In scientific nomenclature, a synonym is a scientific name that applies to a taxon that goes by a different scientific name, although the term is used somewhat differently in the zoological code of nomenclature. For example, Linnaeus was the first to give a scientific name to the Norway spruce, which he called Pinus abies; this name is no longer in use: it is now a synonym of the current scientific name, Picea abies. Unlike synonyms in other contexts, in taxonomy a synonym is not interchangeable with the name of which it is a synonym. In taxonomy, synonyms have a different status. For any taxon with a particular circumscription and rank, only one scientific name is considered to be the correct one at any given time. A synonym cannot exist in isolation: it is always an alternative to a different scientific name. Given that the correct name of a taxon depends on the taxonomic viewpoint used a name, one taxonomist's synonym may be another taxonomist's correct name. Synonyms may arise whenever the same taxon is named more than once, independently.
They may arise when existing taxa are changed, as when two taxa are joined to become one, a species is moved to a different genus, a variety is moved to a different species, etc. Synonyms come about when the codes of nomenclature change, so that older names are no longer acceptable. To the general user of scientific names, in fields such as agriculture, ecology, general science, etc. A synonym is a name, used as the correct scientific name but, displaced by another scientific name, now regarded as correct, thus Oxford Dictionaries Online defines the term as "a taxonomic name which has the same application as another one, superseded and is no longer valid." In handbooks and general texts, it is useful to have synonyms mentioned as such after the current scientific name, so as to avoid confusion. For example, if the much advertised name change should go through and the scientific name of the fruit fly were changed to Sophophora melanogaster, it would be helpful if any mention of this name was accompanied by "".
Synonyms used in this way may not always meet the strict definitions of the term "synonym" in the formal rules of nomenclature which govern scientific names. Changes of scientific name have two causes: they may be taxonomic or nomenclatural. A name change may be caused by changes in the circumscription, position or rank of a taxon, representing a change in taxonomic, scientific insight. A name change may be due to purely nomenclatural reasons, that is, based on the rules of nomenclature. Speaking in general, name changes for nomenclatural reasons have become less frequent over time as the rules of nomenclature allow for names to be conserved, so as to promote stability of scientific names. In zoological nomenclature, codified in the International Code of Zoological Nomenclature, synonyms are different scientific names of the same taxonomic rank that pertain to that same taxon. For example, a particular species could, over time, have had two or more species-rank names published for it, while the same is applicable at higher ranks such as genera, orders, etc.
In each case, the earliest published name is called the senior synonym, while the name is the junior synonym. In the case where two names for the same taxon have been published the valid name is selected accorded to the principle of the first reviser such that, for example, of the names Strix scandiaca and Strix noctua, both published by Linnaeus in the same work at the same date for the taxon now determined to be the snowy owl, the epithet scandiaca has been selected as the valid name, with noctua becoming the junior synonym. One basic principle of zoological nomenclature is that the earliest published name, the senior synonym, by default takes precedence in naming rights and therefore, unless other restrictions interfere, must be used for the taxon. However, junior synonyms are still important to document, because if the earliest name cannot be used the next available junior synonym must be used for the taxon. For other purposes, if a researcher is interested in consulting or compiling all known information regarding a taxon, some of this may well have been published under names now regarded as outdated and so it is again useful to know a list of historic synonyms which may have been used for a given current taxon name.
Objective synonyms refer to taxa with same rank. This may be species-group taxa of the same rank with the same type specimen, genus-group taxa of the same rank with the same type species or if their type species are themselves objective synonyms, of family-group taxa with the same type genus, etc. In the case of subjective synonyms, there is no such shared type, so the synonymy is open to taxonomic judgement, meaning that th
Human betaherpesvirus 5
Human betaherpesvirus 5, sometimes called human cytomegalovirus, is the type species of the virus genus Cytomegalovirus, which in turn is a member of the viral family known as Herpesviridae or herpesviruses. It is commonly called CMV. Within Herpesviridae, HCMV belongs to the Betaherpesvirinae subfamily, which includes cytomegaloviruses from other mammals. Although they may be found throughout the body, HCMV infections are associated with the salivary glands. HCMV infection is unnoticed in healthy people, but can be life-threatening for the immunocompromised, such as HIV-infected persons, organ transplant recipients, or newborn infants. Congenital cytomegalovirus infection can lead to significant morbidity and death. After infection, HCMV remains latent within the body throughout life and can be reactivated at any time, it may cause mucoepidermoid carcinoma and other malignancies such as prostate cancer. HCMV is found in all geographic locations and all socioeconomic groups, infects between 60% and 70% of adults in developed countries and 100% in developing countries.
Of all herpes viruses, HCMV harbors the most genes dedicated to altering innate and adaptive host immunity and represents a lifelong burden of antigenic T cell surveillance and immune dysfunction. It is indicated by the presence of antibodies in the general population. Seroprevalence is age-dependent: 58.9% of individuals aged 6 and older are infected with CMV while 90.8% of individuals aged 80 and older are positive for HCMV. HCMV is the virus most transmitted to a developing fetus. HCMV infection is more widespread in developing countries and in communities with lower socioeconomic status and represents the most significant viral cause of birth defects in industrialized countries. Congenital HCMV is the leading infectious cause of deafness, learning disabilities, intellectual disability in children. CMV "seems to have a large impact on immune parameters in life and may contribute to increased morbidity and eventual mortality." Human betaherpesvirus 5 infection has a classic triad of symptoms: fever, peaking in the late afternoon or early evening.
The mode of HCMV transmission from person to person is unknown, but is presumed to occur through bodily fluids including saliva, urine and tears. Cytomegalovirus is most transmitted through kissing and sexual intercourse, it can be transferred from an infected mother to her unborn child. Infection requires close, intimate contact with a person secreting the virus in their saliva, urine, or other bodily fluids. CMV can be transmitted sexually and via breast milk, occurs through receiving transplanted organs or blood transfusions. Although HCMV is not contagious, it has been shown to spread in households and among young children in day care centers. HCMV replicates within infected endothelial cells at a slow rate, taking about 5 days in cell culture. Like other herpesviruses, HCMV expresses genes in a temporally controlled manner. Immediate early genes are involved in the regulation of transcription, followed by early genes which are involved in viral DNA replication and further transcriptional regulation.
Late genes are expressed during the remainder of infection up to viral egress and code for structural proteins. While HCMV encodes for its own functional DNA polymerase, the virus makes use of the host RNA polymerase for the transcription of all of its genes. Synthesis of the viral double-stranded DNA genome occurs at the host cell nucleus within specialized viral replication compartments. Nearly 75% of the genes encoded by HCMV strain AD169 can be deleted and still result in the production of infectious virus; this suggests that the virus focuses on avoiding the host immune system for a timely entrance into latency. CMV infections are most significant in the perinatal period and in people. HCMV is one of the vertically transmitted infections. Congenital HCMV infection occurs. Up to 5/1000 live births are infected. Five percent develop multiple handicaps, develop cytomegalic inclusion disease with nonspecific signs that resemble rubella. Another 5% develop cerebral calcification. However, infants born preterm and infected with HCMV after birth may experience cognitive and motor impairments in life.
CMV infection or reactivation in people whose immune systems are compromised—for example people who have received transplants or are burned—causes illness and increases the risk of death. CMV reactivation is seen in people with severe colitis. Specific disease entities recognized in those people are CMV hepatitis, which may cause fulminant liver failure cytomegalovirus retinitis cytomegalovirus colitis CMV pneumonitis CMV esophagitis polyradiculopathy, transverse myelitis, subacute encephalitisPeople without CMV infection who are given organ transplants from CMV-infected donors require prophylactic treatment with valganciclovir or ganciclovir, regular serological monitoring to detect a rising CMV titre. CMV infections can still be of clinical significance in adult immunocompetent populations. CMV mononucleosis (some sources reserve "mononucleosis" for Ep
In genetics, a promoter is a region of DNA that initiates transcription of a particular gene. Promoters are located near the transcription start sites of genes, on the same strand and upstream on the DNA. Promoters can be about 100–1000 base pairs long. For transcription to take place, the enzyme that synthesizes RNA, known as RNA polymerase, must attach to the DNA near a gene. Promoters contain specific DNA sequences such as response elements that provide a secure initial binding site for RNA polymerase and for proteins called transcription factors that recruit RNA polymerase; these transcription factors have specific activator or repressor sequences of corresponding nucleotides that attach to specific promoters and regulate gene expression. In bacteria The promoter is recognized by RNA polymerase and an associated sigma factor, which in turn are brought to the promoter DNA by an activator protein's binding to its own DNA binding site nearby. In eukaryotes The process is more complicated, at least seven different factors are necessary for the binding of an RNA polymerase II to the promoter.
Promoters represent critical elements that can work in concert with other regulatory regions to direct the level of transcription of a given gene. A promoter is induced in response to changes in abundance or conformation of regulatory proteins in a cell, which enable activating transcription factors to recruit RNA polymerase; as promoters are immediately adjacent to the gene in question, positions in the promoter are designated relative to the transcriptional start site, where transcription of DNA begins for a particular gene. In the cell nucleus, it seems that promoters are distributed preferentially at the edge of the chromosomal territories for the co-expression of genes on different chromosomes. Furthermore, in humans, promoters show certain structural features characteristic for each chromosome. Core promoter – the minimal portion of the promoter required to properly initiate transcriptionIncludes the transcription start site and elements directly upstream A binding site for RNA polymerase RNA polymerase I: transcribes genes encoding 18S, 5.8S and 28S ribosomal RNAs RNA polymerase II: transcribes genes encoding messenger RNA and certain small nuclear RNAs and microRNA RNA polymerase III: transcribes genes encoding transfer RNA, 5s ribosomal RNAs and other small RNAs General transcription factor binding sites, e.g. TATA box, B recognition element.
Many other elements/motifs may be present. There is no such thing as a set of "universal elements" found in every core promoter. Proximal promoter – the proximal sequence upstream of the gene that tends to contain primary regulatory elements Approximately 250 base pairs upstream of the start site Specific transcription factor binding sites Distal promoter – the distal sequence upstream of the gene that may contain additional regulatory elements with a weaker influence than the proximal promoter Anything further upstream Specific transcription factor binding sites In bacteria, the promoter contains two short sequence elements 10 and 35 nucleotides upstream from the transcription start site; the sequence at -10 has the consensus sequence TATAAT. The sequence at -35 has the consensus sequence TTGACA; the above consensus sequences, while conserved on average, are not found intact in most promoters. On average, only 3 to 4 of the 6 base pairs in each consensus sequence are found in any given promoter.
Few natural promoters have been identified to date that possess intact consensus sequences at both the -10 and -35. The optimal spacing between the -35 and -10 sequences is 17 bp; some promoters contain one or more upstream promoter element subsites. The above promoter sequences are recognized only by RNA polymerase holoenzyme containing sigma-70. RNA polymerase holoenzymes containing other sigma factors recognize different core promoter sequences. <-- upstream downstream --> 5'-XXXXXXXPPPPPPXXXXXXPPPPPPXXXXGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGGXXXX-3' -35 -10 Gene to be transcribed for -10 sequence T A T A A T 77% 76% 60% 61% 56% 82% for -35 sequence T T G A C A 69% 79% 61% 56% 54% 54% Eukaryotic promoters are diverse and can be difficult to characterize, recent studies show that they are divided in more than 10 classes. Gene promoters are located upstream of the gene and can have regulatory elements several kilobases away from the transcriptional start site. In eukaryotes, the transcriptional complex can cause the DNA to bend back on itself, which allows for placement of regulatory sequences far from the actual site of transcription.
Eukaryotic RNA-polymerase-II-dependent promoters can contain a TATA element, recognized by the general transcription factor TATA-binding protein. The TATA element and BRE are located close to the transcriptional start site (
Inclusion bodies, sometimes called elementary bodies, are nuclear or cytoplasmic aggregates of stable substances proteins. They represent sites of viral multiplication in a bacterium or a eukaryotic cell and consist of viral capsid proteins. Inclusion bodies can be hallmarks of genetic diseases, as in the case of neuronal inclusion bodies in disorders like frontotemporal dementia and Parkinson's disease. Inclusion bodies contain little host protein, ribosomal components or DNA/RNA fragments, they almost contain the over expressed protein and aggregation in inclusion bodies has been reported to be reversible. It has been suggested that inclusion bodies are dynamic structures formed by an unbalanced equilibrium between aggregated and soluble proteins of Escherichia coli. There is a growing body of information indicating that formation of inclusion bodies occurs as a result of intracellular accumulation of folded expressed proteins which aggregate through non-covalent hydrophobic or ionic interactions or a combination of both.
Inclusion bodies are dense electron-refractile particles of aggregated protein found in both the cytoplasmic and periplasmic spaces of E. coli during high-level expression of heterologous protein. It is assumed that high level expression of non-native protein and hydrophobic protein is more prone to lead to accumulation as inclusion bodies in E. coli. In the case of proteins having disulfide bonds, formation of protein aggregates as inclusion bodies is anticipated since the reducing environment of bacterial cytosol inhibits the formation of disulfide bonds; the diameter of spherical bacterial inclusion bodies varies from 0.5–1.3 μm and the protein aggregates have either an amorphous or paracrystalline nature depending on the localization. Inclusion bodies have higher density than many of the cellular components, thus can be separated by high-speed centrifugation after cell disruption. Inclusion bodies despite being dense particles are hydrated and have a porous architecture. Inclusion bodies have a non-unit lipid membrane.
Protein inclusion bodies are classically thought to contain misfolded protein. However, this has been contested, as green fluorescent protein will sometimes fluoresce in inclusion bodies, which indicates some resemblance of the native structure and researchers have recovered folded protein from inclusion bodies; when genes from one organism are expressed in another organism the resulting protein sometimes forms inclusion bodies. This is true when large evolutionary distances are crossed: a cDNA isolated from Eukarya for example, expressed as a recombinant gene in a prokaryote risks the formation of the inactive aggregates of protein known as inclusion bodies. While the cDNA may properly code for a translatable mRNA, the protein that results will emerge in a foreign microenvironment; this has fatal effects if the intent of cloning is to produce a biologically active protein. For example, eukaryotic systems for carbohydrate modification and membrane transport are not found in prokaryotes; the internal microenvironment of a prokaryotic cell may differ from that of the original source of the gene.
Mechanisms for folding a protein may be absent, hydrophobic residues that would remain buried may be exposed and available for interaction with similar exposed sites on other ectopic proteins. Processing systems for the cleavage and removal of internal peptides would be absent in bacteria; the initial attempts to clone insulin in a bacterium suffered all of these deficits. In addition, the fine controls that may keep the concentration of a protein low will be missing in a prokaryotic cell, overexpression can result in filling a cell with ectopic protein that if it were properly folded, would precipitate by saturating its environment. Examples of viral inclusion bodies in animals are Intracytoplasmic eosinophilic - Negri bodies in Rabies Guarnieri bodies in vaccinia, variola Paschen bodies in variola Bollinger bodies in fowlpox Henderson-Patterson bodies in Molluscum contagiosum Eosinophilic inclusion bodies in boid inclusion body diseaseIntranuclear eosinophilic - Cowdry type A in Herpes simplex virus and Varicella zoster virus Torres bodies in Yellow fever Cowdry type B in Polio and adenovirusIntranuclear basophilic- Cowdry type B in Adenovirus "Owl's eye appearance" in cytomegalovirusBoth intranuclear and intracytoplasmic- Warthin–Finkeldey bodies in MeaslesExamples of viral inclusion bodies in plants include aggregations of virus particles and aggregations of viral proteins.
Depending on the plant and the plant virus family these inclusions can be found in epidermal cells, mesophyll cells, stomatal cells when plant tissue is properly stained. A red blood cell does not contain inclusions in the cytoplasm. However, it may be seen because of certain hematologic disorders. There are three kinds of erythrocyte inclusions: Developmental Organelles Howell-Jolly bodies: small, round fragments of the nucleus resulting from karyorrhexis or nuclear disintegration of the late reticulocyte and stain reddish-blue with Wright stain. Basophilic stipplings - these stipplings are either fine or coarse, deep blue to purple staining inclusion that appears in erythrocytes on a dried Wright stain. Pappenheimer bodies - are siderotic granules which are small, dark-staining granules that appear near the periphery of a young erythrocyte in a Wright stain. Polychromatophilic red cells - young red cells that no longer have nucleus but still contain some RNA. Cabot R
Humans are the only extant members of the subtribe Hominina. Together with chimpanzees and orangutans, they are part of the family Hominidae. A terrestrial animal, humans are characterized by their erect bipedal locomotion. Early hominins—particularly the australopithecines, whose brains and anatomy are in many ways more similar to ancestral non-human apes—are less referred to as "human" than hominins of the genus Homo. Several of these hominins used fire, occupied much of Eurasia, gave rise to anatomically modern Homo sapiens in Africa about 315,000 years ago. Humans began to exhibit evidence of behavioral modernity around 50,000 years ago, in several waves of migration, they ventured out of Africa and populated most of the world; the spread of the large and increasing population of humans has profoundly affected much of the biosphere and millions of species worldwide. Advantages that explain this evolutionary success include a larger brain with a well-developed neocortex, prefrontal cortex and temporal lobes, which enable advanced abstract reasoning, problem solving and culture through social learning.
Humans use tools better than any other animal. Humans uniquely use such systems of symbolic communication as language and art to express themselves and exchange ideas, organize themselves into purposeful groups. Humans create complex social structures composed of many cooperating and competing groups, from families and kinship networks to political states. Social interactions between humans have established an wide variety of values, social norms, rituals, which together undergird human society. Curiosity and the human desire to understand and influence the environment and to explain and manipulate phenomena have motivated humanity's development of science, mythology, religion and numerous other fields of knowledge. Though most of human existence has been sustained by hunting and gathering in band societies many human societies transitioned to sedentary agriculture some 10,000 years ago, domesticating plants and animals, thus enabling the growth of civilization; these human societies subsequently expanded, establishing various forms of government and culture around the world, unifying people within regions to form states and empires.
The rapid advancement of scientific and medical understanding in the 19th and 20th centuries permitted the development of fuel-driven technologies and increased lifespans, causing the human population to rise exponentially. The global human population was estimated to be near 7.7 billion in 2015. In common usage, the word "human" refers to the only extant species of the genus Homo—anatomically and behaviorally modern Homo sapiens. In scientific terms, the meanings of "hominid" and "hominin" have changed during the recent decades with advances in the discovery and study of the fossil ancestors of modern humans; the clear boundary between humans and apes has blurred, resulting in now acknowledging the hominids as encompassing multiple species, Homo and close relatives since the split from chimpanzees as the only hominins. There is a distinction between anatomically modern humans and Archaic Homo sapiens, the earliest fossil members of the species; the English adjective human is a Middle English loanword from Old French humain from Latin hūmānus, the adjective form of homō "man."
The word's use as a noun dates to the 16th century. The native English term man can refer to the species as well as to human males, or individuals of either sex; the species binomial "Homo sapiens" was coined by Carl Linnaeus in his 18th-century work Systema Naturae. The generic name "Homo" is a learned 18th-century derivation from Latin homō "man," "earthly being"; the species-name "sapiens" means "wise" or "sapient". Note that the Latin word homo refers to humans of either gender, that "sapiens" is the singular form; the genus Homo evolved and diverged from other hominins in Africa, after the human clade split from the chimpanzee lineage of the hominids branch of the primates. Modern humans, defined as the species Homo sapiens or to the single extant subspecies Homo sapiens sapiens, proceeded to colonize all the continents and larger islands, arriving in Eurasia 125,000–60,000 years ago, Australia around 40,000 years ago, the Americas around 15,000 years ago, remote islands such as Hawaii, Easter Island and New Zealand between the years 300 and 1280.
The closest living relatives of humans are gorillas. With the sequencing of the human and chimpanzee genomes, current estimates of similarity between human and chimpanzee DNA sequences range between 95% and 99%. By using the technique called a molecular clock which estimates the time required for the number of divergent mutations to accumulate between two lineages, the approximate date for the split between lineages can be calculated; the gibbons and orangutans were the first groups to split from the line leading to the h
Herpes simplex virus
Herpes simplex virus 1 and 2 known by their taxonomical 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 common and contagious, they can be spread. About 67% of the world population under the age of 50 has HSV-1. In the United States more than one-in-six people have HSV-2. Although it can be transmitted through any intimate contact, it is one of the most common sexually transmitted infections. Many of those who are infected never develop symptoms. Symptoms, when they occur, may include watery blisters in the skin or mucous membranes of the mouth, nose, or genitals. Lesions heal with a scab characteristic of herpetic disease. Sometimes, the viruses cause mild or atypical symptoms during outbreaks. However, they can cause more troublesome forms of herpes simplex; as neurotropic and neuroinvasive viruses, HSV-1 and -2 persist in the body by hiding from the immune system in the cell bodies of neurons.
After the initial or primary infection, some infected people experience sporadic episodes of viral reactivation or outbreaks. In an outbreak, the virus in a nerve cell becomes active and is transported via the neuron's axon to the skin, where virus replication and shedding occur and cause new sores. HSV-1 and HSV-2 are transmitted by contact with an infected person who has reactivations of the virus. HSV-2 is periodically shed in the human genital tract, most asymptomatically. Most sexual transmissions occur during periods of asymptomatic shedding. Asymptomatic reactivation means that the virus causes atypical, subtle, or hard-to-notice symptoms that are not identified as an active herpes infection, so acquiring the virus is possible if no active HSV blisters or sores are present. In one study, daily genital swab samples found HSV-2 at a median of 12–28% of days among those who have had an outbreak, 10% of days among those suffering from asymptomatic infection, with many of these episodes occurring without visible outbreak.
In another study, 73 subjects were randomized to receive valaciclovir 1 g daily or placebo for 60 days each in a two-way crossover design. A daily swab of the genital area was self-collected for HSV-2 detection by polymerase chain reaction, to compare the effect of valaciclovir versus placebo on asymptomatic viral shedding in immunocompetent, HSV-2 seropositive subjects without a history of symptomatic genital herpes infection; the study found that valaciclovir reduced shedding during subclinical days compared to placebo, showing a 71% reduction. About 88% of patients treated with valaciclovir had no recognized signs or symptoms versus 77% for placebo. For HSV-2, subclinical shedding may account for most of the transmission. Studies on discordant partners show that the transmission rate is 5 per 10,000 sexual contacts. Atypical symptoms are attributed to other causes, such as a yeast infection. HSV-1 is acquired orally during childhood, it may be sexually transmitted, including contact with saliva, such as kissing and mouth-to-genital contact.
HSV-2 is a sexually transmitted infection, but rates of HSV-1 genital infections are increasing. Both viruses may be transmitted vertically during childbirth. However, the risk of infection transmission is minimal if the mother has no symptoms or exposed blisters during delivery; the risk is considerable when the mother is infected with the virus for the first time during late pregnancy. Herpes simplex viruses can affect areas of skin exposed to contact with an infected person. An example of this is herpetic whitlow, a herpes infection on the fingers; this was a common affliction of dental surgeons prior to the routine use of gloves when conducting treatment on patients. Animal herpes viruses all share some common properties; the structure of herpes viruses consists of a large, double-stranded, linear DNA genome encased within an icosahedral protein cage called the capsid, wrapped in a lipid bilayer called the envelope. The envelope is joined to the capsid by means of a tegument; this complete particle is known as the virion.
HSV-1 and HSV-2 each contain at least 74 genes within their genomes, although speculation over gene crowding allows as many as 84 unique protein coding genes by 94 putative ORFs. These genes encode a variety of proteins involved in forming the capsid and envelope of the virus, as well as controlling the replication and infectivity of the virus; these genes and their functions are summarized in the table below. The genomes of HSV-1 and HSV-2 are complex and contain two unique regions called the long unique region and the short unique region. Of the 74 known ORFs, UL contains 56 viral genes, whereas US contains only 12. Transcription of HSV genes is catalyzed by RNA polymerase II of the infected host. Immediate early genes, which encode proteins that regulate the expression of early and late viral genes, are the first to be expressed following infection. Early gene expression follows, to allow the synthesis of enzymes involved in DNA replication and the production of certain envelope glycoproteins.
Expression of late genes occurs last. Five proteins from form the viral capsid - UL6, UL18, UL35, UL38, the major capsid p
Lysogeny, or the lysogenic cycle, is one of two cycles of viral reproduction. Lysogeny is characterized by integration of the bacteriophage nucleic acid into the host bacterium's genome or formations of a circular replicon in the bacterial cytoplasm. In this condition the bacterium continues to reproduce normally; the genetic material of the bacteriophage, called a prophage, can be transmitted to daughter cells at each subsequent cell division, at events can release it, causing proliferation of new phages via the lytic cycle. Lysogenic cycles can occur in eukaryotes, although the method of DNA incorporation is not understood; the difference between lysogenic and lytic cycles is that, in lysogenic cycles, the spread of the viral DNA occurs through the usual prokaryotic reproduction, whereas a lytic cycle is more immediate in that it results in many copies of the virus being created quickly and the cell is destroyed. One key difference between the lytic cycle and the lysogenic cycle is that the lysogenic cycle does not lyse the host cell straight away.
Phages that replicate only via the lytic cycle are known as virulent phages while phages that replicate using both lytic and lysogenic cycles are known as temperate phages. In the lysogenic cycle, the phage DNA first integrates into the bacterial chromosome to produce the prophage; when the bacterium reproduces, the prophage is copied and is present in each of the daughter cells. The daughter cells can continue to replicate with the prophage present or the prophage can exit the bacterial chromosome to initiate the lytic cycle. In lysogenic cycle the host DNA is not hydrolysed but in lytic cycle the host DNA is hydrolysed in the lytic phase. Bacteriophages are viruses that replicate within a bacterium. Temperate phages can reproduce using both the lysogenic cycle. Via the lysogenic cycle, the bacteriophage's genome is not expressed and is instead integrated into the bacteria's genome to form the prophage. Since the bacteriophage's genetic information is incorporated into the bacteria's genetic information as a prophage, the bacteriophage replicates passively as the bacterium divides to form daughter bacteria cells.
In this scenario, the daughter bacteria cells are known as lysogens. Lysogens can remain in the lysogenic cycle for many generations but can switch to the lytic cycle at any time via a process known as induction. During induction, prophage DNA is excised from the bacterial genome and is transcribed and translated to make coat proteins for the virus and regulate lytic growth; the model organism for studying lysogeny is lambda phage. Prophage integration, maintenance of lysogeny and control of phage genome excision in induction is described in detail in the lambda phage article. Bacteriophages are parasitic because they infect their hosts, use bacterial machinery to replicate, lyse the bacteria. Temperate phages can lead to both advantages and disadvantages for their hosts via the lysogenic cycle. During the lysogenic cycle, the virus genome is incorporated as prophage and a repressor prevents viral replication. Nonetheless, a temperate phage can escape repression to replicate, produce viral particles, lyse the bacteria.
The temperate phage escaping repression would be a disadvantage for the bacteria. On the other hand, the prophage may transfer genes that enhance host virulence and resistance to the immune system; the repressor produced by the prophage that prevents prophage genes from being expressed confers an immunity for the host bacteria from lytic infection by related viruses. In some interactions between lysogenic phages and bacteria, lysogenic conversion may occur, which can be called phage conversion, it is when a temperate phage induces a change in the phenotype of the infected bacteria, not part of a usual phage cycle. Changes can involve the external membrane of the cell by making it impervious to other phages or by increasing the pathogenic capability of the bacteria for a host. In this way, temperate bacteriophages play a role in the spread of virulence factors, such as exotoxins and exoenzymes, amongst bacteria; this change stays in the genome of the infected bacteria and is copied and passed down to daughter cells.
Lysogenic conversion has shown to enable biofilm formation in Bacillus anthracis Strains of B. anthracis cured of all phage were unable to form biofilms, which are surface-adhered bacterial communities that enable bacteria to better access nutrients and survive environmental stresses. In addition to biofilm formation in B. anthracis, lysogenic conversion of Bacillus subtilis, Bacillus thuringiensis, Bacillus cereus has shown an enhanced rate or extent of sporulation. Sporulation produces endospores, which are metabolically dormant forms of the bacteria that are resistant to temperature, ionizing radiation, desiccation and disinfectants. Non-virulent bacteria have been shown to transform into virulent pathogens through lysogenic conversion with the virulence factors carried on the lysogenic prophage. Virulence genes carried within prophages as discrete autonomous genetic elements, known as morons, confer an advantage to the bacteria that indirectly benefits the virus through enhanced lysogen survival.
Examples: Corynebacterium diphtheriae produces the toxin of diphtheria only when it is infected by the phage β. In this case, the gene that codes for the toxin is carried by the phage, not the bacteria. Vibrio cholerae is a non-toxic strain that can become toxic, producing cholera toxin, when it is infected with the phage CTXφ. Shigella dysenteriae, which produces dysentery has toxins that fall into two major