Introduction to viruses

Last updated

Illustration of a SARS-CoV-2 virion Coronavirus. SARS-CoV-2.png
Illustration of a SARS-CoV-2 virion

A virus is a tiny infectious agent that reproduces inside the cells of living hosts. When infected, the host cell is forced to rapidly produce thousands of identical copies of the original virus. Unlike most living things, viruses do not have cells that divide; new viruses assemble in the infected host cell. But unlike simpler infectious agents like prions, they contain genes, which allow them to mutate and evolve. Over 4,800 species of viruses have been described in detail [1] out of the millions in the environment. Their origin is unclear: some may have evolved from plasmids—pieces of DNA that can move between cells—while others may have evolved from bacteria.

Contents

Viruses are made of either two or three parts. All include genes. These genes contain the encoded biological information of the virus and are built from either DNA or RNA. All viruses are also covered with a protein coat to protect the genes. Some viruses may also have an envelope of fat-like substance that covers the protein coat, and makes them vulnerable to soap. A virus with this "viral envelope" uses it—along with specific receptors—to enter a new host cell. Viruses vary in shape from the simple helical and icosahedral to more complex structures. Viruses range in size from 20 to 300 nanometres; it would take 33,000 to 500,000 of them, side by side, to stretch to 1 centimetre (0.4 in).

Viruses spread in many ways. Although many are very specific about which host species or tissue they attack, each species of virus relies on a particular method to copy itself. Plant viruses are often spread from plant to plant by insects and other organisms, known as vectors . Some viruses of humans and other animals are spread by exposure to infected bodily fluids. Viruses such as influenza are spread through the air by droplets of moisture when people cough or sneeze. Viruses such as norovirus are transmitted by the faecal–oral route, which involves the contamination of hands, food and water. Rotavirus is often spread by direct contact with infected children. The human immunodeficiency virus, HIV, is transmitted by bodily fluids transferred during sex. Others, such as the dengue virus, are spread by blood-sucking insects.

Viruses, especially those made of RNA, can mutate rapidly to give rise to new types. Hosts may have little protection against such new forms. Influenza virus, for example, changes often, so a new vaccine is needed each year. Major changes can cause pandemics, as in the 2009 swine influenza that spread to most countries. Often, these mutations take place when the virus has first infected other animal hosts. Some examples of such "zoonotic" diseases include coronavirus in bats, and influenza in pigs and birds, before those viruses were transferred to humans.

Viral infections can cause disease in humans, animals and plants. In healthy humans and animals, infections are usually eliminated by the immune system, which can provide lifetime immunity to the host for that virus. Antibiotics, which work against bacteria, have no impact, but antiviral drugs can treat life-threatening infections. Those vaccines that produce lifelong immunity can prevent some infections.

Discovery

Scanning electron micrograph of HIV-1 viruses, coloured green, budding from a lymphocyte HIV-budding-Color cropped.jpg
Scanning electron micrograph of HIV-1 viruses, coloured green, budding from a lymphocyte

In 1884, French microbiologist Charles Chamberland invented the Chamberland filter (or Chamberland–Pasteur filter), that contains pores smaller than bacteria. He could then pass a solution containing bacteria through the filter, and completely remove them. In the early 1890s, Russian biologist Dmitri Ivanovsky used this method to study what became known as the tobacco mosaic virus. His experiments showed that extracts from the crushed leaves of infected tobacco plants remain infectious after filtration. [2]

At the same time, several other scientists showed that, although these agents (later called viruses) were different from bacteria and about one hundred times smaller, they could still cause disease. In 1899, Dutch microbiologist Martinus Beijerinck observed that the agent only multiplied when in dividing cells. He called it a "contagious living fluid" (Latin : contagium vivum fluidum )—or a "soluble living germ" because he could not find any germ-like particles. [3] In the early 20th century, English bacteriologist Frederick Twort discovered viruses that infect bacteria, [4] and French-Canadian microbiologist Félix d'Herelle described viruses that, when added to bacteria growing on agar, would lead to the formation of whole areas of dead bacteria. Counting these dead areas allowed him to calculate the number of viruses in the suspension. [5]

The invention of the electron microscope in 1931 brought the first images of viruses. [6] In 1935, American biochemist and virologist Wendell Meredith Stanley examined the tobacco mosaic virus (TMV) and found it to be mainly made from protein. [7] A short time later, this virus was shown to be made from protein and RNA. [8] Rosalind Franklin developed X-ray crystallographic pictures and determined the full structure of TMV in 1955. [9] Franklin confirmed that viral proteins formed a spiral hollow tube, wrapped by RNA, and also showed that viral RNA was a single strand, not a double helix like DNA. [10]

A problem for early scientists was that they did not know how to grow viruses without using live animals. The breakthrough came in 1931, when American pathologists Ernest William Goodpasture and Alice Miles Woodruff grew influenza, and several other viruses, in fertilised chickens' eggs. [11] Some viruses could not be grown in chickens' eggs. This problem was solved in 1949, when John Franklin Enders, Thomas Huckle Weller, and Frederick Chapman Robbins grew polio virus in cultures of living animal cells. [12] Over 4,800 species of viruses have been described in detail. [1]

Origins

Viruses co-exist with life wherever it occurs. They have probably existed since living cells first evolved. Their origin remains unclear because they do not fossilize, so molecular techniques have been the best way to hypothesise about how they arose. These techniques rely on the availability of ancient viral DNA or RNA, but most viruses that have been preserved and stored in laboratories are less than 90 years old. [13] [14] Molecular methods have only been successful in tracing the ancestry of viruses that evolved in the 20th century. [15] New groups of viruses might have repeatedly emerged at all stages of the evolution of life. [16] There are three major theories about the origins of viruses: [16] [17]

Regressive theory
Viruses may have once been small cells that parasitised larger cells. Eventually, the genes they no longer needed for a parasitic way of life were lost. The bacteria Rickettsia and Chlamydia are living cells that, like viruses, can reproduce only inside host cells. This lends credence to this theory, as their dependence on being parasites may have led to the loss of the genes that once allowed them to live on their own. [18]
Cellular origin theory
Some viruses may have evolved from bits of DNA or RNA that "escaped" from the genes of a larger organism. The escaped DNA could have come from plasmids—pieces of DNA that can move between cells—while others may have evolved from bacteria. [19]
Coevolution theory
Viruses may have evolved from complex molecules of protein and DNA at the same time as cells first appeared on earth, and would have depended on cellular life for many millions of years. [20]

There are problems with all of these theories. The regressive hypothesis does not explain why even the smallest of cellular parasites do not resemble viruses in any way. The escape or the cellular origin hypothesis does not explain the presence of unique structures in viruses that do not appear in cells. The coevolution, or "virus-first" hypothesis, conflicts with the definition of viruses, because viruses depend on host cells. [20] [21] Also, viruses are recognised as ancient, and to have origins that pre-date the divergence of life into the three domains. [22] This discovery has led modern virologists to reconsider and re-evaluate these three classical hypotheses. [16] [22]

Structure

Simplified diagram of the structure of a virus Basic Scheme of Virus en.svg
Simplified diagram of the structure of a virus

A virus particle, also called a virion, consists of genes made from DNA or RNA which are surrounded by a protective coat of protein called a capsid. [23] The capsid is made of many smaller, identical protein molecules called capsomers. The arrangement of the capsomers can either be icosahedral (20-sided), helical, or more complex. There is an inner shell around the DNA or RNA called the nucleocapsid, made out of proteins. Some viruses are surrounded by a bubble of lipid (fat) called an envelope, which makes them vulnerable to soap and alcohol. [24]

Size

Virions of some of the most common human viruses with their relative size. The nucleic acids are not to scale. Virus size.png
Virions of some of the most common human viruses with their relative size. The nucleic acids are not to scale.

Viruses are among the smallest infectious agents, and are too small to be seen by light microscopy; most of them can only be seen by electron microscopy. Their sizes range from 20 to 300  nanometres; it would take 30,000 to 500,000 of them, side by side, to stretch to one centimetre (0.4 in). [23] In comparison, bacteria are typically around 1000 nanometres (1 micrometer) in diameter, and host cells of higher organisms are typically a few tens of micrometers. Some viruses such as megaviruses and pandoraviruses are relatively large viruses. At around 1000 nanometres, these viruses, which infect amoebae, were discovered in 2003 and 2013. [25] [26] They are around ten times wider (and thus a thousand times larger in volume) than influenza viruses, and the discovery of these "giant" viruses astonished scientists. [27]

Genes

The genes of viruses are made from DNA (deoxyribonucleic acid) and, in many viruses, RNA (ribonucleic acid). The biological information contained in an organism is encoded in its DNA or RNA. Most organisms use DNA, but many viruses have RNA as their genetic material. The DNA or RNA of viruses consists of either a single strand or a double helix. [28]

Viruses can reproduce rapidly because they have relatively few genes. For example, influenza virus has only eight genes and rotavirus has eleven. In comparison, humans have 20,000–25,000. Some viral genes contain the code to make the structural proteins that form the virus particle. Other genes make non-structural proteins found only in the cells the virus infects. [29] [30]

All cells, and many viruses, produce proteins that are enzymes that drive chemical reactions. Some of these enzymes, called DNA polymerase and RNA polymerase, make new copies of DNA and RNA. A virus's polymerase enzymes are often much more efficient at making DNA and RNA than the equivalent enzymes of the host cells, [31] but viral RNA polymerase enzymes are error-prone, causing RNA viruses to mutate and form new strains. [32]

In some species of RNA virus, the genes are not on a continuous molecule of RNA, but are separated. The influenza virus, for example, has eight separate genes made of RNA. When two different strains of influenza virus infect the same cell, these genes can mix and produce new strains of the virus in a process called reassortment. [33]

Protein synthesis

Diagram of a typical eukaryotic cell, showing subcellular components. Organelles: (1) nucleolus (2) nucleus (3) ribosome (4) vesicle (5) rough endoplasmic reticulum (ER) (6) Golgi apparatus (7) cytoskeleton (8) smooth ER (9) mitochondria (10) vacuole (11) cytoplasm (12) lysosome (13) centrioles within centrosome (14) a virus shown to approximate scale Cell with Virus.png
Diagram of a typical eukaryotic cell, showing subcellular components. Organelles: (1) nucleolus (2) nucleus (3) ribosome (4) vesicle (5) rough endoplasmic reticulum (ER) (6) Golgi apparatus (7) cytoskeleton (8) smooth ER (9) mitochondria (10) vacuole (11) cytoplasm (12) lysosome (13) centrioles within centrosome (14) a virus shown to approximate scale

Proteins are essential to life. Cells produce new protein molecules from amino acid building blocks based on information coded in DNA. Each type of protein is a specialist that usually only performs one function, so if a cell needs to do something new, it must make a new protein. Viruses force the cell to make new proteins that the cell does not need, but are needed for the virus to reproduce. Protein synthesis consists of two major steps: transcription and translation. [34]

Transcription is the process where information in DNA, called the genetic code, is used to produce RNA copies called messenger RNA (mRNA). These migrate through the cell and carry the code to ribosomes where it is used to make proteins. This is called translation because the protein's amino acid structure is determined by the mRNA's code. Information is hence translated from the language of nucleic acids to the language of amino acids. [34]

Some nucleic acids of RNA viruses function directly as mRNA without further modification. For this reason, these viruses are called positive-sense RNA viruses. [35] In other RNA viruses, the RNA is a complementary copy of mRNA and these viruses rely on the cell's or their own enzyme to make mRNA. These are called negative-sense RNA viruses. In viruses made from DNA, the method of mRNA production is similar to that of the cell. The species of viruses called retroviruses behave completely differently: they have RNA, but inside the host cell a DNA copy of their RNA is made with the help of the enzyme reverse transcriptase. This DNA is then incorporated into the host's own DNA, and copied into mRNA by the cell's normal pathways. [36]

Life-cycle

Life-cycle of a typical virus (left to right); following infection of a cell by a single virus, hundreds of offspring are released. HepC replication.png
Life-cycle of a typical virus (left to right); following infection of a cell by a single virus, hundreds of offspring are released.

When a virus infects a cell, the virus forces it to make thousands more viruses. It does this by making the cell copy the virus's DNA or RNA, making viral proteins, which all assemble to form new virus particles. [37]

There are six basic, overlapping stages in the life cycle of viruses in living cells: [38]

Effects on the host cell

Viruses have an extensive range of structural and biochemical effects on the host cell. [39] These are called cytopathic effects . [40] Most virus infections eventually result in the death of the host cell. The causes of death include cell lysis (bursting), alterations to the cell's surface membrane and apoptosis (cell "suicide"). [41] Often cell death is caused by cessation of its normal activity due to proteins produced by the virus, not all of which are components of the virus particle. [42]

Some viruses cause no apparent changes to the infected cell. Cells in which the virus is latent (inactive) show few signs of infection and often function normally. [43] This causes persistent infections and the virus is often dormant for many months or years. This is often the case with herpes viruses. [44] [45]

Some viruses, such as Epstein–Barr virus, often cause cells to proliferate without causing malignancy; [46] but some other viruses, such as papillomavirus, are an established cause of cancer. [47] When a cell's DNA is damaged by a virus such that the cell cannot repair itself, this often triggers apoptosis. One of the results of apoptosis is destruction of the damaged DNA by the cell itself. Some viruses have mechanisms to limit apoptosis so that the host cell does not die before progeny viruses have been produced; HIV, for example, does this. [48]

Viruses and diseases

There are many ways in which viruses spread from host to host but each species of virus uses only one or two. Many viruses that infect plants are carried by organisms; such organisms are called vectors. Some viruses that infect animals, including humans, are also spread by vectors, usually blood-sucking insects, but direct transmission is more common. Some virus infections, such as norovirus and rotavirus, are spread by contaminated food and water, by hands and communal objects, and by intimate contact with another infected person, while others like SARS-CoV-2 and influenza viruses are airborne. Viruses such as HIV, hepatitis B and hepatitis C are often transmitted by unprotected sex or contaminated hypodermic needles. To prevent infections and epidemics, it is important to know how each different kind of virus is spread. [49]

In humans

Common human diseases caused by viruses include the common cold, influenza, chickenpox and cold sores. Serious diseases such as Ebola and AIDS are also caused by viruses. [50] Many viruses cause little or no disease and are said to be "benign". The more harmful viruses are described as virulent. [51] Viruses cause different diseases depending on the types of cell that they infect. Some viruses can cause lifelong or chronic infections where the viruses continue to reproduce in the body despite the host's defence mechanisms. [52] This is common in hepatitis B virus and hepatitis C virus infections. People chronically infected with a virus are known as carriers. They serve as important reservoirs of the virus. [53] [54]

Endemic

If the proportion of carriers in a given population reaches a given threshold, a disease is said to be endemic. [55] Before the advent of vaccination, infections with viruses were common and outbreaks occurred regularly. In countries with a temperate climate, viral diseases are usually seasonal. Poliomyelitis, caused by poliovirus often occurred in the summer months. [56] By contrast colds, influenza and rotavirus infections are usually a problem during the winter months. [57] [58] Other viruses, such as measles virus, caused outbreaks regularly every third year. [59] In developing countries, viruses that cause respiratory and enteric infections are common throughout the year. Viruses carried by insects are a common cause of diseases in these settings. Zika and dengue viruses for example are transmitted by the female Aedes mosquitoes, which bite humans particularly during the mosquitoes' breeding season. [60]

Pandemic and emergent

Left to right: the African green monkey, source of SIV; the sooty mangabey, source of HIV-2; and the chimpanzee, source of HIV-1 SIV primates.jpg
Left to right: the African green monkey, source of SIV; the sooty mangabey, source of HIV-2; and the chimpanzee, source of HIV-1
Origin and evolution of (A) SARS-CoV (B) MERS-CoV, and (C) SARS-CoV-2 in different hosts. All the viruses came from bats as coronavirus-related viruses before mutating and adapting to intermediate hosts and then to humans and causing the diseases SARS, MERS and COVID-19.(Adapted from Ashour et al. (2020) ) Orgin and evolution of SARS.jpg
Origin and evolution of (A) SARS-CoV (B) MERS-CoV, and (C) SARS-CoV-2 in different hosts. All the viruses came from bats as coronavirus-related viruses before mutating and adapting to intermediate hosts and then to humans and causing the diseases SARS, MERS and COVID-19.(Adapted from Ashour et al. (2020) )

Although viral pandemics are rare events, HIV—which evolved from viruses found in monkeys and chimpanzees—has been pandemic since at least the 1980s. [62] During the 20th century there were four pandemics caused by influenza virus and those that occurred in 1918, 1957 and 1968 were severe. [63] Before its eradication, smallpox was a cause of pandemics for more than 3,000 years. [64] Throughout history, human migration has aided the spread of pandemic infections; first by sea and in modern times also by air. [65]

With the exception of smallpox, most pandemics are caused by newly evolved viruses. These "emergent" viruses are usually mutants of less harmful viruses that have circulated previously either in humans or in other animals. [66]

Severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) are caused by new types of coronaviruses. Other coronaviruses are known to cause mild infections in humans, [67] so the virulence and rapid spread of SARS infections—that by July 2003 had caused around 8,000 cases and 800 deaths—was unexpected and most countries were not prepared. [68]

A related coronavirus emerged in Wuhan, China, in November 2019 and spread rapidly around the world. Thought to have originated in bats and subsequently named severe acute respiratory syndrome coronavirus 2, infections with the virus cause a disease called COVID-19, that varies in severity from mild to deadly, [69] and led to a pandemic in 2020. [61] [70] [71] Restrictions unprecedented in peacetime were placed on international travel, [72] and curfews imposed in several major cities worldwide. [73]

In plants

Peppers infected by mild mottle virus Pepper mild mottle virus.png
Peppers infected by mild mottle virus

There are many types of plant virus, but often they only cause a decrease in yield, and it is not economically viable to try to control them. Plant viruses are frequently spread from plant to plant by organisms called "vectors". These are normally insects, but some fungi, nematode worms and single-celled organisms have also been shown to be vectors. When control of plant virus infections is considered economical (perennial fruits, for example) efforts are concentrated on killing the vectors and removing alternate hosts such as weeds. [74] Plant viruses are harmless to humans and other animals because they can only reproduce in living plant cells. [75]

Bacteriophages

The structure of a typical bacteriophage PhageExterior.svg
The structure of a typical bacteriophage

Bacteriophages are viruses that infect bacteria and archaea. [76] They are important in marine ecology: as the infected bacteria burst, carbon compounds are released back into the environment, which stimulates fresh organic growth. Bacteriophages are useful in scientific research because they are harmless to humans and can be studied easily. These viruses can be a problem in industries that produce food and drugs by fermentation and depend on healthy bacteria. Some bacterial infections are becoming difficult to control with antibiotics, so there is a growing interest in the use of bacteriophages to treat infections in humans. [77]

Host resistance

Innate immunity of animals

Animals, including humans, have many natural defences against viruses. Some are non-specific and protect against many viruses regardless of the type. This innate immunity is not improved by repeated exposure to viruses and does not retain a "memory" of the infection. The skin of animals, particularly its surface, which is made from dead cells, prevents many types of viruses from infecting the host. The acidity of the contents of the stomach destroys many viruses that have been swallowed. When a virus overcomes these barriers and enters the host, other innate defences prevent the spread of infection in the body. A special hormone called interferon is produced by the body when viruses are present, and this stops the viruses from reproducing by killing the infected cells and their close neighbours. Inside cells, there are enzymes that destroy the RNA of viruses. This is called RNA interference. Some blood cells engulf and destroy other virus-infected cells. [78]

Adaptive immunity of animals

Two rotavirus particles: the one on the right is coated with antibodies which stop its attaching to cells and infecting them Rotavirus with antibody.jpg
Two rotavirus particles: the one on the right is coated with antibodies which stop its attaching to cells and infecting them

Specific immunity to viruses develops over time and white blood cells called lymphocytes play a central role. Lymphocytes retain a "memory" of virus infections and produce many special molecules called antibodies. These antibodies attach to viruses and stop the virus from infecting cells. Antibodies are highly selective and attack only one type of virus. The body makes many different antibodies, especially during the initial infection. After the infection subsides, some antibodies remain and continue to be produced, usually giving the host lifelong immunity to the virus. [79]

Plant resistance

Plants have elaborate and effective defence mechanisms against viruses. One of the most effective is the presence of so-called resistance (R) genes. Each R gene confers resistance to a particular virus by triggering localised areas of cell death around the infected cell, which can often be seen with the unaided eye as large spots. This stops the infection from spreading. [80] RNA interference is also an effective defence in plants. [81] When they are infected, plants often produce natural disinfectants that destroy viruses, such as salicylic acid, nitric oxide and reactive oxygen molecules. [82]

Resistance to bacteriophages

The major way bacteria defend themselves from bacteriophages is by producing enzymes which destroy foreign DNA. These enzymes, called restriction endonucleases, cut up the viral DNA that bacteriophages inject into bacterial cells. [83]

Prevention and treatment of viral disease

Vaccines

The structure of DNA showing the position of the nucleosides and the phosphorus atoms that form the "backbone" of the molecule DNA chemical structure.svg
The structure of DNA showing the position of the nucleosides and the phosphorus atoms that form the "backbone" of the molecule

Vaccines simulate a natural infection and its associated immune response, but do not cause the disease. Their use has resulted in the eradication of smallpox and a dramatic decline in illness and death caused by infections such as polio, measles, mumps and rubella. [84] Vaccines are available to prevent over fourteen viral infections of humans [85] and more are used to prevent viral infections of animals. [86] Vaccines may consist of either live or killed viruses. [87] Live vaccines contain weakened forms of the virus, but these vaccines can be dangerous when given to people with weak immunity. In these people, the weakened virus can cause the original disease. [88] Biotechnology and genetic engineering techniques are used to produce "designer" vaccines that only have the capsid proteins of the virus. Hepatitis B vaccine is an example of this type of vaccine. [89] These vaccines are safer because they can never cause the disease. [87]

Antiviral drugs

The structure of the DNA base guanosine and the antiviral drug aciclovir which functions by mimicking it Guanosine aciclovir comparison.svg
The structure of the DNA base guanosine and the antiviral drug aciclovir which functions by mimicking it

Since the mid-1980s, the development of antiviral drugs has increased rapidly, mainly driven by the AIDS pandemic. Antiviral drugs are often nucleoside analogues, which masquerade as DNA building blocks (nucleosides). When the replication of virus DNA begins, some of the fake building blocks are used. This prevents DNA replication because the drugs lack the essential features that allow the formation of a DNA chain. When DNA production stops the virus can no longer reproduce. [90] Examples of nucleoside analogues are aciclovir for herpes virus infections and lamivudine for HIV and hepatitis B virus infections. Aciclovir is one of the oldest and most frequently prescribed antiviral drugs. [91]

Other antiviral drugs target different stages of the viral life cycle. HIV is dependent on an enzyme called the HIV-1 protease for the virus to become infectious. There is a class of drugs called protease inhibitors, which bind to this enzyme and stop it from functioning. [92]

Hepatitis C is caused by an RNA virus. In 80% of those infected, the disease becomes chronic, and they remain infectious for the rest of their lives unless they are treated. There are effective treatments that use direct-acting antivirals. [93] Treatments for chronic carriers of the hepatitis B virus have been developed by a similar strategy, using lamivudine and other anti-viral drugs. In both diseases, the drugs stop the virus from reproducing and the interferon kills any remaining infected cells. [94]

HIV infections are usually treated with a combination of antiviral drugs, each targeting a different stage in the virus's life cycle. There are drugs that prevent the virus from attaching to cells, others that are nucleoside analogues and some poison the virus's enzymes that it needs to reproduce. The success of these drugs is proof of the importance of knowing how viruses reproduce. [92]

Role in ecology

Viruses are the most abundant biological entity in aquatic environments; [95] one teaspoon of seawater contains about ten million viruses, [96] and they are essential to the regulation of saltwater and freshwater ecosystems. [97] Most are bacteriophages, [98] which are harmless to plants and animals. They infect and destroy the bacteria in aquatic microbial communities and this is the most important mechanism of recycling carbon in the marine environment. The organic molecules released from the bacterial cells by the viruses stimulate fresh bacterial and algal growth. [99]

Microorganisms constitute more than 90% of the biomass in the sea. It is estimated that viruses kill approximately 20% of this biomass each day and that there are fifteen times as many viruses in the oceans as there are bacteria and archaea. They are mainly responsible for the rapid destruction of harmful algal blooms, [100] which often kill other marine life. [101] The number of viruses in the oceans decreases further offshore and deeper into the water, where there are fewer host organisms. [102]

Their effects are far-reaching; by increasing the amount of respiration in the oceans, viruses are indirectly responsible for reducing the amount of carbon dioxide in the atmosphere by approximately 3 gigatonnes of carbon per year. [102]

Marine mammals are also susceptible to viral infections. In 1988 and 2002, thousands of harbour seals were killed in Europe by phocine distemper virus. [103] Many other viruses, including caliciviruses, herpesviruses, adenoviruses and parvoviruses, circulate in marine mammal populations. [102]

Viruses can also serve as an alternative food source for microorganisms which engage in virovory, supplying nucleic acids, nitrogen, and phosphorus through their consumption. [104] [105]

See also

Related Research Articles

<span class="mw-page-title-main">Retrovirus</span> Family of viruses

A retrovirus is a type of virus that inserts a DNA copy of its RNA genome into the DNA of a host cell that it invades, thus changing the genome of that cell. After invading a host cell's cytoplasm, the virus uses its own reverse transcriptase enzyme to produce DNA from its RNA genome, the reverse of the usual pattern, thus retro (backward). The new DNA is then incorporated into the host cell genome by an integrase enzyme, at which point the retroviral DNA is referred to as a provirus. The host cell then treats the viral DNA as part of its own genome, transcribing and translating the viral genes along with the cell's own genes, producing the proteins required to assemble new copies of the virus. Many retroviruses cause serious diseases in humans, other mammals, and birds.

<span class="mw-page-title-main">Virology</span> Study of viruses

Virology is the scientific study of biological viruses. It is a subfield of microbiology that focuses on their detection, structure, classification and evolution, their methods of infection and exploitation of host cells for reproduction, their interaction with host organism physiology and immunity, the diseases they cause, the techniques to isolate and culture them, and their use in research and therapy.

<span class="mw-page-title-main">Antiviral drug</span> Medication used to treat a viral infection

Antiviral drugs are a class of medication used for treating viral infections. Most antivirals target specific viruses, while a broad-spectrum antiviral is effective against a wide range of viruses. Antiviral drugs are a class of antimicrobials, a larger group which also includes antibiotic, antifungal and antiparasitic drugs, or antiviral drugs based on monoclonal antibodies. Most antivirals are considered relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from virucides, which are not medication but deactivate or destroy virus particles, either inside or outside the body. Natural virucides are produced by some plants such as eucalyptus and Australian tea trees.

Gene silencing is the regulation of gene expression in a cell to prevent the expression of a certain gene. Gene silencing can occur during either transcription or translation and is often used in research. In particular, methods used to silence genes are being increasingly used to produce therapeutics to combat cancer and other diseases, such as infectious diseases and neurodegenerative disorders.

Viral evolution is a subfield of evolutionary biology and virology that is specifically concerned with the evolution of viruses. Viruses have short generation times, and many—in particular RNA viruses—have relatively high mutation rates. Although most viral mutations confer no benefit and often even prove deleterious to viruses, the rapid rate of viral mutation combined with natural selection allows viruses to quickly adapt to changes in their host environment. In addition, because viruses typically produce many copies in an infected host, mutated genes can be passed on to many offspring quickly. Although the chance of mutations and evolution can change depending on the type of virus, viruses overall have high chances for mutations.

<i>Orthomyxoviridae</i> Family of RNA viruses including the influenza viruses

Orthomyxoviridae is a family of negative-sense RNA viruses. It includes seven genera: Alphainfluenzavirus, Betainfluenzavirus, Gammainfluenzavirus, Deltainfluenzavirus, Isavirus, Thogotovirus, and Quaranjavirus. The first four genera contain viruses that cause influenza in birds and mammals, including humans. Isaviruses infect salmon; the thogotoviruses are arboviruses, infecting vertebrates and invertebrates. The Quaranjaviruses are also arboviruses, infecting vertebrates (birds) and invertebrates (arthropods).

<span class="mw-page-title-main">Oncovirus</span> Viruses that can cause cancer

An oncovirus or oncogenic virus is a virus that can cause cancer. This term originated from studies of acutely transforming retroviruses in the 1950–60s, when the term oncornaviruses was used to denote their RNA virus origin. With the letters RNA removed, it now refers to any virus with a DNA or RNA genome causing cancer and is synonymous with tumor virus or cancer virus. The vast majority of human and animal viruses do not cause cancer, probably because of longstanding co-evolution between the virus and its host. Oncoviruses have been important not only in epidemiology, but also in investigations of cell cycle control mechanisms such as the retinoblastoma protein.

<span class="mw-page-title-main">Plant virus</span> Virus that affects plants

Plant viruses are viruses that have the potential to affect plants. Like all other viruses, plant viruses are obligate intracellular parasites that do not have the molecular machinery to replicate without a host. Plant viruses can be pathogenic to vascular plants.

<i>Gammaretrovirus</i> Genus of viruses

Gammaretrovirus is a genus in the Retroviridae family. Example species are the murine leukemia virus and the feline leukemia virus. They cause various sarcomas, leukemias and immune deficiencies in mammals, reptiles and birds.

<span class="mw-page-title-main">Viral envelope</span> Outermost layer of many types of the infectious agent

A viral envelope is the outermost layer of many types of viruses. It protects the genetic material in their life cycle when traveling between host cells. Not all viruses have envelopes. A viral envelope protein or E protein is a protein in the envelope, which may be acquired by the capsid from an infected host cell.

<span class="mw-page-title-main">H5N1 genetic structure</span> Genetic structure of Influenza A virus

The genetic structure of H5N1, a highly pathogenic avian influenza virus, is characterized by a segmented RNA genome consisting of eight gene segments that encode for various viral proteins essential for replication, host adaptation, and immune evasion.

<span class="mw-page-title-main">Herpes simplex virus</span> Species of virus

Herpes simplex virus1 and 2, also known by their taxonomic names Human alphaherpesvirus 1 and Human alphaherpesvirus 2, are two members of the human Herpesviridae family, a set of viruses that produce viral infections in the majority of humans. Both HSV-1 and HSV-2 are very common and contagious. They can be spread when an infected person begins shedding the virus.

<i>Murine coronavirus</i> Species of virus

Murine coronavirus (M-CoV) is a virus in the genus Betacoronavirus that infects mice. Belonging to the subgenus Embecovirus, murine coronavirus strains are enterotropic or polytropic. Enterotropic strains include mouse hepatitis virus (MHV) strains D, Y, RI, and DVIM, whereas polytropic strains, such as JHM and A59, primarily cause hepatitis, enteritis, and encephalitis. Murine coronavirus is an important pathogen in the laboratory mouse and the laboratory rat. It is the most studied coronavirus in animals other than humans, and has been used as an animal disease model for many virological and clinical studies.

Yizhi Jane Tao is a Chinese biochemist, structural biologist, and professor of biochemistry and cell biology at Rice University in Houston, Texas. Professor Tao led a team of researchers to be the first to map the structure of the influenza A virus nucleoprotein to an atomic level, a feat which circulated widely in the popular press. She was named among the top ten most influential Chinese of 2006 by a consortium of China's leading media outlets including Phoenix Satellite Television, China News Service, Asia Newsweek, and World Journal.

<span class="mw-page-title-main">History of virology</span>

The history of virology – the scientific study of viruses and the infections they cause – began in the closing years of the 19th century. Although Edward Jenner and Louis Pasteur developed the first vaccines to protect against viral infections, they did not know that viruses existed. The first evidence of the existence of viruses came from experiments with filters that had pores small enough to retain bacteria. In 1892, Dmitri Ivanovsky used one of these filters to show that sap from a diseased tobacco plant remained infectious to healthy tobacco plants despite having been filtered. Martinus Beijerinck called the filtered, infectious substance a "virus" and this discovery is considered to be the beginning of virology.

<span class="mw-page-title-main">Virus</span> Infectious agent that replicates in cells

A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism. Viruses infect all life forms, from animals and plants to microorganisms, including bacteria and archaea. Viruses are found in almost every ecosystem on Earth and are the most numerous type of biological entity. Since Dmitri Ivanovsky's 1892 article describing a non-bacterial pathogen infecting tobacco plants and the discovery of the tobacco mosaic virus by Martinus Beijerinck in 1898, more than 11,000 of the millions of virus species have been described in detail. The study of viruses is known as virology, a subspeciality of microbiology.

<span class="mw-page-title-main">Influenza</span> Infectious disease

Influenza, commonly known as the flu, is an infectious disease caused by influenza viruses. Symptoms range from mild to severe and often include fever, runny nose, sore throat, muscle pain, headache, coughing, and fatigue. These symptoms begin one to four days after exposure to the virus and last for about two to eight days. Diarrhea and vomiting can occur, particularly in children. Influenza may progress to pneumonia from the virus or a subsequent bacterial infection. Other complications include acute respiratory distress syndrome, meningitis, encephalitis, and worsening of pre-existing health problems such as asthma and cardiovascular disease.

In biology, a pathogen, in the oldest and broadest sense, is any organism or agent that can produce disease. A pathogen may also be referred to as an infectious agent, or simply a germ.

<i>Influenza D virus</i> Species of virus

Influenza D virus is a species in the virus genus Deltainfluenzavirus, in the family Orthomyxoviridae, that causes influenza.

<i>Orthornavirae</i> Kingdom of viruses

Orthornavirae is a kingdom of viruses that have genomes made of ribonucleic acid (RNA), including genes which encode an RNA-dependent RNA polymerase (RdRp). The RdRp is used to transcribe the viral RNA genome into messenger RNA (mRNA) and to replicate the genome. Viruses in this kingdom share a number of characteristics which promote rapid evolution, including high rates of genetic mutation, recombination, and reassortment.

References

Notes

  1. 1 2 King AM, Lefkowitz EJ, Mushegian AR, Adams MJ, Dutilh BE, Gorbalenya AE, Harrach B, Harrison RL, Junglen S, Knowles NJ, Kropinski AM, Krupovic M, Kuhn JH, Nibert ML, Rubino L, Sabanadzovic S, Sanfaçon H, Siddell SG, Simmonds P, Varsani A, Zerbini FM, Davison AJ (September 2018). "Changes to taxonomy and the International Code of Virus Classification and Nomenclature ratified by the International Committee Taxonomy of Viruses (2018)" (PDF). Archives of Virology. 163 (9): 2601. doi:10.1007/s00705-018-3847-1. PMID   29754305. S2CID   21670772.
  2. Shors 2017 , p. 6
  3. Collier, Balows & Sussman 1998 , p. 3
  4. Shors 2017 , p. 827
  5. D'Herelle F (2007). "On an invisible microbe antagonistic toward dysenteric bacilli: brief note by Mr. F. D'Herelle, presented by Mr. Roux. 1917". Research in Microbiology. 158 (7): 553–554. doi: 10.1016/j.resmic.2007.07.005 . PMID   17855060.
  6. From Nobel Lectures, Physics 1981–1990, (1993) Editor-in-Charge Tore Frängsmyr, Editor Gösta Ekspång, World Scientific Publishing Co., Singapore
  7. Stanley WM, Loring HS (1936). "The isolation of crystalline tobacco mosaic virus protein from diseased tomato plants". Science. 83 (2143): 85. Bibcode:1936Sci....83...85S. doi:10.1126/science.83.2143.85. PMID   17756690.
  8. Stanley WM, Lauffer MA (1939). "Disintegration of tobacco mosaic virus in urea solutions". Science. 89 (2311): 345–347. Bibcode:1939Sci....89..345S. doi:10.1126/science.89.2311.345. PMID   17788438.
  9. Creager AN, Morgan GJ (June 2008). "After the double helix: Rosalind Franklin's research on Tobacco mosaic virus". Isis; an International Review Devoted to the History of Science and Its Cultural Influences. 99 (2): 239–272. doi:10.1086/588626. PMID   18702397. S2CID   25741967.
  10. Johnson B (25 July 2017). "Rosalind Franklin's contributions to virology". Nature Portfolio Microbiology Community. Retrieved 7 January 2022.
  11. Goodpasture EW, Woodruff AM, Buddingh GJ (October 1931). "The Cultivation Of Vaccine and other Viruses In The Chorioallantoic Membrane of Chick Embryos". Science. 74 (1919): 371–372. Bibcode:1931Sci....74..371G. doi:10.1126/science.74.1919.371. PMID   17810781.
  12. Rosen FS (October 2004). "Isolation of poliovirus – John Enders and the Nobel Prize". N. Engl. J. Med. 351 (15): 1481–1483. doi:10.1056/NEJMp048202. PMID   15470207.
  13. Shors 2017 , p. 16
  14. Collier, Balows & Sussman 1998 , pp. 18–19
  15. Liu Y, Nickle DC, Shriner D, Jensen MA, Learn GH, Mittler JE, Mullins JI (November 2004). "Molecular clock-like evolution of human immunodeficiency virus type 1". Virology. 329 (1): 101–108. doi: 10.1016/j.virol.2004.08.014 . PMID   15476878.
  16. 1 2 3 Krupovic M, Dooja W, Koonin EV (2019). "Origin of viruses: primordial replicators recruiting capsids from hosts" (PDF). Nature Reviews Microbiology. 17 (7): 449–458. doi:10.1038/s41579-019-0205-6. PMID   31142823. S2CID   169035711.
  17. Collier, Balows & Sussman 1998 , pp. 11–21
  18. Collier, Balows & Sussman 1998 , p. 11
  19. Collier, Balows & Sussman 1998 , pp. 11–12
  20. 1 2 Wessner DR (2010). "The Origins of Viruses". Nature Education. 3 (9): 37.
  21. Nasir A, Kim KM, Caetano-Anollés G (2012). "Viral evolution: Primordial cellular origins and late adaptation to parasitism". Mobile Genetic Elements. 2 (5): 247–252. doi:10.4161/mge.22797. PMC   3575434 . PMID   23550145.
  22. 1 2 Mahy WJ, Van Regenmortel MH (2009). Desk Encyclopedia of General Virology. Oxford: Academic Press. p. 28. ISBN   978-0-12-375146-1.
  23. 1 2 Collier, Balows & Sussman 1998 , pp. 33–55
  24. Rotter ML (August 2001). "Arguments for alcoholic hand disinfection". The Journal of Hospital Infection. 48 (Suppl A): S4–S8. doi:10.1016/s0195-6701(01)90004-0. PMID   11759024.
  25. Abergel C, Legendre M, Claverie JM (November 2015). "The rapidly expanding universe of giant viruses: Mimivirus, Pandoravirus, Pithovirus and Mollivirus". FEMS Microbiol. Rev. 39 (6): 779–796. doi: 10.1093/femsre/fuv037 . PMID   26391910.
  26. Philippe N, Legendre M, Doutre G, Couté Y, Poirot O, Lescot M, Arslan D, Seltzer V, Bertaux L, Bruley C, Garin J, Claverie JM, Abergel C (July 2013). "Pandoraviruses: amoeba viruses with genomes up to 2.5 Mb reaching that of parasitic eukaryotes" (PDF). Science. 341 (6143): 281–286. Bibcode:2013Sci...341..281P. doi:10.1126/science.1239181. PMID   23869018. S2CID   16877147.
  27. Zimmer C (18 July 2013). "Changing View on Viruses: Not So Small After All". The New York Times. Retrieved 20 December 2014.
  28. Shors 2017 , p. 81
  29. Shors 2017 , p. 129
  30. International Human GS (2004). "Finishing the euchromatic sequence of the human genome". Nature. 431 (7011): 931–945. Bibcode:2004Natur.431..931H. doi: 10.1038/nature03001 . PMID   15496913. S2CID   186242248.
  31. Shors 2017 , pp. 129–31
  32. Shors 2017 , p. 652
  33. Shors 2017 , p. 654
  34. 1 2 de Klerk E, 't Hoen PA (March 2015). "Alternative mRNA transcription, processing, and translation: insights from RNA sequencing". Trends in Genetics. 31 (3): 128–139. doi:10.1016/j.tig.2015.01.001. PMID   25648499.
  35. Collier, Balows & Sussman 1998 , pp. 75–82
  36. Shors 2017 , p. 698
  37. Shors 2017 , pp. 6–13
  38. Shors 2017 , pp. 121–123
  39. Oxford, Kellam & Collier 2016, p. 34–36.
  40. Oxford, Kellam & Collier 2016, p. 34.
  41. Okamoto T, Suzuki T, Kusakabe S, Tokunaga M, Hirano J, Miyata Y, Matsuura Y (2017). "Regulation of Apoptosis during Flavivirus Infection". Viruses. 9 (9): 243. doi: 10.3390/v9090243 . PMC   5618009 . PMID   28846635.
  42. Alwine JC (2008). "Modulation of host cell stress responses by human cytomegalovirus". Current Topics in Microbiology and Immunology. 325: 263–79. doi:10.1007/978-3-540-77349-8_15. PMID   18637511.
  43. Sinclair J (March 2008). "Human cytomegalovirus: Latency and reactivation in the myeloid lineage". J. Clin. Virol. 41 (3): 180–185. doi:10.1016/j.jcv.2007.11.014. PMID   18164651.
  44. Jordan MC, Jordan GW, Stevens JG, Miller G (June 1984). "Latent herpesviruses of humans". Ann. Intern. Med. 100 (6): 866–880. doi:10.7326/0003-4819-100-6-866. PMID   6326635.
  45. Sissons JG, Bain M, Wills MR (February 2002). "Latency and reactivation of human cytomegalovirus". J. Infect. 44 (2): 73–77. doi:10.1053/jinf.2001.0948. PMID   12076064. S2CID   24879226.
  46. Barozzi P, Potenza L, Riva G, Vallerini D, Quadrelli C, Bosco R, Forghieri F, Torelli G, Luppi M (December 2007). "B cells and herpesviruses: a model of lymphoproliferation". Autoimmun Rev. 7 (2): 132–136. doi:10.1016/j.autrev.2007.02.018. PMID   18035323.
  47. Graham SV (2017). "The human papillomavirus replication cycle, and its links to cancer progression: a comprehensive review". Clinical Science. 131 (17): 2201–2221. doi: 10.1042/CS20160786 . PMID   28798073.
  48. Roulston A, Marcellus RC, Branton PE (1999). "Viruses and apoptosis". Annu. Rev. Microbiol. 53: 577–628. doi:10.1146/annurev.micro.53.1.577. PMID   10547702.
  49. Shors 2017 , p. 32
  50. Shors 2017 , p. 271
  51. Berngruber TW, Froissart R, Choisy M, Gandon S (2013). "Evolution of Virulence in Emerging Epidemics". PLOS Pathogens. 9 (3): e1003209. doi: 10.1371/journal.ppat.1003209 . PMC   3597519 . PMID   23516359.
  52. Shors 2017 , p. 464
  53. Tanaka J, Akita T, Ko K, Miura Y, Satake M (September 2019). "Countermeasures against viral hepatitis B and C in Japan: An epidemiological point of view". Hepatology Research. 49 (9): 990–1002. doi:10.1111/hepr.13417. PMC   6852166 . PMID   31364248.
  54. Lai CC, Liu YH, Wang CY, Wang YH, Hsueh SC, Yen MY, Ko WC, Hsueh PR (March 2020). "Asymptomatic carrier state, acute respiratory disease, and pneumonia due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2): Facts and myths". Journal of Microbiology, Immunology, and Infection = Wei Mian Yu Gan Ran Za Zhi. 53 (3): 404–412. doi:10.1016/j.jmii.2020.02.012. PMC   7128959 . PMID   32173241.
  55. Oxford, Kellam & Collier 2016, p. 63.
  56. Strand LK (July 2018). "The Terrible Summer of 1952 … When Polio Struck Our Family". Seminars in Pediatric Neurology. 26: 39–44. doi:10.1016/j.spen.2017.04.001. PMID   29961515. S2CID   49640682.
  57. Moorthy M, Castronovo D, Abraham A, Bhattacharyya S, Gradus S, Gorski J, Naumov YN, Fefferman NH, Naumova EN (October 2012). "Deviations in influenza seasonality: odd coincidence or obscure consequence?". Clinical Microbiology and Infection. 18 (10): 955–962. doi:10.1111/j.1469-0691.2012.03959.x. PMC   3442949 . PMID   22958213.
  58. Barril PA, Fumian TM, Prez VE, Gil PI, Martínez LC, Giordano MO, Masachessi G, Isa MB, Ferreyra LJ, Ré VE, Miagostovich M, Pavan JV, Nates SV (April 2015). "Rotavirus seasonality in urban sewage from Argentina: effect of meteorological variables on the viral load and the genetic diversity". Environmental Research. 138: 409–415. Bibcode:2015ER....138..409B. doi:10.1016/j.envres.2015.03.004. hdl: 11336/61497 . PMID   25777068.
  59. Durrheim DN, Crowcroft NS, Strebel PM (December 2014). "Measles – The epidemiology of elimination". Vaccine. 32 (51): 6880–6883. doi: 10.1016/j.vaccine.2014.10.061 . hdl: 1959.13/1299149 . PMID   25444814.
  60. Mbanzulu KM, Mboera LE, Luzolo FK, Wumba R, Misinzo G, Kimera SI (February 2020). "Mosquito-borne viral diseases in the Democratic Republic of the Congo: a review". Parasites & Vectors. 13 (1): 103. doi: 10.1186/s13071-020-3985-7 . PMC   7045448 . PMID   32103776.
  61. 1 2 Ashour HM, Elkhatib WF, Rahman MM, Elshabrawy HA (March 2020). "Insights into the Recent 2019 Novel Coronavirus (SARS-CoV-2) in Light of Past Human Coronavirus Outbreaks". Pathogens (Basel, Switzerland). 9 (3): 186. doi: 10.3390/pathogens9030186 . PMC   7157630 . PMID   32143502.
  62. Eisinger RW, Fauci AS (March 2018). "Ending the HIV/AIDS Pandemic1". Emerging Infectious Diseases. 24 (3): 413–416. doi:10.3201/eid2403.171797. PMC   5823353 . PMID   29460740.
  63. Qin Y, Zhao MJ, Tan YY, Li XQ, Zheng JD, Peng ZB, Feng LZ (August 2018). "[History of influenza pandemics in China during the past century]". Zhonghua Liu Xing Bing Xue Za Zhi = Zhonghua Liuxingbingxue Zazhi (in Chinese). 39 (8): 1028–1031. doi:10.3760/cma.j.issn.0254-6450.2018.08.003. PMID   30180422.
  64. Nishiyama Y, Matsukuma S, Matsumura T, Kanatani Y, Saito T (April 2015). "Preparedness for a smallpox pandemic in Japan: public health perspectives". Disaster Medicine and Public Health Preparedness. 9 (2): 220–223. doi:10.1017/dmp.2014.157. PMID   26060873. S2CID   37149836.
  65. Houghton F (2019). "Geography, global pandemics & air travel: Faster, fuller, further & more frequent". Journal of Infection and Public Health. 12 (3): 448–449. doi:10.1016/j.jiph.2019.02.020. PMC   7129534 . PMID   30878442.
  66. "Virology Journal". Virology Journal.
  67. Weiss SR, Leibowitz JL (2011). Coronavirus pathogenesis. Advances in Virus Research. Vol. 81. pp. 85–164. doi:10.1016/B978-0-12-385885-6.00009-2. ISBN   978-0-12-385885-6. PMC   7149603 . PMID   22094080.
  68. Wong AT, Chen H, Liu SH, Hsu EK, Luk KS, Lai CK, Chan RF, Tsang OT, Choi KW, Kwan YW, Tong AY, Cheng VC, Tsang DC (May 2017). "From SARS to Avian Influenza Preparedness in Hong Kong". Clinical Infectious Diseases. 64 (suppl_2): S98–S104. doi: 10.1093/cid/cix123 . PMID   28475794.
  69. Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19) (PDF) (Report). World Health Organization (WHO). 16–24 February 2020. Retrieved 21 March 2020.
  70. Deng SQ, Peng HJ (February 2020). "Characteristics of and Public Health Responses to the Coronavirus Disease 2019 Outbreak in China". Journal of Clinical Medicine. 9 (2): 575. doi: 10.3390/jcm9020575 . PMC   7074453 . PMID   32093211.
  71. Han Q, Lin Q, Jin S, You L (February 2020). "Coronavirus 2019-nCoV: A brief perspective from the front line". The Journal of Infection. 80 (4): 373–377. doi:10.1016/j.jinf.2020.02.010. PMC   7102581 . PMID   32109444.
  72. Londoño E, Ortiz A (16 March 2020). "Coronavirus Travel Restrictions, Across the Globe". The New York Times via NYTimes.com.
  73. "US takes more big pandemic response steps; Europe COVID-19 cases soar". CIDRAP. 15 March 2020.
  74. Shors 2017 , p. 822
  75. Shors 2017 , pp. 802–803
  76. Oxford, Kellam & Collier 2016, p. 19.
  77. Shors 2017 , p. 803
  78. Shors 2017 , pp. 116–117
  79. Shors 2017 , pp. 225–233
  80. Garcia-Ruiz H (2018). "Susceptibility Genes to Plant Viruses". Viruses. 10 (9): 484. doi: 10.3390/v10090484 . PMC   6164914 . PMID   30201857.
  81. Shors 2017 , p. 812
  82. Soosaar JL, Burch-Smith TM, Dinesh-Kumar SP (2005). "Mechanisms of plant resistance to viruses". Nature Reviews Microbiology. 3 (10): 789–798. doi:10.1038/nrmicro1239. PMID   16132037. S2CID   27311732.
  83. Horvath P, Barrangou R (January 2010). "CRISPR/Cas, the immune system of bacteria and archaea" (PDF). Science. 327 (5962): 167–170. Bibcode:2010Sci...327..167H. doi:10.1126/science.1179555. PMID   20056882. S2CID   17960960. Archived from the original (PDF) on 27 March 2020.
  84. Shors 2017 , pp. 237–255
  85. Small JC, Ertl HC (2011). "Viruses – from pathogens to vaccine carriers". Current Opinion in Virology. 1 (4): 241–245. doi:10.1016/j.coviro.2011.07.009. PMC   3190199 . PMID   22003377.
  86. Burakova Y, Madera R, McVey S, Schlup JR, Shi J (2018). "Adjuvants for Animal Vaccines". Viral Immunology. 31 (1): 11–22. doi:10.1089/vim.2017.0049. PMID   28618246.
  87. 1 2 Shors 2017 , p. 237
  88. Thomssen R (1975). "Live attenuated versus killed virus vaccines". Monographs in Allergy. 9: 155–176. PMID   1090805.
  89. Shors 2017 , p. 238
  90. Shors 2017 , pp. 514–515
  91. Shors 2017 , p. 514
  92. 1 2 Shors 2017 , p. 568
  93. Falade-Nwulia O, Suarez-Cuervo C, Nelson DR, Fried MW, Segal JB, Sulkowski MS (May 2017). "Oral Direct-Acting Agent Therapy for Hepatitis C Virus Infection: A Systematic Review". Annals of Internal Medicine. 166 (9): 637–648. doi:10.7326/M16-2575. PMC   5486987 . PMID   28319996.
  94. Paul N, Han SH (June 2011). "Combination Therapy for Chronic Hepatitis B: Current Indications". Curr Hepat Rep. 10 (2): 98–105. doi:10.1007/s11901-011-0095-1. PMC   3085106 . PMID   21654909.
  95. Koonin EV, Senkevich TG, Dolja VV (September 2006). "The ancient Virus World and evolution of cells". Biol. Direct. 1: 29. doi: 10.1186/1745-6150-1-29 . PMC   1594570 . PMID   16984643.
  96. Dávila-Ramos S, Castelán-Sánchez HG, Martínez-Ávila L, Sánchez-Carbente MD, Peralta R, Hernández-Mendoza A, Dobson AD, Gonzalez RA, Pastor N, Batista-García RA (2019). "A Review on Viral Metagenomics in Extreme Environments". Frontiers in Microbiology. 10: 2403. doi: 10.3389/fmicb.2019.02403 . PMC   6842933 . PMID   31749771.
  97. Shors 2017 , p. 5
  98. Breitbart M, Bonnain C, Malki K, Sawaya NA (July 2018). "Phage puppet masters of the marine microbial realm". Nature Microbiology. 3 (7): 754–766. doi:10.1038/s41564-018-0166-y. PMID   29867096. S2CID   46927784.
  99. Shors 2017 , pp. 25–26
  100. Suttle CA (September 2005). "Viruses in the sea". Nature. 437 (7057): 356–361. Bibcode:2005Natur.437..356S. doi:10.1038/nature04160. PMID   16163346. S2CID   4370363.
  101. "Harmful Algal Blooms: Red Tide: Home | CDC HSB". www.cdc.gov. Retrieved 23 August 2009.
  102. 1 2 3 Suttle CA (October 2007). "Marine viruses – major players in the global ecosystem". Nat. Rev. Microbiol. 5 (10): 801–812. doi:10.1038/nrmicro1750. PMID   17853907. S2CID   4658457.
  103. Hall A, Jepson P, Goodman S, Harkonen T (2006). "Phocine distemper virus in the North and European Seas – Data and models, nature and nurture". Biological Conservation. 131 (2): 221–229. Bibcode:2006BCons.131..221H. doi:10.1016/j.biocon.2006.04.008.
  104. DeLong JP, Van Etten JL, Al-Ameeli Z, Agarkova IV, Dunigan DD (3 January 2023). "The consumption of viruses returns energy to food chains". Proceedings of the National Academy of Sciences. 120 (1): e2215000120. Bibcode:2023PNAS..12015000D. doi:10.1073/pnas.2215000120. ISSN   0027-8424. PMC   9910503 . PMID   36574690.
  105. Irving M (28 December 2022). "First "virovore" discovered: An organism that eats viruses". New Atlas. Archived from the original on 29 December 2022. Retrieved 29 December 2022.

Bibliography

  • Collier L, Balows A, Sussman M, eds. (1998). Topley & Wilson's Microbiology and Microbial Infections. Vol. 1, Virology (9th ed.). Arnold. ISBN   0-340-66316-2.
  • Oxford J, Kellam P, Collier L (2016). Human Virology. Oxford: Oxford University Press. ISBN   978-0-19-871468-2. OCLC   968152575.
  • Shors T (2017). Understanding Viruses. Jones and Bartlett Publishers. ISBN   978-1284025927.