Gammaherpesvirinae is a subfamily of viruses in the order Herpesvirales, in the family Herpesviridae. Viruses in Gammaherpesvirinae are distinguished by reproducing at a more variable rate than other subfamilies of Herpesviridae. Mammals serve as natural hosts. There are 32 species in this subfamily, divided among 4 genera. Diseases associated with this subfamily include: HHV-4: infectious mononucleosis. HHV-8: kaposi's sarcoma. Herpesviruses represent a group of double-stranded DNA viruses distributed within the animal kingdom; the family Herpesviridae, which contains eight viruses that infect humans, is the most extensively studied group within this order and comprises three subfamilies, namely Alphaherpesvirinae, Betaherpesvirinae and Gammaherpesvirinae. Gammaherpesviruses belong to four separate genera: the well-established genera Lymphocryptovirus and Rhadinovirus and the more defined genera Macavirus and Percavirus. Gammaherpesviruses are of primary interest due to the two human viruses, EBV and KSHV and the diseases they cause.
The gammaherpesviruses replicate and persist in lymphoid cells but some are capable of undergoing lytic replication in epithelial or fibroblast cells. Gammaherpesviruses may be a cause of chronic fibrotic lung diseases in animals; these viruses can be subdivided into two genera: lymphocryptoviruses and rhadinoviruses: * Note: Animal viruses can and do infect humans and human cells to various degrees, just not commonly. Murid herpesvirus 68 is an important model system for the study of gammaherpesviruses with tractable genetics; the gammaherpesviruses, including HVS, EBV, KSHV, RRV, are capable of establishing latent infection in lymphocytes. Unclassified viruses. Within this genus there are a number of unclassified viruses including cynomys herpesvirus 1 Elephantid herpesvirus 3, Elephantid herpesvirus 4, Elephantid herpesvirus 5, Procavid herpesvirus 1, Trichechid herpesvirus 1 and Common bottlenose dolphin gammaherpesvirus 1. Group: dsDNA Viruses in Gammaherpesvirinae are enveloped, with icosahedral, spherical to pleomorphic, round geometries, T=16 symmetry.
The diameter is around 150-200 nm. Genomes are non-segmented, around 180kb in length; the main stages in the lifecycle of Gamma herpes virus are namely • Virus attachment and entry • Viral DNA injection through nuclear pore complex into nucleus • Assembly of nucleocapsids and encapsidation of viral genome • Primary envelopment, invaginations of nuclear membrane and nuclear egress • Tegumentation and secondary envelopment in the cytoplasm • Egress and extracellularvirions release The lytic cycle of the gammaherpesviruses is initiated only on rare occasions. Therefore, the least contribution to pathogenicity has to be expected from this stage; the ORFs expressed during that stage are further divided into immediate-early and late. Promoter activation mediated by these proteins has a strong effect on DNA synthesis from the origins of lytic DNA replication; as a result, virions are released from the productively infected cells. Herpesviruses have large genomes containing a wide array of genes. Although the first ORF in these gammaherpesviruses have oncogenic potential, other viral genes may play a role in viral transformation.
A striking feature of the four gammaherpesviruses is that they contain distinct ORFs involved in lymphocyte signaling events. At the left end of each viral genome are located ORFs encoding distinct transforming proteins; the Gammaherpes viral genes are capable of modulating cellular signals such that cell proliferation and viral replication occur at the appropriate times in the viral life cycle. Viruses that establish lifelong latent infections must ensure that the viral genome is maintained within the latently infected cell throughout the life of the host, yet at the same time must be capable of avoiding elimination by the immune surveillance system must avoid being detected by host CD8+ cytotoxic T lymphocytes; the gamma-herpesviruses are characteristically latent in lymphocytes and drive the proliferation that requires the expression of latent viral antigens. The majority of gammaherpesviruses encode a specific protein, critical for maintenance of the viral genome within latently infected cells termed the genome maintenance protein.
GMPs are DNA-binding proteins that ensures that, as the host cell progresses through mitosis, the viral episomes are partitioned to daughter cells. This provides continuous existence of the viral genome within the host cells. Attenuated virus mutants represent a promising approach towards gamma-herpesvirus infection control. Latency-deficient and, apathogenic MHV-68 mutants are found to be effective vaccines against these viruses. Research in this area is exclusively performed using MHV68 as KSHV and EBV do not productively infect model organisms used for this type of experimentation. Gammaherpesvirinae at the US National Library of Medicine Medical Subject Headings ICTVdb Overview ICTVdb Details Taxonomic Proposals from the Herpesviridae Study Group Viralzone: Gammaherpesvirinae ICTV
Infection of the skin is distinguished from dermatitis, inflammation of the skin, but a skin infection can result in skin inflammation. Skin inflammation due to skin infection is called infective dermatitis. Bacterial skin infections affected about 155 million people and cellulitis occurred in about 600 million people in 2013. Bacterial skin infections include: Folliculitis is an infection of the hair follicle that can resemble pimples. Impetigo is a contagious bacterial skin infection most common among pre-school children, it is caused by Staphylococcus aureus, sometimes by Streptococcus pyogenes. Erysipelas is an acute streptococcus bacterial infection of the deep epidermis with lymphatic spread. Cellulitis is a diffuse inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. Cellulitis can be caused by normal skin flora or by exogenous bacteria, occurs where the skin has been broken: cracks in the skin, blisters, insect bites, surgical wounds, intravenous drug injection or sites of intravenous catheter insertion.
Skin on the face or lower legs is most affected by this infection, though cellulitis can occur on any part of the body. Fungal skin infections may present as either a superficial or deep infection of the skin, and/or nails; as of 2010, they affect about one billion people globally. Parasitic infestations and bites in humans are caused by several groups of organisms belonging to the following phyla: Annelida, Bryozoa, Cnidaria, Echinodermata, Nemathelminthes and Protozoa. Virus-related cutaneous conditions are caused by two main groups of viruses–DNA and RNA types–both of which are obligatory intracellular parasites. Dempster-Shafer Theory is used for detecting skin infection and displaying the result of the detection process
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
Human herpesvirus 6
Human herpesvirus 6 is the common collective name for Human betaherpesvirus 6A and Human betaherpesvirus 6B. These related viruses are two of the nine herpesviruses known to have humans as their primary host. HHV-6A and HHV-6B are double stranded DNA viruses within the Betaherpesvirinae subfamily and of the genus Roseolovirus. HHV-6A and HHV-6B infect all of the human populations that have been tested. HHV-6A has been described as more neurovirulent, as such is more found in patients with neuroinflammatory diseases such as multiple sclerosis. HHV-6 levels in the brain are elevated in people with Alzheimer's disease. HHV-6B primary infection is the cause of the common childhood illness exanthema subitum. Additionally, HHV-6B reactivation is common in transplant recipients, which can cause several clinical manifestations such as encephalitis, bone marrow suppression, pneumonitis. A variety of tests are used in the detection HHV-6, some of which do not differentiate the two species. During 1986, Syed Zaki Salahuddin, Dharam Ablashi, Robert Gallo cultivated peripheral blood mononuclear cells from patients with AIDS and lymphoproliferative illnesses.
Short-lived, refractile cells that contained intranuclear and/or intracytoplasmic inclusion bodies were documented. Electron microscopy revealed a novel virus. Shortly after its discovery, Ablashi et al. described five cell lines that can be infected by the newly discovered HBLV. They published that HSB-2, a particular T-cell line, is susceptible to infection. Ablashi's pioneering research concluded by suggesting that the virus name be changed from HBLV to HHV-6, in accord with the published provisional classification of herpes viruses. Years HHV-6 was divided into subtypes. Early research described two similar, yet unique variants: HHV-6A and HHV-6B; the distinction was warranted due to unique restriction endonuclease cleavages, monoclonal antibody reactions, growth patterns. HHV-6A includes several adult-derived strains and its disease spectrum is not well defined, although it is thought by some to be more neurovirulent. HHV-6B is detected in children with roseola infantum, as it is the etiologic agent for this condition.
Within these two viruses is a sequence homology of 95%. In 2012, HHV-6A and HHV-6B were recognized as distinct species. HHV-6A and HHV-6B were recognized by the International Committee on Taxonomy of Viruses as distinct species in 2012. Human Roseoloviruses include HHV-6A, HHV-6B and HHV-7. Herpesvirus was established as a genus in 1971 in the first report of the ICTV; this genus consisted of 23 viruses among 4 groups. In 1976, a second ICTV report was released in which this genus was elevated to the family level — the herpetoviridae; because of possible confusion with viruses derived from reptiles, the family name was changed in the third report to herpesviridae. In this report, the family Herpesviridae was divided into 5 unnamed genera. In 2009, the order Herpesvirales was created; this was necessitated by the discovery that the herpes viruses of fish and molluscs are only distantly related to those of birds and mammals. Order Herpesvirales contains three families, the Herpesviridae, which contains the long-recognized herpesviruses of mammals and reptiles, plus two new families — the family Alloherpesviridae which incorporates herpes viruses of bony fish and frogs, the family Malacoherpesviridae which contains viruses of molluscs.
As of 2012, this order has 3 families, 4 subfamilies, 18 genera and 97 species. The diameter of an HHV-6 virion is about 2000 Angstroms; the virion's outer portion consists of a lipid bilayer membrane that contains viral glycoproteins and is derived from that of the host. Below this membrane envelope is a tegument which surrounds an icosahedral capsid, composed of 162 capsomeres; the protective capsid of HHV-6 contains double stranded linear DNA. During maturation of HHV-6 virions, human cell membranes are used to form viral lipid envelopes. During this process HHV-6 utilizes lipid rafts, which are membranous microdomains enriched by cholesterol and glycosylphosphatidylinositol-anchored proteins. Early researchers suspected. However, researched published in 2009 suggests that the HHV-6 virus utilizes trans-Golgi-network-derived vesicles for assembly; the genetic material of HHV-6 is composed of linear, double stranded DNA which contains an origin of replication, two 8–10 kb left and right direct repeat termini, a unique segment, 143–145kb.
The origin of replication is. The direct repeat termini possess a repeated TTAGGG sequence. Variability in the number of telomeric repeats is observed in the range of 15–180; these termini contain pac-1 and pac-2 cleavage and packing signals that are conserved among herpesviruses. The unique segment contains seven major core gene blocks, characteristic of herpesviruses; these conserved genes code for proteins that are involved in replication and packing of the viral genome into a mature virion. Additionally, they code for a number of immunomo
A DNA virus is a virus that has DNA as its genetic material and replicates using a DNA-dependent DNA polymerase. The nucleic acid is double-stranded DNA but may be single-stranded DNA. DNA viruses belong to either Group Group II of the Baltimore classification system for viruses. Single-stranded DNA is expanded to double-stranded in infected cells. Although Group VII viruses such as hepatitis B contain a DNA genome, they are not considered DNA viruses according to the Baltimore classification, but rather reverse transcribing viruses because they replicate through an RNA intermediate. Notable diseases like smallpox and the chickenpox are caused by such DNA viruses. Genome organization within this group varies considerably; some have circular genomes. Some families have circularly permuted linear genomes. Others have linear genomes with covalently closed ends. A virus infecting archaea was first described in 1974. Several others have been described since: most have head-tail morphologies and linear double-stranded DNA genomes.
Other morphologies have been described: spindle shaped, rod shaped, filamentous and spherical. Additional morphological types may exist. Orders within this group are defined on the basis of morphology rather than DNA sequence similarity, it is thought that morphology is more conserved in this group than sequence similarity or gene order, variable. Three orders and 31 families are recognised. A fourth order — Megavirales — for the nucleocytoplasmic large DNA viruses has been proposed; this proposal has yet to be ratified by the ICTV. Four genera are recognised. Fifteen families are enveloped; these include all three families in the order Herpesvirales and the following families: Ascoviridae, Asfarviridae, Fuselloviridae, Guttaviridae, Iridoviridae, Lipothrixviridae and Poxviridae. Bacteriophages belonging to the families Tectiviridae and Corticoviridae have a lipid bilayer membrane inside the icosahedral protein capsid and the membrane surrounds the genome; the crenarchaeal virus Sulfolobus turreted.
The genomes in this group vary from ~10 kilobases to over 2.5 megabases in length. The largest bacteriophage known is Klebsiella Phage vB_KleM-RaK2 which has a genome of 346 kilobases; the virophages are a group of viruses. A virus with a novel method of genome packing infecting species of the genus Sulfolobus has been described; as this virus does not resemble any known virus it has been classified into a new family, the Portogloboviridae. Another Sulfolobus infecting virus - Sulfolobus ellipsoid virus 1 - has been described; this enveloped virus may be classified into a new taxon. Species of the order Caudovirales and of the families Corticoviridae and Tectiviridae infect bacteria. Species of the order Ligamenvirales and the families Ampullaviridae, Clavaviridae, Globuloviridae, Guttaviridae and Turriviridae infect hyperthermophilic archaea species of the Crenarchaeota. Species of the order Herpesvirales and of the families Adenoviridae, Iridoviridae, Papillomaviridae and Poxviridae infect vertebrates.
Species of the families Ascovirus, Hytrosaviridae and Polydnaviruses and of the genus Nudivirus infect insects. Species of the family Mimiviridae and the species Marseillevirus, Mavirus virophage and Sputnik virophage infect protozoa. Species of the family Nimaviridae infect crustaceans. Species of the family Phycodnaviridae and the species Organic Lake virophage infect algae; these are the only known dsDNA viruses. Species of the family Plasmaviridae infect species of the class Mollicutes. Species of the family Pandoraviridae infect amoebae. Species of the genus Dinodnavirus infect dinoflagellates; these are the only known viruses. Species of the genus Rhizidiovirus infect stramenopiles; these are the only known dsDNA viruses. Species of the genus Salterprovirus and Sphaerolipoviridae infect species of the Euryarchaeota. Order Caudovirales Family Myoviridae—includes Enterobacteria phage T4 Family Podoviridae—includes Enterobacteria phage T7 Family Siphoviridae—includes Enterobacteria phage λ Order Herpesvirales Family Alloherpesviridae Family Herpesviridae—includes human herpesviruses, Varicella Zoster virus Family Malacoherpesviridae Order Ligamenvirales Family Lipothrixviridae Family Rudiviridae Unassigned families Family Adenoviridae—includes viruses which cause human adenovirus infection Family Ampullaviridae Family Ascoviridae Family Asfarviridae—includes African swine fever virus Family Baculoviridae Family Bicaudaviridae Family Clavaviridae Family Corticoviridae Family Fuselloviridae Family Globuloviridae Family Guttaviridae Family Hytrosaviridae Family Iridoviridae Family Lavidaviridae Family Marseilleviridae Family Mimiviridae Family Nudiviridae Family Nimaviridae Family Pandoraviridae Family Papillomaviridae Family Phycodnaviridae Family Plasmaviridae Family Polydnaviruses Family Polyomaviridae—includes Simian virus 40, JC virus, BK virus Family Poxviridae—includes Cowpox virus, smallpox Family Sphaerolipoviridae Family Tectiviridae Family Tristromaviridae Family Turriviridae Unassigned genera Dinodnavirus Salterprovirus Rhizidiovirus Unassigned species Abalone shriveling syndrome-associated virus Bandicoot papillomatosis carcinomatosis vi
Human alphaherpesvirus 3
Human alphaherpesvirus 3 referred to as the varicella-zoster virus, is one of eight herpesviruses known to infect humans. It causes chickenpox, a disease most affecting children and young adults, shingles in adults. VZV is a worldwide pathogen known by many names: chickenpox virus, varicella virus, zoster virus, Human herpesvirus 3. VZV infections are species-specific to humans, but can survive in external environments for a few hours, maybe a day or two. VZV multiplies in the lungs, causes a wide variety of symptoms. After the primary infection, the virus goes dormant in the nerves, including the cranial nerve ganglia, dorsal root ganglia, autonomic ganglia. Many years after the person has recovered from chickenpox, VZV can reactivate to cause neurologic conditions. Primary varicella zoster virus infection results in chickenpox, which may result in complications including encephalitis, pneumonia, or bronchitis; when clinical symptoms of chickenpox have resolved, VZV remains dormant in the nervous system of the infected person, in the trigeminal and dorsal root ganglia.
VZV enters through the respiratory system. Having an incubation period of 10–21 days, averaging at 14 days. Targeting the skin and peripheral nerve, the period of illness is from 3 to 4 days. 1 -- 2 days before the rashes appear, is. Some signs and symptoms are vesicles that fill with pus and scab before healing. Lesions tend to stay towards the face and lower back sometimes on the chest and shoulders. Shingles stay located around the waist. In about 10–20% of cases, VZV reactivates in life, producing a disease known as shingles or herpes zoster. VZV can infect the central nervous system, with a 2013 article reporting an incidence rate of 1.02 cases per 100,000 inhabitants in Switzerland, an annual incidence rate of 1.8 cases per 100,000 inhabitants in Sweden. Other serious complications of varicella zoster infection include postherpetic neuralgia, Mollaret's meningitis, zoster multiplex, inflammation of arteries in the brain leading to stroke, herpes ophthalmicus, or zoster sine herpete. In Ramsay Hunt syndrome, VZV affects the geniculate ganglion giving lesions that follow specific branches of the facial nerve.
Symptoms may include painful blisters on the tongue and ear along with one sided facial weakness and hearing loss. If infected during initial stages of pregnancy severe damage to the fetus can take place. Reye’s syndrome can happen after initial infection, continuous vomiting and shows signs of brain dysfunction: extreme drowsiness or combative behavior. In some cases, death or coma can follow. Reye’s syndrome affects children and teenagers, using aspirin during infection can increase this risk. VZV is related to the herpes simplex viruses, sharing much genome homology; the known envelope glycoproteins correspond with those in HSV. VZV fails to produce the LAT that play an important role in establishing HSV latency. VZV virons are 180 -- 200 nm in diameter, their lipid envelope encloses the 100 nm nucleocapsid of 162 hexameric and pentameric capsomeres arranged in an icosahedral form. Its DNA is a single, double-stranded molecule, 125,000 nt long; the capsid is surrounded by loosely associated proteins known collectively as the tegument.
The tegument is in turn covered by a lipid envelope studded with glycoproteins that are displayed on the exterior of the virion, each 8 nm long. The genome was first sequenced in 1986, it is a linear duplex DNA molecule, a laboratory strain has 124,884 base pairs. The genome has 2 predominant isomers, depending on the orientation of the S segment, P and IS which are present with equal frequency for a total frequency of 90–95%; the L segment can be inverted resulting in a total of four linear isomers. This is distinct from HSV's equiprobable distribution, the discriminatory mechanism is not known. A small percentage of isolated molecules are circular genomes. There are at least 70 open reading frames in the genome. There are at least five clades of this virus. Clades 1 and 3 include European/North American strains. Clade 4 includes some strains from Europe but its geographic origins need further clarification. Commonality with HSV1 and HSV2 indicates a common ancestor. Relation with other human herpes viruses is less strong, but many homologues and conserved gene blocks are still found.
There are four genotypes that do not fit into these clades. The current distribution of these clades is Europe. Allocation of VZV strains to clades required sequence of whole virus genome. All molecular epidemiological data on global VZV strains distribution obtained with targeted sequencing of selected regions. Phylogenetic analysis of VZV genomic sequences resolves wild-type strains into 9 genotypes. Complete sequences for M3 and M4 strains are unavailable, but targeted analyses of representative strains suggest they are stable, cir