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No one knows exactly when viruses emerged or from where they came, since viruses do not leave historical footprints such as fossils. Viruses were first discovered after the development of a porcelain filter, called the Chamberland-Pasteur filter, which could remove all bacteria visible under the microscope from any liquid sample. It was not until the development of the electron microscope in the 1940s that scientists got their first good view of the structure of the tobacco mosaic virus ([link]) and others. The use of this technology has allowed for the discovery of many viruses of all types of living organisms.
A virion consists of a nucleic-acid core, an outer protein coating, and sometimes an outer envelope made of protein and phospholipid membranes derived from the host cell.
Viruses come in many shapes and sizes, but these are consistent and distinct for each viral family ([link]).
Adenovirus, a nonenveloped animal virus that causes respiratory illnesses in humans, uses protein spikes protruding from its capsomeres to attach to the host cell.
Enveloped virions like HIV (human immunodeficiency virus), the causative agent in AIDS (acquired immune deficiency syndrome), consist of nucleic acid (RNA in the case of HIV) and capsid proteins surrounded by a phospholipid bilayer envelope and its associated proteins ([link]). Overall, the shape of the virion and the presence or absence of an envelope tells us little about what diseases the viruses may cause or what species they might infect, but is still a useful means to begin viral classification. Unlike all living organisms that use DNA as their genetic material, viruses may use either DNA or RNA as theirs. A virus attaches to a specific receptor site on the host-cell membrane through attachment proteins in the capsid or proteins embedded in its envelope.
Unlike animal viruses, the nucleic acid of bacteriophages is injected into the host cell naked, leaving the capsid outside the cell. The last stage of viral replication is the release of the new virions into the host organism, where they are able to infect adjacent cells and repeat the replication cycle. Click through this tutorial on viruses to identify structures, modes of transmission, replication, and more. Viruses cause a variety of diseases in animals, including humans, ranging from the common cold to potentially fatal illnesses like meningitis ([link]). While we do have limited numbers of effective antiviral drugs, such as those used to treat HIV and influenza, the primary method of controlling viral disease is by vaccination, which is intended to prevent outbreaks by building immunity to a virus or virus family. Weakened live viral vaccines are designed in the laboratory to cause few symptoms in recipients while giving them immunity against future infections. Live vaccines are usually made by attenuation (weakening) of the “wild-type” (disease-causing) virus by growing it in the laboratory in tissues or at temperatures different from what the virus is accustomed to in the host. Some vaccines are in continuous development because certain viruses, such as influenza and HIV, have a high mutation rate compared to other viruses or host cells.
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 inhibit viral replication at many different phases of the HIV replicative cycle.
When any of these drugs are used individually, the virus’ high mutation rate allows the virus to rapidly evolve resistance to the drug. Viral replication within a living cell always produces changes in the cell, sometimes resulting in cell death and sometimes slowly killing the infected cells. The virus cannot attach to dog cells because dog cells do not express the receptors for the virus or there is no cell within the dog that is permissive for viral replication. Rabies vaccine works after a bite because it takes two weeks for the virus to travel from the site of the bite to the central nervous system, where the most severe symptoms of the disease occur.
When checked, Shutterstock's safe search screens restricted content and excludes it from your search results. Also called ‘flat warts’, these are most common in humans, which are although sometimes unsightly and sometimes painful. Modern viruses are thought to be a mosaic of bits and pieces of nucleic acids picked up from various sources along their respective evolutionary paths. They vary in their structure, their replication methods, and in their target hosts or even host cells.
In 1886, Adolph Meyer demonstrated that a disease of tobacco plants, tobacco mosaic disease, could be transferred from a diseased plant to a healthy one through liquid plant extracts.
The surface structure of virions can be observed by both scanning and transmission electron microscopy, whereas the internal structures of the virus can only be observed in images from a transmission electron microscope ([link]).
They were initially grouped by shared morphology, meaning their size, shape, and distinguishing structures.
The most visible difference between members of viral families is their morphology, which is quite diverse. All virions have a nucleic-acid genome covered by a protective layer of protein, called a capsid. Nonenveloped viruses also include those that cause polio (poliovirus), plantar warts (papillomavirus), and hepatitis A (hepatitis A virus).
Chicken pox, influenza, and mumps are examples of diseases caused by viruses with envelopes.
The viral DNA directs the host cell’s replication proteins to synthesize new copies of the viral genome and to transcribe and translate that genome into viral proteins.
To replicate their genomes in the host cell, the genomes of RNA viruses encode enzymes not found in host cells. The 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 the virus can infect other cells and ultimately other individuals. The viral replication cycle can produce dramatic biochemical and structural changes in the host cell, which may cause cell damage. The attachment is specific, and typically a virus will only attach to cells of one or a few species and only certain cell types within those species with the appropriate receptors. Plant and animal viruses can enter their cells through endocytosis, in which the cell membrane surrounds and engulfs the entire virus. DNA viruses usually use host cell proteins and enzymes to make additional DNA that is used to copy the genome or be transcribed to messenger RNA (mRNA), which is then used in protein synthesis. 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.


These diseases can be treated by antiviral drugs or by vaccines, but some viruses, such as HIV, are capable of avoiding the immune response and mutating so as to become resistant to antiviral drugs.
A vaccine may be prepared using weakened live viruses, killed viruses, or molecular subunits of the virus. For example, the virus may be grown in cells in a test tube, in bird embryos, or in live animals. With influenza, mutation in genes for the surface molecules helps the virus evade the protective immunity that may have been obtained in a previous influenza season, making it necessary for individuals to get vaccinated every year.
In the case of rabies, a fatal neurological disease transmitted in the saliva of rabies virus-infected animals, the progression of the disease from the time of the animal bite to the time it enters the central nervous system may be two weeks or longer. 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 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. 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).
The breakthrough in the treatment of HIV was the development of highly active anti-retroviral therapy (HAART), which involves a mixture of different drugs, sometimes called a drug “cocktail.” By attacking the virus at different stages of its replication cycle, it is difficult for the virus to develop resistance to multiple drugs at the same time.
Their genomes contain either DNA or RNA, and they replicate using the replication proteins of a host cell.
There are six basic stages in the virus replication cycle: attachment, penetration, uncoating, replication, assembly, and release. Many of these diseases can be prevented by the use of viral vaccines, which stimulate protective immunity against the virus without causing major disease. The vaccine is able to cause an immune response in the body during this time that clears the infection before it reaches the nervous system.
Viruses are acellular, parasitic entities that are not classified within any domain because they are not considered alive. While most biological diversity can be understood through evolutionary history, such as how species have adapted to conditions and environments, much about virus origins and evolution remains unknown. In 1892, Dmitri Ivanowski showed that this disease could be transmitted in this way even after the Chamberland-Pasteur filter had removed all viable bacteria from the extract.
Unlike bacteria (which are about 100 times larger), we cannot see viruses with a light microscope, with the exception of some large virions of the poxvirus family ([link]).
Later, groups of viruses were classified by the type of nucleic acid they contained, DNA or RNA, and whether their nucleic acid was single- or double-stranded. An interesting feature of viral complexity is that the complexity of the host does not correlate to the complexity of the virion. Nonenveloped viruses tend to be more robust and more likely to survive under harsh conditions, such as the gut. Because of the fragility of the envelope, nonenveloped viruses are more resistant to changes in temperature, pH, and some disinfectants than enveloped viruses. Viral genomes tend to be small compared to bacteria or eukaryotes, containing only those genes that code for proteins the virus cannot get from the host cell. DNA viruses cause human diseases such as chickenpox, hepatitis B, and some venereal diseases like herpes and genital warts. RNA polymerase enzymes are not as stable as DNA polymerases and often make mistakes during transcription.
These changes, called cytopathic effects, can change cell functions or even destroy the cell. Some enveloped viruses enter the cell when the viral envelope fuses directly with the cell membrane. RNA viruses, such as the influenza virus, usually use the RNA core as a template for synthesis of viral genomic RNA and mRNA. In general, live viruses lead to better immunity, but have the possibility of causing disease at some low frequency. The adaptation to these new cells or temperature induces mutations in the virus’ genomes, allowing them to grow better in the laboratory while inhibiting their ability to cause disease when reintroduced into the conditions found in the host. Other viruses, such as those that cause the childhood diseases measles, mumps, and rubella, mutate so little that the same vaccine is used year after year. This is enough time to vaccinate an individual who suspects being bitten by a rabid animal, and the boosted immune response from the vaccination is enough to prevent the virus from entering nervous tissue. For most viruses, these drugs inhibit the virus by blocking the actions of one or more of its proteins.
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. Still, even with the use of combination HAART therapy, there is concern that, over time, the virus will evolve resistance to this therapy.
A viral infection may be productive, resulting in new virions, or nonproductive, meaning the virus remains inside the cell without producing new virions. Viral vaccines may also be used in active viral infections, boosting the ability of the immune system to control or destroy the virus. They have no plasma membrane, internal organelles, or metabolic processes, and they do not divide. Still, it was many years before it was proven that these “filterable” infectious agents were not simply very small bacteria but were a new type of tiny, disease-causing particle.
More recently, molecular analysis of viral replication cycles has further refined their classification. Some of the most complex virion structures are observed in bacteriophages, viruses that infect the simplest living organisms, bacteria. Some viral capsids are simple polyhedral “spheres,” whereas others are quite complex in structure. For this reason, mutations, changes in the nucleotide sequence, in RNA viruses occur more frequently than in DNA 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.


Some infected cells, such as those infected by the common cold virus (rhinovirus), die through lysis (bursting) or apoptosis (programmed cell death or “cell suicide”), releasing all the progeny virions at once. Once inside the cell, the viral capsid is degraded and the viral nucleic acid is released, which then becomes available for replication and transcription.
The viral mRNA is translated into viral enzymes and capsid proteins to assemble new virions ([link]). Killed viral vaccine and the subunit viruses are both incapable of causing disease, but in general lead to less effective or long-lasting immunity. These attenuated viruses thus still cause an infection, but they do not grow very well, allowing the immune response to develop in time to prevent major disease.
Thus, the fatal neurological consequences of the disease are averted and the individual only has to recover from the infected bite. 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. For influenza, drugs like Tamiflu can reduce the duration of “flu” symptoms by one or two days, but the drug does not prevent symptoms entirely. Thus, new anti-HIV drugs are constantly being developed with the hope of continuing the battle against this highly fatal virus.
Viruses consist of a nucleic-acid core surrounded by a protein capsid with or without an outer lipid envelope. Antiviral drugs that target enzymes and other protein products of viral genes have been developed and used with mixed success. Along with the lips, these warts can be found on chin, cheeks, forehead, neck, arms and hand.Person, who has developed this type of condition, should avoid picking them.
Instead, they infect a host cell and use the host’s replication processes to produce progeny virus particles. Also, metabolic differences seen in different cell types based on differential gene expression are a likely factor in which cells a virus may use to replicate. 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.
The success of the polio vaccine paved the way for the routine dispensation of childhood vaccines against measles, mumps, rubella, chickenpox, and other diseases. The danger of using live vaccines, which are usually more effective than killed vaccines, is the low but significant risk that these viruses will revert back to their disease-causing form by back mutations. This approach is also being used for the treatment of Ebola, one of the fastest and most deadly viruses affecting humans, though usually infecting limited populations.
Other antiviral drugs, such as Ribavirin, have been used to treat a variety of viral infections. Combinations of anti-HIV drugs have been used to effectively control the virus, extending the lifespan of infected individuals.
Viruses infect all forms of organisms including bacteria, archaea, fungi, plants, and animals. All viruses use some sort of glycoprotein to attach to their host cells at molecules on the cell called viral receptors.
While most viruses contain a single segment of nucleic acid, others have genomes that consist of several segments.
For example, the fact that influenza is an RNA virus is one reason a new flu vaccine is needed every year. The cell must be making the substances the virus needs, such as enzymes the virus genome itself does not have genes for, or the virus will not be able to replicate using that cell.
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. 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. Back mutations occur when the vaccine undergoes mutations in the host such that it readapts to the host and can again cause disease, which can then be spread to other humans in an epidemic. There are large numbers of antiviral drugs available to treat infections, some specific for a particular virus and others that can affect multiple viruses.
The virus exploits these cell-surface molecules, which the cell uses for some other purpose, as a way to recognize and infect specific cell types. Retroviruses, such as HIV, have an RNA genome that must be reverse transcribed to make DNA, which then is inserted into the host’s DNA.
This happened as recently as 2007 in Nigeria where mutations in a polio vaccine led to an epidemic of polio in that country. Transmitted by bats and great apes, this virus can cause death in 70–90 percent of the infected within two weeks. For example, the measles virus uses a cell-surface glycoprotein in humans that normally functions in immune reactions and possibly in the sperm-egg interaction at fertilization.
However, the damage to the cells that HIV infects may make it impossible for the cells to function as mediators of immunity, even though the cells remain alive for a period of time. To convert RNA into DNA, retroviruses contain genes that encode the virus-specific enzyme reverse transcriptase that transcribes an RNA template to DNA.
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. Since most warts are the result of virus, it is important for people to be well cleaned after vising public places. Attachment is a requirement for viruses to later penetrate the cell membrane, inject the viral genome, and complete their replication inside the cell. Most productive viral infections follow similar steps in the virus replication cycle: attachment, penetration, uncoating, replication, assembly, and release.
The fact that HIV produces some of its own enzymes, which are 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.



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