Other proteins, invariably glycoproteins, make up the peplomers projecting from the envelope; a second type of envelope protein is the nonglycosylated matrix protein that occurs as a layer at the inner surface of the lipid envelope of orthomyxoviruses, paramyxoviruses, and rhabdoviruses. One or more of the proteins on the surface of the virion has a specific affinity for complementary receptors present on the surface of susceptible cells; the same viral protein contains the antigenic determinants against which neutralizing antibodies are made.
Virions of several families carry a limited number of enzymes, transcriptases being the most important Table As a consequence, the composition of lipids of particular viruses differs according to the composition of the membrane lipids of the cells in which they have replicated. The poxviruses, ranaviruses, and African swine fever virus contain cellular lipid in their envelopes, and other lipids in the inner part of the virion. Lipid occurs in the outer membrane of poxviruses, and has a different composition from that of host cell lipids.
In ranaviruses and African swine fever virus the additional viral lipid occurs within the icosahedral capsid. Apart from that associated with viral nucleic acid, carbohydrate occurs as a component of viral glycoproteins, which usually occur as peplomers, with their hydrophobic ends buried in the lipid bilayer of the envelope, while their glycosylated hydrophilic ends project into the medium.
Poxviruses also contain internal glycoproteins, in the membrane of the core, and one of the outer capsid proteins of rotaviruses is glycosylated. In general, viruses are more sensitive than bacteria or fungi to inactivation by physical and chemical agents. A knowledge of their sensitivity to environmental conditions is therefore important for ensuring the preservation of the infectivity of viruses as reference reagents, and in clinical specimens collected for diagnosis, as well as for their deliberate inactivation for such practical ends as sterilization, disinfection, and the production of inactivated vaccines see Chapter 14 and Chapter The principal environmental condition that may adversely affect the infectivity of viruses in clinical specimens is too high a temperature; other important conditions are pH and lipid solvents.
Viruses vary considerably in heat stability. At ambient temperature the rate of decay of infectivity is slower but significant, expecially in hot summer weather or in the tropics in any season. The enveloped viruses are more heat labile than nonenveloped viruses. Some enveloped viruses, notably respiratory syncytial virus, tend to be inactivated by the process of freezing and subsequent thawing, probably as a result of disruption of the virion by ice crystals.
This poses problems in the collection and transportation of clinical specimens. The most practical way of avoiding such problems is to deliver specimens to the laboratory as rapidly as practicable, packed without freezing, on ice see Chapter In the laboratory, it is often necessary to preserve stocks of viable virus for years. Freeze-drying prolongs viability significantly even at ambient temperatures, and is important in enabling live viral vaccines to be used in tropical countries.
On the whole, viruses prefer an isotonic environment at physiological pH, but some virions tolerate a wide ionic and pH range. For example, whereas most enveloped viruses are inactivated at pH 5—6, adenoviruses and many picornaviruses survive the acidic pH of the stomach.
The infectivity of enveloped viruses is readily destroyed by lipid solvents such as ether or chloroform, or detergents like sodium deoxycholate, so that these agents must be avoided in laboratory procedures concerned with maintaining the viability of viruses. On the other hand, detergents are commonly used by virologists to solubilize viral envelopes and liberate proteins for use as vaccines or for chemical analysis. Sensitivity to lipid solvents is also employed as a preliminary screening test in the identification of new viral isolates, especially by arbovirologists.
National Center for Biotechnology Information , U. Veterinary Virology. Published online Jun PAUL J. Copyright and License information Disclaimer. Published by Elsevier Inc. All rights reserved. Elsevier hereby grants permission to make all its COVIDrelated research that is available on the COVID resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source.
Publisher Summary Viruses are smaller and simpler in construction than unicellular microorganisms, and they contain only one type of nucleic acid—either DNA or RNA—never both. Open in a separate window. Viral Structure In the simpler viruses the virion consists of a single molecule of nucleic acid surrounded by a protein coat, the capsid; the capsid and its enclosed nucleic acid together constitute the nucleocapsid.
PLATE Helical Symmetry The nucleocapsids of several RNA viruses have a different type of symmetry: the capsomers and nucleic acid molecule s self-assemble as a helix Fig. Nucleic Acid Any particular virus contains only a single kind of nucleic acid. DNA The genome of all DNA viruses consists of a single molecule, which is double-stranded except in the case of the parvoviruses, and may be linear or circular.
Protein Some virus-coded proteins are structural, i. Carbohydrate Apart from that associated with viral nucleic acid, carbohydrate occurs as a component of viral glycoproteins, which usually occur as peplomers, with their hydrophobic ends buried in the lipid bilayer of the envelope, while their glycosylated hydrophilic ends project into the medium. Temperature Viruses vary considerably in heat stability. Ionic Environment and pH On the whole, viruses prefer an isotonic environment at physiological pH, but some virions tolerate a wide ionic and pH range.
Lipid Solvents The infectivity of enveloped viruses is readily destroyed by lipid solvents such as ether or chloroform, or detergents like sodium deoxycholate, so that these agents must be avoided in laboratory procedures concerned with maintaining the viability of viruses.
Morphology: virus structure. In: Brown F. Williams and Wilkins; Baltimore: Design principles in virus particle construction. In: Horsfall F. Lippincott; Philadelphia: Viral membranes. In: Fraenkel-Conrat H. Plenum Press; New York: Structures of viruses. In: Mahy B. Cambridge University Press; Cambridge: Part I. Using newly developed vaccines that boost the immune response, there is hope that immune systems of affected individuals will be better able to control the virus, potentially reducing mortality rates.
Another way of treating viral infections is the use of antiviral drugs. These drugs often have limited ability to cure viral disease but have been used to control and reduce symptoms for a wide variety of viral diseases. For most viruses, these drugs inhibit the virus by blocking the actions of one or more of its proteins. It is important that the targeted proteins be encoded for by viral genes and that these molecules are not present in a healthy host cell. In this way, viral growth is inhibited without damaging the host.
There are large numbers of antiviral drugs available to treat infections, some specific for a particular virus and others that can affect multiple viruses. Antivirals have been developed to treat genital herpes herpes simplex II and influenza. For genital herpes, drugs such as acyclovir can reduce the number and duration of the episodes of active viral disease during which patients develop viral lesions in their skins cells. As the virus remains latent in nervous tissue of the body for life, this drug is not a cure but can make the symptoms of the disease more manageable.
Other antiviral drugs, such as Ribavirin, have been used to treat a variety of viral infections. By far the most successful use of antivirals has been in the treatment of the retrovirus HIV, which causes a disease that, if untreated, is usually fatal within 10—12 years after being infected. Anti-HIV drugs have been able to control viral replication to the point that individuals receiving these drugs survive for a significantly longer time than the untreated.
Drugs have been developed that inhibit the fusion of the HIV viral envelope with the plasma membrane of the host cell fusion inhibitors , the conversion of its RNA genome to double-stranded DNA reverse transcriptase inhibitors , the integration of the viral DNA into the host genome integrase inhibitors , and the processing of viral proteins protease inhibitors.
Still, even with the use of combination HAART therapy, there is concern that, over time, the virus will evolve resistance to this therapy. Thus, new anti-HIV drugs are constantly being developed with the hope of continuing the battle against this highly fatal virus. Viruses are acellular entities that can usually only be seen with an electron microscope. Viruses are diverse, infecting archaea, bacteria, fungi, plants, and animals.
Viruses consist of a nucleic-acid core surrounded by a protein capsid with or without an outer lipid envelope. Viral replication within a living cell always produces changes in the cell, sometimes resulting in cell death and sometimes slowly killing the infected cells. There are six basic stages in the virus replication cycle: attachment, penetration, uncoating, replication, assembly, and release. A viral infection may be productive, resulting in new virions, or nonproductive, meaning the virus remains inside the cell without producing new virions.
Viruses cause a variety of diseases in humans. Many of these diseases can be prevented by the use of viral vaccines, which stimulate protective immunity against the virus without causing major disease. Viral vaccines may also be used in active viral infections, boosting the ability of the immune system to control or destroy the virus.
Antiviral drugs that target enzymes and other protein products of viral genes have been developed and used with mixed success. Combinations of anti-HIV drugs have been used to effectively control the virus, extending the lifespan of infected individuals.
Learning Objectives By the end of this section, you will be able to: Describe how viruses were first discovered and how they are detected Explain the detailed steps of viral replication Describe how vaccines are used in prevention and treatment of viral diseases. Figure This figure shows three relatively complex virions: the bacteriophage T4, with its DNA-containing head group and tail fibers that attach to host cells; adenovirus, which uses spikes from its capsid to bind to the host cells; and HIV, which uses glycoproteins embedded in its envelope to do so.
Notice that HIV has proteins called matrix proteins, internal to the envelope, which help stabilize virion shape. A All viruses are encased in a viral membrane. B The capsomere is made up of small protein subunits called capsids.
C DNA is the genetic material in all viruses. D Glycoproteins help the virus attach to the host cell. As a result, the virus is engulfed. RNA and proteins are made and assembled into new virions.
The infected bacterium is referred to as a lysogen or lysogenic bacterium. In this state, the virus enjoys a stable relationship with its host, where it does not interfere with host cell metabolism or reproduction. The host cell enjoys immunity from reinfection from the same virus.
Exposure of the host cell to stressful conditions i. This event triggers the remaining steps of the lytic cycle, synthesis, maturation, and release, leading to lysis of the host cell and release of newly formed virions. OpenStax, Virus Infections and Hosts. OpenStax CNX. So, what dictates the replication type that will be used by a temperate phage? If there are plenty of host cells around, it is likely that a temperate phage will engage in the lytic cycle of replication, leading to a large increase in viral production.
If host cells are scarce, a temperate phage is more likely to enter lysogeny, allowing for viral survival until host cell numbers increase. The same is true if the number of phage in an environment greatly outnumber the host cells, since lysogeny would allow for host cells numbers to rebound, ensuring long term viral survival.
One of the best examples of this is for the bacterium Corynebacterium diphtheriae , the causative agent of diphtheria. The diphtheria toxin that causes the disease is encoded within the phage genome, so only C. Eukaryotic viruses can cause one of four different outcomes for their host cell. The most common outcome is host cell lysis, resulting from a virulent infection essentially the lytic cycle of replication seen in phage.
Some viruses can cause a latent infection , co-existing peacefully with their host cells for years much like a temperate phage during lysogeny. Some enveloped eukaryotic viruses can also be released one at a time from an infected host cell, in a type of budding process, causing a persistent infection. Lastly, certain eukaryotic viruses can cause the host cell to transform into a malignant or cancerous cell, a mechanism known as transformation.
There are many different causes of cancer, or unregulated cell growth and reproduction. Some known causes include exposure to certain chemicals or UV light. There are also certain viruses that have a known associated with the development of cancer.
Such viruses are referred to as oncoviruses. Oncoviruses can cause cancer by producing proteins that bind to host proteins known as tumor suppressor proteins , which function to regulate cell growth and to initiate programmed cell death, if needed. Projections from the envelope are known as spikes. The spikes sometimes contain essential elements for attachment of the virus to the host cell. The virus of AIDS, the human immunodeficiency virus, uses its spikes for this purpose.
Bacteriophages are viruses that multiply within bacteria. These viruses are among the more complex viruses. They often have icosahedral heads and helical tails. Viral replication. During the process of viral replication , a virus induces a living host cell to synthesize the essential components for the synthesis of new viral particles.
The particles are then assembled into the correct structure, and the newly formed virions escape from the cell to infect other cells. The first step in the replication process is attachment. In this step, the virus adsorbs to a susceptible host cell. High specificity exists between virus and cell, and the envelope spikes may unite with cell surface receptors. Receptors may exist on bacterial pili or flagella or on the host cell membrane. The next step is penetration of the virus or the viral genome into the cell.
The latter situation occurs with the bacteriophage when the tail of the phage unites with the bacterial cell wall and enzymes open a hole in the wall. The DNA of the phage penetrates through this hole. The replication steps of the process occur next. The protein capsid is stripped away from the genome, and the genome is freed in the cell cytoplasm. If the genome consists of RNA, the genome acts as a messenger RNA molecule and provides the genetic codes for the synthesis of enzymes.
The enzymes are used for the synthesis of viral genomes and capsomeres and the assembly of these components into new viruses.
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