cell death cytocidal, cytolytic infection.

Figure Development and progression of viral cytopathology. Figure Alteration of cytoskeleton organization by virus infection. Figure Formation of multinucleated cells. Effects on Cell Physiology Research into the pathogenesis of virus infections suggests a close correlation between cellular physiologic responses and the replication of some viruses Fig.

Figure Relationship of morphological, physiological, and biochemical cellular effects to the replication of human cytomegalovirus. Effects on Cell Biochemistry Virus binding to the cell membrane in concert with immediate early e.

Genotoxic Effects Chromosome damage may be caused directly by the virus particle or indirectly by events occurring during synthesis of new viral macromolecules RNA, DNA, protein. Figure Chromosomal aberrations resulting from cytomegalovirus infection of human peripheral blood lymphocytes.

Biologic Effects The biologic consequences of virus infection results from the aforementioned biochemical, physiological, structural, morphological and genetic changes. Relation of Cellular Effects to Viral Pathogenesis Although most of the events that damage or modify the host cell during lytic infection are difficult to separate from viral replication, the effects are not always linked directly to the production of progeny virions.

Persistent Infections Types of Persistent Infection In a persistent infection the virus is not eliminated from all of the host tissues after initial infection or the acute phase of disease. One common symptom is hyperplasia , the abnormal proliferation of cells that causes the appearance of plant tumors known as galls. Other viruses induce hypoplasia , or decreased cell growth, in the leaves of plants, causing thin, yellow areas to appear.

Still other viruses affect the plant by directly killing plant cells, a process known as cell necrosis. Other symptoms of plant viruses include malformed leaves; black streaks on the stems of the plants; altered growth of stems, leaves, or fruits; and ring spots, which are circular or linear areas of discoloration found in a leaf. Plant viruses can seriously disrupt crop growth and development, significantly affecting our food supply. They are responsible for poor crop quality and quantity globally, and can bring about huge economic losses annually.

Others viruses may damage plants used in landscaping. Some viruses that infect agricultural food plants include the name of the plant they infect, such as tomato spotted wilt virus, bean common mosaic virus, and cucumber mosaic virus. In plants used for landscaping, two of the most common viruses are peony ring spot and rose mosaic virus. There are far too many plant viruses to discuss each in detail, but symptoms of bean common mosaic virus result in lowered bean production and stunted, unproductive plants.

In the ornamental rose, the rose mosaic disease causes wavy yellow lines and colored splotches on the leaves of the plant. Animal viruses, unlike the viruses of plants and bacteria, do not have to penetrate a cell wall to gain access to the host cell. The virus may even induce the host cell to cooperate in the infection process.

As a protein in the viral capsid binds to its receptor on the host cell, the virus may be taken inside the cell via a vesicle during the normal cell process of receptor-mediated endocytosis. An alternative method of cell penetration used by non-enveloped viruses is for capsid proteins to undergo shape changes after binding to the receptor, creating channels in the host cell membrane.

Enveloped 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 that seen in 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. 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 such as intravenous drug use.

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 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.

Chronic infection of the liver by this virus leads to a much greater chance of developing liver cancer, sometimes as much as 30 years after the initial infection. As already discussed, herpes simplex virus can remain in a state of latency in nervous tissue for months, even years. 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 or weeks by destroying viruses in the skin. As a result of this type of replicative cycle, appearances of cold sores and genital herpes 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. 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 introducing genes that stimulate unregulated cell growth oncogenes or by interfering with the expression of genes that inhibit cell growth. Cancers known to be associated with viral infections include cervical cancer, caused by human papillomavirus HPV Figure 5 , liver cancer caused by hepatitis B virus, T-cell leukemia, and several types of lymphoma.

View this video to learn the various stages of the replicative cycles of animal viruses and click on the flash animation links. All Rights Reserved. Skip to content By the end of this section, you will be able to do the following: List the steps of replication and explain what occurs at each step Describe the lytic and lysogenic cycles of virus replication Explain the transmission of plant and animal viruses Discuss some of the diseases caused by plant and animal viruses Discuss the economic impact of plant and animal viruses.

Steps of Virus Infections A virus must use its host-cell processes to replicate. 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. They cause damage to fruit, leaves, and stems, which has a large economic impact. Create a visual representation to describe how viruses differ from bacteria in their modes of reproduction.

What characteristics do viruses share with living organisms? How do they differ? What evidence supports the claim that viruses do not fit our usual definition of life? This way, the virus can exit the host cell without killing it. What advantage does the virus gain by keeping the host alive? As an Amazon Associate we earn from qualifying purchases. Want to cite, share, or modify this book?

This book is Creative Commons Attribution License 4. Skip to Content Go to accessibility page. My highlights. Table of contents. The Chemistry of Life. The Cell. Evolutionary Processes. Biological Diversity.

Plant Structure and Function. Animal Structure and Function. Learning Objectives In this section, you will explore the following questions: What are the steps in viral replication, and what events occur in each? What is the difference between the lytic and lysogenic cycles of virus replication? How are plant and animal viruses transmitted, what are examples of virus-caused diseases in plants and animals, and what are the economic impacts of plant viruses? Big Idea 3 Living systems store, retrieve, transmit and respond to information essential to life processes.

Enduring Understanding 3. C The processing of genetic information is imperfect and is a source of genetic variation. Essential Knowledge 3.

Science Practice 6. Learning Objective 3. Science Practice 1. Table The video shows how viruses replicate in our body. Using the terminology provided in the video, explain how a virus attaches to a cell in our body? Figure As a result, the virus is engulfed. RNA and proteins are made and assembled into new virions. Influenza virus is packaged in a viral envelope that fuses with the plasma membrane. What advantage does the virus gain by keeping the host cell alive? Graham Beards; scale-bar data from Matt Russell.

In the lytic cycle, the phage replicates and lyses the host cell. In the lysogenic cycle, phage DNA is incorporated into the host genome, where it is passed on to subsequent generations. Environmental stressors such as starvation or exposure to toxic chemicals may cause the prophage to excise and enter the lytic cycle.

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. Erskine Palmer, B. The virus, is oncogenic and can lead to cervical cancer. Before a virus can replicate in a host cell, the capsid or envelope must be released. Larsen, Wikimedia Commons. What symptoms of plant viral diseases do you see in this light micrograph of the cells of a plant root?

By not killing the host, more viruses can be made and released from the host cell, thus ensuring the continued spread of viruses. Previous Next. Order a print copy As an Amazon Associate we earn from qualifying purchases. We recommend using a citation tool such as this one. Living systems store, retrieve, transmit and respond to information essential to life processes.