What determines the host specificity for viruses




















Publication types Research Support, Non-U. Gov't Review. Substances Viral Proteins. 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.

Entry Viruses may enter a host cell either with or without the viral capsid. Replication and Assembly The replication mechanism depends on the viral genome. 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. Figure 1: The influenza reproductive cycle. In influenza virus infection, glycoproteins on the capsid attach to a host epithelial cell.

Following this, the virus is engulfed. RNA and proteins are then made and assembled into new virions. Bacteriophages Figure 2: Bacteriophages attached to a host cell transmission electron micrograph. In bacteriophage with tails, like the one shown here, the tails serve as a passageway for transmission of the phage genome. Shao, Q. RIG-I from waterfowl and mammals differ in their abilities to induce antiviral responses against influenza A viruses.

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Jason S. You can also search for this author in PubMed Google Scholar. Correspondence to Wendy S. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

The worldwide spread of a novel pathogen. Influenza pandemics occur when a new influenza virus emerges owing to a lack of immunity in the human population. Human-adapted influenza viruses that regularly circulate and cause epidemics in the human population.



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