Skip to ContentGo to accessibility pageKeyboard shortcuts menu
OpenStax Logo
Biology

21.2 Virus Infections and Hosts

Biology21.2 Virus Infections and Hosts

Learning Objectives

By the end of this section, you will be able to:
  • List the steps of replication and explain what occurs at each step
  • Describe the lytic and lysogenic cycles of virus replication
  • Explain the transmission and diseases of animal and plant viruses
  • Discuss the economic impact of animal and plant viruses

Viruses can be seen as obligate, intracellular parasites. A virus must attach to a living cell, be taken inside, manufacture its proteins and copy its genome, and find a way to escape the cell so that the virus can infect other cells. Viruses can infect only certain species of hosts and only certain cells within that host. Cells that a virus may use to replicate are called permissive. For most viruses, the molecular basis for this specificity is that a particular surface molecule known as the viral receptor must be found on the host cell surface for the virus to attach. Also, metabolic and host cell immune response differences seen in different cell types based on differential gene expression are a likely factor in which cells a virus may target for replication. The permissive cell must make the substances that the virus needs or the virus will not be able to replicate there.

Steps of Virus Infections

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 or “cell suicide”), 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 the virus from the body, and from cell damage caused by the virus. Many animal viruses, such as HIV (human immunodeficiency virus), 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.

Link to Learning

Link to Learning

QR Code representing a URL

This video explains how influenza attacks the body.

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, such as HIV, 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 HIV produces some of its own enzymes not found in the host has allowed researchers to develop drugs that inhibit these enzymes. These drugs, including the reverse transcriptase inhibitor AZT, inhibit HIV 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 HIV and has been effective at reducing the number of infectious virions (copies of viral RNA) in the blood to non-detectable levels in many HIV-infected individuals.

Egress

The last stage of viral replication is the release of the new virions produced in the host organism, where they are able to infect adjacent cells and repeat the replication cycle. As you’ve learned, some viruses are released when the host cell dies, and other viruses can leave infected cells by budding through the membrane without directly killing the cell.

Visual Connection

Art Connection

The illustration shows the steps of an influenza virus infection. In step 1, influenza virus becomes attached to a target epithelial cell. In step 2, the cell engulfs the virus by endocytosis, and the virus becomes encased in the cell’s plasma membrane. In step 3, the membrane dissolves, and the viral contents are released into the cytoplasm. Viral mRNA enters the nucleus, where it is replicated by viral RNA polymerase. In step 4, viral mRNA exits to the cytoplasm, where it is used to make viral proteins. In step 5, new viral particles are released into the extracellular fluid. The cell, which is not killed in the process, continues to make new virus.
Figure 21.8 In influenza virus infection, glycoproteins attach to a host epithelial cell. 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. This way, the virus can exit the host cell without killing it. What advantage does the virus gain by keeping the host cell alive?

Link to Learning

Link to Learning

QR Code representing a URL

Watch a video on viruses, identifying structures, modes of transmission, replication, and more.

Different Hosts and Their Viruses

As you’ve learned, viruses are often very specific as to which hosts and which cells within the host they will infect. This feature of a virus makes it specific to one or a few species of life on Earth. On the other hand, so many different types of viruses exist on Earth that nearly every living organism has its own set of viruses that tries to infect its cells. Even the smallest and simplest of cells, prokaryotic bacteria, may be attacked by specific types of viruses.

Bacteriophages

The micrograph shows hexagonal bacteriophage capsids attached to a host bacterial cell by slender stalks.
Figure 21.9 This transmission electron micrograph shows bacteriophages attached to a bacterial cell. (credit: modification of work by Dr. Graham Beards; scale-bar data from Matt Russell)

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 the E. coli bacterium. Viruses that infect plant or animal cells may also undergo infections where they are not producing virions for long periods. An example is the animal herpesviruses, including herpes simplex viruses, the cause of oral and genital herpes in humans. In a process called latency, these viruses can exist in nervous tissue for long periods of time without producing new virions, only to leave latency periodically and cause lesions in the skin where the virus replicates. Even though there are similarities between lysogeny and latency, the term lysogenic cycle is usually reserved to describe bacteriophages. Latency will be described in more detail below.

Visual Connection

Art Connection

The bacteriophage lytic cycle begins when the phage attaches via a slender stalk to the host cell. Linear DNA from the viral head is injected into the host cell. The phage DNA circularizes, remaining separate from the host DNA. The phage DNA replicates, and new phage proteins are made. New phage particles are assembled. The cell lyses, releasing the phage. The bacteriophage lysogenic cycle begins the same way as the lytic cycle, with phage infecting a host cell. However, the phage DNA becomes incorporated into the host genome. The cell divides, and phage DNA is passed on to daughter cells. Under stressful conditions, the phage DNA is excised from the bacterial chromosome and enters the lytic cycle.
Figure 21.10 A temperate bacteriophage has both lytic and lysogenic cycles. 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.

Which of the following statements is false?

  1. In the lytic cycle, new phage are produced and released into the environment.
  2. In the lysogenic cycle, phage DNA is incorporated into the host genome.
  3. An environmental stressor can cause the phage to initiate the lysogenic cycle.
  4. Cell lysis only occurs in the lytic cycle.

Animal Viruses

Animal viruses, unlike the viruses of plants and bacteria, do not have to penetrate a cell wall to gain access to the host cell. Non-enveloped or “naked” animal viruses may enter cells in two different ways. 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. The viral genome is then “injected” into the host cell through these channels in a manner analogous to that used by many bacteriophages. 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 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. As we have already discussed using the example of HIV, 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 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 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. 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. 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 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. 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).

Part a shows a micrograph of the varicella-zoster virus, which has an icosahedral capsid surrounded by an irregularly shaped envelope. Part b shows a red, bumpy shingles rash on a person’s face.
Figure 21.11 (a) Varicella-zoster, the virus that causes chickenpox, has an enveloped icosahedral capsid visible in this 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)

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 inhibit cell growth. Oncogenic viruses can be either DNA or RNA viruses. Cancers known to be associated with viral infections include cervical cancer caused by human papillomavirus (HPV) (Figure 21.12), liver cancer caused by hepatitis B virus, T-cell leukemia, and several types of lymphoma.

The micrograph shows an icosahedral virus with glycoproteins protruding from its capsid.
Figure 21.12 HPV, or human papillomavirus, has a naked icosahedral capsid visible in this transmission electron micrograph and a double-stranded DNA genome that is incorporated into the host DNA. The virus, which is sexually transmitted, is oncogenic and can lead to cervical cancer. (credit: modification of work by NCI, NIH; scale-bar data from Matt Russell)

Link to Learning

Link to Learning

QR Code representing a URL

Visit the interactive animations showing the various stages of the replicative cycles of animal viruses and click on the flash animation links.

Plant Viruses

Plant viruses, like other viruses, contain a core of either DNA or RNA. You have already learned about one of these, the tobacco mosaic virus. As plant cells have a cell wall to protect their cells, these viruses do not use receptor-mediated endocytosis to enter host cells as is seen with animal viruses. For many plant viruses to be transferred from plant to plant, damage to some of the plants’ cells must occur to allow the virus to enter a new host. This damage is often caused by weather, insects, animals, fire, or human activities like farming or landscaping. Additionally, plant offspring may inherit viral diseases from parent plants. Plant viruses can be transmitted by a variety of vectors, through contact with an infected plant’s sap, by living organisms such as insects and nematodes, and through pollen. When plants viruses are transferred between different plants, this is known as horizontal transmission, and when they are inherited from a parent, this is called vertical transmission.

Symptoms of viral diseases vary according to the virus and its host (Table 21.4). 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.

Some Common Symptoms of Plant Viral Diseases
Symptom Appears as
Hyperplasia Galls (tumors)
Hypoplasia Thinned, yellow splotches on leaves
Cell necrosis Dead, blackened stems, leaves, or fruit
Abnormal growth patterns Malformed stems, leaves, or fruit
Discoloration Yellow, red, or black lines, or rings in stems, leaves, or fruit
Table 21.4

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.

Order a print copy

As an Amazon Associate we earn from qualifying purchases.

Citation/Attribution

This book may not be used in the training of large language models or otherwise be ingested into large language models or generative AI offerings without OpenStax's permission.

Want to cite, share, or modify this book? This book uses the Creative Commons Attribution License and you must attribute OpenStax.

Attribution information
  • If you are redistributing all or part of this book in a print format, then you must include on every physical page the following attribution:
    Access for free at https://openstax.org/books/biology/pages/1-introduction
  • If you are redistributing all or part of this book in a digital format, then you must include on every digital page view the following attribution:
    Access for free at https://openstax.org/books/biology/pages/1-introduction
Citation information

© Feb 14, 2022 OpenStax. Textbook content produced by OpenStax is licensed under a Creative Commons Attribution License . The OpenStax name, OpenStax logo, OpenStax book covers, OpenStax CNX name, and OpenStax CNX logo are not subject to the Creative Commons license and may not be reproduced without the prior and express written consent of Rice University.