Virus Famili Herpesviridae

The Herpesviridae are a large family of DNA viruses that cause diseases in animals, including humans. The members of this family are also known as herpesviruses. The family name is derived from the Greek word herpein ("to creep"), referring to the latent, recurring infections typical of this group of viruses. Herpesviridae can cause latent or lytic infections.
Viral structure

Herpesviruses all share a common structure—all herpesviruses are composed of relatively large double-stranded, linear DNA genomes encoding 100-200 genes encased within an icosahedral protein cage called the capsid which is itself wrapped in a protein layer called the tegument containing both viral proteins and viral mRNAs and a lipid bilayer membrane called the envelope. This whole particle is known as a virion.
Herpes virus life-cycle

All herpesviruses are nuclear-replicating—the viral DNA is transcribed to RNA within the infected cell's nucleus.

Infection is initiated when a viral particle contacts a cell with specific types of receptor molecules on the cell surface. Following binding of viral envelope glycoproteins to cell membrane receptors, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus. Within the nucleus, replication of viral DNA and transcription of viral genes occurs.

During symptomatic infection, infected cells transcribe lytic viral genes. In some host cells, a small number of viral genes termed latency associated transcript (LAT) accumulate instead. In this fashion the virus can persist in the cell (and thus the host) indefinitely. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free.

Reactivation of latent viruses has been implicated in a number of diseases (e.g. Shingles, Pityriasis Rosea). Following activation, transcription of viral genes transitions from latency-associated LAT to multiple lytic genes; these lead to enhanced replication and virus production. Often, lytic activation leads to cell death. Clinically, lytic activation is often accompanied by emergence of non-specific symptoms such as low grade fever, headache, sore throat, malaise, and rash as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.
Taxonomy

The genus Herpesvirus was established in 1971 in the first report of the International Committee on Taxonomy of Viruses (ICTV). This genus consisted of 23 viruses and 4 groups of viruses. In the second ICTV report in 1976 this genus was elevated to family level - the Herpetoviridae. Because of possible confusion with viruses derived from reptiles this name was changed in the third report in 1979 to Herpesviridae. In this report the family Herpesviridae was divided into 3 subfamilies (Alphaherpesvirinae, Betaherpesvirinae and Gammaherpesvirinae) and 5 unnamed genera: 21 viruses were listed. In 2009 the family Herpesviridae was elevated to the order Herpesvirales. This elevation was necessitated by the discovery that the herpes viruses of fish and molluscs were only distantly related to those of birds and mammals. Two new families were created - the family Alloherpesviridae which incorporates bony fish and frog viruses and the family Malacoherpesviridae which contains those of molluscs.

This order currently has 3 families, 3 subfamilies plus 1 unassigned, 17 genera, 90 species and plus 48 as yet unassigned viruses.
Virus naming system

The system of naming herpes viruses was originated in 1973 and has been elaborated considerably since. The recommended naming system specified that each herpes virus should be named after the taxon (family or subfamily) to which its primary natural host belongs. The subfamily name is used for viruses from members of the family Bovidae or from primates (the virus name ending in –ine, e.g. bovine) and the host family name for other viruses (ending in –id, e.g. equid). Human herpes viruses have been treated as an exception (human rather than hominid). Following the host-derived term, the word herpes virus is added, followed by an arabic number (1,2,3,...). These last two additions bear no implied meaning about taxonomic or biological properties of the virus.

Some exceptions to this system exist. A number of viruses' names (e.g. Epstein–Barr virus) are so widely used that it is impractical to attempt to insist on their replacement. This has led to the a dual nomenclature in the literature for some herpes viruses. All herpes viruses described since this system was adopted have been named in accordance with it.
Immune system evasions
cmvIL-10

Herpesviruses are known for their ability to establish lifelong infections. One way this is possible is through immune evasion. Herpesviruses have found many different ways to evade the immune system. One such way is by encoding a protein mimicking human interleukin 10 (hIL-10) and another is by downregulation of the Major Histocompatibility Complex II (MHC II) in infected cells. Research conducted on cytomegalovirus (CMV) indicates that the viral human IL-10 homolog, cmvIL-10, is important in inhibiting pro-inflammatory cytokine synthesis. The cmvIL-10 protein has 27% identity with hIL-10 and only one conserved residue out of the nine amino acids that make up the functional site for cytokine synthesis inhibition on hIL-10. There is, however, much similarity in the functions of hIL-10 and cmvIL-10. Both have been shown to down regulate IFN-γ, IL-1α, GM-CSF, IL-6 and TNF- α, which are all pro-inflammatory cytokines. They have also been shown to play a role in downregulating MHC I and MHC II and up regulating HLA-G (non-classical MHC I). These two events allow for immune evasion by suppressing the cell-mediated immune response and natural killer cell response, respectively. The similarities between hIL-10 and cmvIL-10 may be explained by the fact that hIL-10 and cmvIL-10 both use the same cell surface receptor, the hIL-10 receptor. One difference in the function of hIL-10 and cmvIL-10 is that hIL-10 causes human peripheral blood mononuclear cells (PBMC) to both increase and decrease in proliferation whereas cmvIL-10 only causes a decrease in proliferation of PBMCs. This indicates that cmvIL-10 may lack the stimulatory effects that hIL-10 has on these cells.

It was found that cmvIL-10 functions through phosphorylation of the Stat3 protein. It was originally thought that this phosphorylation was a result of the JAK-STAT pathway. However, despite evidence that JAK does indeed phosphorylate Stat3, its inhibition has no significant influence on cytokine synthesis inhibition. Another protein, PI3K, was also found to phosphorylate Stat3. PI3K inhibition, unlike JAK inhibition, did have a significant impact on cytokine synthesis. The difference between PI3K and JAK in Stat3 phosphorylation is that PI3K phosphorylates Stat3 on the S727 residue whereas JAK phosphorylates Stat3 on the Y705 residue. This difference in phosphorylation positions seems to be the key factor in Stat3 activation leading to inhibition of pro-inflammatory cytokine synthesis. In fact, when a PI3K inhibitor is added to cells, the cytokine synthesis levels are significantly restored. The fact that cytokine levels are not completely restored indicates there is another pathway activated by cmvIL-10 that is inhibiting cytokine synthesis. The proposed mechanism is that cmvIL-10 activates PI3K which in turn activates PKB (Akt). PKB may then activate mTOR, which may target Stat3 for phosphorylation on the S727 residue.[6]

Another one of the many ways in which herpes viruses evade the immune system is by down regulation of MHC I and MHC II. This is observed in almost every human herpesvirus. Down regulation of MHC I and MHC II can come about by many different mechanisms, most causing the MHC to be absent from the cell surface. As discussed above, one way is by a viral chemokine homolog such as IL-10. Another mechanism to down regulate MHCs is to encode viral proteins that detain the newly formed MHC in the endoplasmic reticulum (ER). The MHC cannot reach the cell surface and therefore cannot activate the T cell response. The MHCs can also be targeted for destruction in the proteasome or lysosome. The ER protein TAP also plays a role in MHC down regulation. Viral proteins inhibit TAP preventing the MHC from picking up a viral antigen peptide. This prevents proper folding of the MHC and therefore the MHC does not reach the cell surface.

It is important to note that HLA-G is often up regulated in addition to downregulation of MHC I and MHC II. This prevents the natural killer cell response.[citation needed]


There are eight distinct viruses in this family known to cause disease in humans.[8][9]
Human Herpesvirus (HHV) classification
Type     Synonym     Subfamily     Primary Target Cell     Pathophysiology     Site of Latency     Means of Spread
HHV‑1     Herpes simplex virus-1 (HSV-1)     α (Alpha)     Mucoepithelial     Oral and/or genital herpes (predominantly orofacial), as well as other herpes simplex infections     Neuron     Close contact (sexually transmitted disease)
HHV-2     Herpes simplex virus-2 (HSV-2)     α     Mucoepithelial     Oral and/or genital herpes (predominantly genital), as well as other herpes simplex infections     Neuron     Close contact (sexually transmitted disease)
HHV-3     Varicella zoster virus (VZV)     α     Mucoepithelial     Chickenpox and shingles     Neuron     Respiratory and close contact (including sexually transmitted disease)
HHV-4     Epstein-Barr virus (EBV), lymphocryptovirus     γ (Gamma)     B cells and epithelial cells     Infectious mononucleosis, Burkitt's lymphoma, CNS lymphoma in AIDS patients,
post-transplant lymphoproliferative syndrome (PTLD), nasopharyngeal carcinoma, HIV-associated hairy leukoplakia     B cell     Close contact, transfusions, tissue transplant, and congenital
HHV-5     Cytomegalovirus (CMV)     β (Beta)     Monocyte, lymphocyte, and epithelial cells     Infectious mononucleosis-like syndrome,[10] retinitis, etc.     Monocyte, lymphocyte, and ?     Saliva
HHV-6     Roseolovirus, Herpes lymphotropic virus     β     T cells and ?     Sixth disease (roseola infantum or exanthem subitum)     T cells and ?     Respiratory and close contact?
HHV-7     Roseolovirus     β     T cells and ?     Sixth disease (roseola infantum or exanthem subitum)     T cells and ?      ?
HHV-8     Kaposi's sarcoma-associated herpesvirus
(KSHV), a type of rhadinovirus     γ     Lymphocyte and other cells     Kaposi's sarcoma, primary effusion lymphoma, some types of multicentric Castleman's disease     B cell     Close contact (sexual), saliva?


[edit] Herpesviruses of other animals

In addition to the herpesviruses considered endemic in humans, some viruses associated primarily with animals may infect humans. These are zoonotic infections:
Zoonotic Herpesviruses
Species     Type     Synonym     Subfamily     Human Pathophysiology
Macaque monkey     CeHV-1     Cercopithecine herpesvirus-1, (Monkey B virus)     α     Very unusual, with only approximately 25 human cases reported.[11] Untreated infection is often deadly; sixteen of the 25 cases resulted in fatal encephalomyelitis. At least four cases resulted in survival with severe neurologic impairment.[11][12] Symptom awareness and early treatment are important for laboratory workers facing exposure.
Mouse     MuHV‑4     Murine gammaherpesvirus-68 (MHV-68)     γ     Zoonotic infection found in 4.5% of general population and more common in laboratory workers handling infected mice.[14] ELISA tests show factor-of-four (x4) false positive results, due to antibody cross-reaction with other Herpes viruses.


In animal virology the most important herpesviruses belong to the Alphaherpesvirinae. Research on pseudorabies virus (PrV), the causative agent of Aujeszky's disease in pigs, has pioneered animal disease control with genetically modified vaccines. PrV is now extensively studied as a model for basic processes during lytic herpesvirus infection, and for unravelling molecular mechanisms of herpesvirus neurotropism, whereas bovine herpesvirus 1, the causative agent of bovine infectious rhinotracheitis and pustular vulvovaginitis, is analyzed to elucidate molecular mechanisms of latency. The avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline similarity and diversity within the Alphaherpesvirinae.

    Subfamily Alphaherpesvirinae
        Genus Simplexvirus
            Bovine herpesvirus 2 causes bovine mammillitis and pseudo-lumpyskin disease.
            Cercopithecine herpesvirus 1, also known as Herpes B virus, causes a Herpes simplex-like disease in Macaques, usually fatal if symptomatic and untreated in humans.
            Ateline herpesvirus 1, Spider monkey herpesvirus.
        Genus Varicellovirus
            Bovine herpesvirus 1 causes infectious bovine rhinotracheitis, vaginitis, balanoposthitis, and abortion in cattle.
            Bovine herpesvirus 5 causes encephalitis in cattle.
            Caprine herpesvirus 1 causes conjunctivitis and respiratory disease in goats.
            Porcine herpesvirus 1 causes pseudorabies.
            Equine herpesvirus 1 causes respiratory disease, neurological disease/paralysis, and spontaneous abortion in horses.
            Equine herpesvirus 3 causes coital exanthema in horses.
            Equine herpesvirus 4 causes rhinopneumonitis in horses.
            Canine herpesvirus 1 causes a severe hemorrhagic disease in puppies.
            Feline herpesvirus 1 causes feline viral rhinotracheitis and keratitis in cats.
            Duck herpesvirus 1 causes duck plague.
        Genus Mardivirus
            Gallid herpesvirus 2 causes Marek's disease.
            Gallid herpesvirus 3 (GaHV-3 or MDV-2)
            Herpesvirus of turkeys (HVT)
        Genus Iltovirus
            Gallid herpesvirus 1 causes infectious laryngotracheitis in birds.
    Subfamily Betaherpesvirinae
        Porcine herpesvirus 2 causes inclusion body rhinitis in swine.
    Subfamily Gammaherpesvirinae
        Genus Rhadinovirus
            Alcelaphine herpesvirus 1 causes bovine malignant catarrhal fever.
            Alcelaphine herpesvirus 2 causes an antelope and hartebeest version of MCF.
            Bovine herpesvirus 4
            Equine herpesvirus 2 causes equine cytomegalovirus infection.
            Equine herpesvirus
            Murid herpesvirus 4 Also known as Murine gammaherpesvirus-68 (MHV-68)

[edit] Family Herpesviridae

The following genera are included in the family Herpesviridae:

    Subfamily Alphaherpesvirinae
        Genus Iltovirus; type species: Gallid herpesvirus 1
            Species: Gallid herpesvirus 1, Psittacid herpesvirus 1
        Genus Mardivirus; type species: Gallid herpesvirus 2
            Species: Columbid herpesvirus 1, Gallid herpesvirus 2, Gallid herpesvirus 3, Meleagrid herpesvirus 1
        Genus Simplexvirus; type species: Human herpesvirus 1
            Species: Ateline herpesvirus 1, Bovine herpesvirus 2, Cercopithecine herpesvirus 2, Human herpesvirus 1, Human herpesvirus 2, Leporid herpesvirus 4, Macacine herpesvirus 1, Macropodid herpesvirus 1, Macropodid herpesvirus 2, Papiine herpesvirus 2, Saimiriine herpesvirus 1
        Genus Unassigned
            Species: Chelonid herpesvirus 5, Chelonid herpesvirus 6
        Genus Varicellovirus; type species: Human herpesvirus 3
            Species: Bovine herpesvirus 1, Bovine herpesvirus 5, Bubaline herpesvirus 1, Canid herpesvirus 1, Caprine herpesvirus 1, Cercopithecine herpesvirus 9, Cervid herpesvirus 1, Cervid herpesvirus 2, Equid herpesvirus 1, Equid herpesvirus 3, Equid herpesvirus 4, Equid herpesvirus 8, Equid herpesvirus 9, Felid herpesvirus 1, Human herpesvirus 3, Phocid herpesvirus 1, Suid herpesvirus
    Subfamily Betaherpesvirinae
        Genus Cytomegalovirus; type species: Human herpesvirus 5
            Species: Cercopithecine herpesvirus 5, Human herpesvirus 5, Macacine herpesvirus 3, Panine herpesvirus 2
        Genus Muromegalovirus; type species: Murid herpesvirus 1
            Species: Murid herpesvirus 1, Murid herpesvirus 2
        Genus Proboscivirus; type species: Elephantid herpesvirus 1
        Genus Roseolovirus; type species: Human herpesvirus 6
            Species: Human herpesvirus 6, Human herpesvirus 7
        Genus Unassigned
            Species: Caviid herpesvirus 2, Suid herpesvirus 2, Tupaiid herpesvirus 1
    Subfamily Gammaherpesvirinae
        Genus Lymphocryptovirus; type species: Human herpesvirus 4
            Species: Callitrichine herpesvirus 3, Cercopithecine herpesvirus 14, Gorilline herpesvirus 1, Human herpesvirus 4, Macacine herpesvirus 4, Panine herpesvirus 1, Papiine herpesvirus 1, Pongine herpesvirus 2
        Genus Macavirus; type species: Alcelaphine herpesvirus 1
            Species: Alcelaphine herpesvirus 1, Alcelaphine herpesvirus 2, Bovine herpesvirus 6, Caprine herpesvirus 2, Hippotragine herpesvirus 1, Ovine herpesvirus 2, Suid herpesvirus 3, Suid herpesvirus 4, Suid herpesvirus 5
        Genus Percavirus; type species: Equid herpesvirus 2
            Species: Equid herpesvirus 2, Equid herpesvirus 5, Mustelid herpesvirus 1
        Genus Rhadinovirus; type species: Saimiriine herpesvirus 2
            Species: Ateline herpesvirus 2, Ateline herpesvirus 3, Bovine herpesvirus 4, Human herpesvirus 8, Macacine herpesvirus 5, Murid herpesvirus 4, Saimiriine herpesvirus 2
        Genus Unassigned
            Species: Equid herpesvirus 7, Phocid herpesvirus 2, Saguinine herpesvirus 1
    Subfamily Unassigned
        Genus Unassigned
            Species: Iguanid herpesvirus 2
            Species: duck enteritis virus


Research is currently ongoing into a variety of side-effect or co-conditions related to the herpesviruses. These include:

    Alzheimer's disease (This database compiles Alzheimer's disease susceptibility genes related to the Herpes simplex life cycle)
    atherosclerosis
    cholangiocarcinoma
    Crohn's disease
    chronic fatigue syndrome
    dysautonomia
    fibromyalgia
    Irritable bowel syndrome
    multiple sclerosis
    labile hypertension
    lupus
    pancreatic cancer
    pancreatitis
    pityriasis rosea
    Type II Diabetes

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Virus Famili Myoviridae

Description and Significance

Myoviruses are a family of bacteriophages (from "bacteria" and the Greek phagein, "to eat"), or viruses that infect bacteria. Myoviruses, along with several other bacteriophages, have a "head and tail" morphology that is not found in other groups of viruses. In myoviruses, the tail contracts; this is related to the virus' mode of penetration of the host cell. Bacteriophage T4, a myovirus, infects E. coli.

The myovirus genome is non-segmented and contains a molecule of linear, double-stranded DNA. The complete genome is 33600-170000 nucleotides long, and has terminally redundant sequences. Guanine + cytosine content is 35%.

Myoviruses are not enveloped and consist of a head and a tail separated by a neck. The head has icosahedral symmetry, while the tail is tubular and has helical symmetry. The capsid that constitutes the head is made up of 152 capsomers. The head has a diameter of 50-110nm; the tail is 16-20nm in diameter. The tail consists of a central tube, a contractile sheath, a collar, a base plate, six tail pins and six long fibers. Tail structure is similar to tectiviridae, but differs in the fact that a myovirus' tail is permanent. Contractions of the tail require ATP. When the sheath is contracted, it measures 10-15 nm in length.

After a myovirus attaches to a host cell, it uses its contractile sheath to function like a syringe, piercing the cell wall with its central tube and injecting its genetic material into the host. The myovirus' genetic information takes over the host cell's mechanisms for transcription and translation and begins making new viruses. Once the cell has created as many myoviruses as it can, lysis occurs and the new viruses escape from the dead host cell.

Myoviruses, being bacteriophages, infect bacteria. The most commonly infected bacteria is Escherichia coli. Myoviruses are virulent phages, meaning they do not integrate their genetic material with their host cell's, and they usually kill their host cell.

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Virus Alloherpesviridae

Alloherpesviridae is a family of viruses within the order Herpesvirales. This family includes the species that infect fish and amphibians. Phylogenetic studies have confirmed the validity of this family and suggest that it may be divided into two clades: one consisting of viruses from cyprinid and anguillid hosts and the other of viruses from ictalurid, salmonid, acipenserid and ranid hosts.1
History

This family was created in 2005.
Taxonomy

Four genera have been recognised in this family but a number of species remain unclassified. The family appears to be divisible into three families2 but this probably needs confirmation with additioanl studies before being generally accepted.

Genus Batrachovirus
Species
Ranid herpesvirus 1 (Lucké tumor herpesvirus) – type species
Ranid herpesvirus 2

Genus Cyprinivirus
Species
Cyprinid herpesvirus 1
Cyprinid herpesvirus 2
Cyprinid herpesvirus 3 (Koi herpesvirus)

Genus Ictalurivirus
Species
Acipenserid herpesvirus 2 – host: white sturgeon (Acipenser transmontanus)
Ictalurid herpesvirus 1 (Channel cat fish virus) – type species
Ictalurid herpesvirus 2 (Ictalurus melas herpesvirus) – host: black bullhead (Ameiurus melas)

Genus Salmonivirus
Species
Salmonid herpesvirus 1
Salmonid herpesvirus 2
Salmonid herpesvirus 3

Unclassified
Acipenserid herpesvirus 1
Ameiurid alloherpesvirus 1
Anguillid herpesvirus 1
Australian pilchard herpesvirus
Esocid herpesvirus
Percid herpresvirus 1

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Vius Siphoviridae

Fusobacterium nucleatum is a periodontal pathogen that has been directly associated with the development and progression of periodontal disease, a widespread pathology that affects the support tissues of the tooth. We isolated a new bacteriophage (FnpΦ02) that specifically infects this bacterium. Transmission electron microscopy showed that the virion is composed of an icosahedral head and a segmented tail. The size of the phage genome was estimated to be approximately 59 kbp of double-stranded DNA. The morphological features and the genetic characteristics suggest that FnpΦ02 is part of the Siphoviridae family. Using one-step growth and adsorption experiments, the latent period, burst size, and adsorption rate were estimated to be 15 h, 100 infectious units per cell, and 7.5 × 10⁻¹⁰ ml min⁻¹, respectively. A small fragment of phage DNA was cloned and sequenced, showing 93% nucleotide identity with the phage PA6 of Propionibacterium acnes and amino acid identity with fragments of two proteins (Gp3 and Gp4) of this phage. To our knowledge, FnpΦ02 is the first phage described to infect Fusobacterium nucleatum and provides the base for future exploration of phages in the control of periodontal disease.
Most cited papers:
Arch Virol. 2002 Dec ;147 (12):2419-29  12491107  Cit:29
Remarkable morphological diversity of viruses and virus-like particles in hot terrestrial environments.
R Rachel, M Bettstetter, B P Hedlund, M Häring, A Kessler, K O Stetter, D Prangishvili
Lehrstuhl für Mikrobiologie und Archaeenzentrum, Universität Regensburg, Germany.
Electron microscopic studies of the viruses in two hot springs (85 degrees C, pH 1.5-2.0, and 75-93 degrees C, pH 6.5) in Yellowstone National Park revealed particles with twelve different morphotypes. This diversity encompassed known viruses of hyperthermophilic archaea, filamentous Lipothrixviridae, rod-shaped Rudiviridae, and spindle-shaped Fuselloviridae, and novel morphotypes previously not observed in nature. Two virus types resembled head-and-tail bacteriophages from the families Siphoviridae and Podoviridae, and constituted the first observation of these viruses in a hydrothermal environment. Viral hosts in the acidic spring were members of the hyperthermophilic archaeal genus Acidianus.
J Struct Biol. ;138 (1-2):105-13  12160706  Cit:25
Segmentation of two- and three-dimensional data from electron microscopy using eigenvector analysis.
Achilleas S Frangakis, Reiner Hegerl
Max-Planck-Institut für Biochemie, Am Klopferspitz 18a, D-8215 Martinsried, Germany.
An automatic image segmentation method is used to improve processing and visualization of data obtained by electron microscopy. Exploiting affinity criteria between pixels, e.g., proximity and gray level similarity, in conjunction with an eigenvector analysis, the image is subdivided into areas which correspond to objects or meaningful regions. Extending a proposal by Shi and Malik (1997, Proceedings of the IEEE conference on Computer Vision and Pattern Recognition, pp. 731-737) the approach was adapted to the field of electron microscopy, especially to three-dimensional application as needed by electron tomography. Theory, implementation, parameter setting, and results obtained with a variety of data are presented and discussed. The method turns out to be a powerful tool for visualization with the potential for further improvement by developing and tuning new affinity.
Science. 2001 Apr 27;292 (5517):744-8  11326105  Cit:14
Virus maturation involving large subunit rotations and local refolding.
J F Conway, W R Wikoff, N Cheng, R L Duda, R W Hendrix, J E Johnson, A C Steven
Laboratory of Structural Biology Research, National Institute of Arthritis, Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA.
Large-scale conformational changes transform viral precursors into infectious virions. The structure of bacteriophage HK97 capsid, Head-II, was recently solved by crystallography, revealing a catenated cross-linked topology. We have visualized its precursor, Prohead-II, by cryoelectron microscopy and modeled the conformational change by appropriately adapting Head-II. Rigid-body rotations ( approximately 40 degrees) cause switching to an entirely different set of interactions; in addition, two motifs undergo refolding. These changes stabilize the capsid by increasing the surface area buried at interfaces and bringing the cross-link-forming residues, initially approximately 40 angstroms apart, close together. The inner surface of Prohead-II is negatively charged, suggesting that the transition is triggered electrostatically by DNA packaging.
J Bacteriol. 2005 Jun ;187 (12):4187-97  15937180  Cit:12
Structural characterization and assembly of the distal tail structure of the temperate lactococcal bacteriophage TP901-1.
Christina S Vegge, Lone Brøndsted, Horst Neve, Stephen Mc Grath, Douwe van Sinderen, Finn K Vogensen
Department of Food Science, The Royal Veterinary and Agricultural University, Rolighedsvej 30, DK-1958 Frederiksberg C, Denmark.
The tail structures of bacteriophages infecting gram-positive bacteria are largely unexplored, although the phage tail mediates the initial interaction with the host cell. The temperate Lactococcus lactis phage TP901-1 of the Siphoviridae family has a long noncontractile tail with a distal baseplate. In the present study, we investigated the distal tail structures and tail assembly of phage TP901-1 by introducing nonsense mutations into the late transcribed genes dit (orf46), tal(TP901-1)(orf47), bppU (orf48), bppL (orf49), and orf50. Transmission electron microscopy examination of mutant and wild-type TP901-1 phages showed that the baseplate consisted of two different disks and that a central tail fiber is protruding below the baseplate. Evaluation of the mutant tail morphologies with protein profiles and Western blots revealed that the upper and lower baseplate disks consist of the proteins BppU and BppL, respectively. Likewise, Dit and Tal(TP901-1) were shown to be structural tail proteins essential for tail formation, and Tal(TP901-1) was furthermore identified as the tail fiber protein by immunogold labeling experiments. Determination of infection efficiencies of the mutant phages showed that the baseplate is fundamental for host infection and the lower disk protein, BppL, is suggested to interact with the host receptor. In contrast, ORF50 was found to be nonessential for tail assembly and host infection. A model for TP901-1 tail assembly, in which the function of eight specific proteins is considered, is presented.
Appl Environ Microbiol. 2005 Mar ;71 (3):1598-609  15746365  Cit:11
Genomic analysis of bacteriophage PhiJL001: insights into its interaction with a sponge-associated alpha-proteobacterium.
Jayme E Lohr, Feng Chen, Russell T Hill
Center of Marine Biotechnology, Columbus Center Suite 236, 701 East Pratt Street, Baltimore, MD 21202, USA.
Bacteriophage PhiJL001 infects a novel marine bacterium in the alpha subclass of the Proteobacteria isolated from the marine sponge Ircinia strobilina. PhiJL001 is a siphovirus and forms turbid plaques on its host. The genome sequence of PhiJL001 was determined in order to better understand the interaction between the marine phage and its sponge-associated host bacterium. The complete genome sequence of PhiJL001 comprised 63,469 bp with an overall G+C content of 62%. The genome has 91 predicted open reading frames (ORFs), and 17 ORFs have been assigned putative functions. PhiJL001 appears to be a temperate phage, and the integrase gene was identified in the genome. DNA hybridization analysis showed that the PhiJL001 genome does not integrate into the host chromosome under the conditions tested. DNA hybridization experiments therefore suggested that PhiJL001 has some pseudolysogenic characteristics. The genome of PhiJL001 contains many putative genes involved in phage DNA replication (e.g., helicase, DNA polymerase, and thymidylate synthase genes) and also contains a putative integrase gene associated with the lysogenic cycle. Phylogeny based on DNA polymerase gene sequences indicates that PhiJL001 is related to a group of siphoviruses that infect mycobacteria. Designation of PhiJL001 as a siphovirus is consistent with the morphology of the phage visualized by transmission electron microscopy. The unique marine phage-host system described here provides a model system for studying the role of phages in sponge microbial communities.
Virology. 2000 Oct 25;276 (2):315-28  11040123  Cit:9
Mutational analysis of two structural genes of the temperate lactococcal bacteriophage TP901-1 involved in tail length determination and baseplate assembly.
M Pedersen, S Ostergaard, J Bresciani, F K Vogensen
Department of Dairy and Food Science, The Royal Veterinary and Agricultural University, Rolighedsvej 30, Frederiksberg C, DK-1958, Denmark.
Two putative structural genes, orf tmp (tape measure protein) and orf bpp (baseplate protein), of the temperate lactococcal phage TP901-1 were examined by introduction of specific mutations in the prophage strain Lactococcus lactic ssp. cremoris 901-1. The adsorption efficiencies of the mutated phages to the indicator strain L. lactic ssp. cremoris 3107 were determined and electron micrographs were obtained. Specific mutations in orf tmp resulted in the production of mostly phage head structures without tails and a few wild-type looking phages. Furthermore, construction of an inframe deletion or duplication of 29% in orf tmp was shown to shorten or lengthen the phage tail by approximately 30%, respectively. The orf tmp is proposed to function as a tape measure protein, TMP, important for assembly of the TP901-1 phage tail and involved in tail length determination. Specific mutations in orf bpp produced phages which were unable to adsorb to the indicator strain and electron microscopy revealed particles lacking the baseplate structure. The orf bpp is proposed to encode a highly immunogenic structural baseplate protein, BPP, important for assembly of the baseplate. Finally, an assembly pathway of the TP901-1 tail and baseplate structure is presented.
J Appl Microbiol. 1999 Sep ;87 (3):402-9  10540243  Cit:9
Study of the potential relationship between the morphology of infectious somatic coliphages and their persistence in the environment.
M Muniesa, F Lucena, J Jofre
Departament de Microbiologia, Facultat de Biologia, Universitat de Barcelona, Spain.
The proportions of different morphological types of infectious somatic coliphages were determined in faecally polluted freshwaters. Myoviridae, followed by Siphoviridae, were the most frequently isolated morphological types in raw sewage, treated sewage and river water collected a few metres downstream from a sewage outfall. However, in river water collected further downstream from the pollution point, in river water after ‘in situ’ inactivation experiments and in chlorinated raw and treated sewage significant changes in the proportions of the different somatic coliphage morphological types occurred. In all cases, Siphoviridae, especially those with flexible and curled tails, became more abundant to the detriment of Myoviridae.
Arch Virol. 1996 ;141 (2):209-18  8634015  Cit:8
Frequency of morphological phage descriptions in 1995.
H W Ackermann
Félix d’Hérelle Reference Center for Bacterial Viruses, Department ofMicrobiology, Faculty of Medicine, Laval University, Québec, Cananda.
At least 4500 bacterial viruses have been examined in the electron microscope since 1959. About 4400 phages (96%) are tailed and only 162 phages (4%) are cubic, filamentous, or pleomorphic. Phages belong to 12 virus families and occur in about 130 bacterial genera. Phages are listed by morphotypes and host genera. Siphoviridae or phages with long, noncontractile tails include about 60% of tailed phages.
Arch Virol. 1997 ;142 (7):1381-90  9267450  Cit:7
Taxonomic changes in tailed phages of enterobacteria.
H W Ackermann, M S DuBow, M Gershman, B Karska-Wysocki, S S Kasatiya, M J Loessner, M D Mamet-Bratley, M Regué
Félix d’Hérelle Reference Center for Bacterial Viruses, Department of Microbiology, Faculty of Medicine, Laval University, Quebec, Canada.
Out of 136 new phages, 80 (59%) are classified into 23 species according to morphology and physicochemical properties. Six new species are described and species beta 4, from a previous classification scheme, is renamed T1. The morphology of 36 phage species is schematically represented.
Arch Virol. 1994 ;135 (3-4):345-54  7979972  Cit:7
Classification of Acinetobacter phages.
H W Ackermann, G Brochu, H P Emadi Konjin
Félix d’Hérelle Reference Center for Bacterial Viruses, Department of Microbiology, Faculty of Medicine, Laval University, Quebec, Sainte-Foy, Canada.
Eight phage species and type viruses are proposed. They belong to the Myoviridae, Siphoviridae, and Podoviridae families of tailed phages and are characterized by a combination of morphological and physicochemical properties. An unusual siphovirus species has an elongated head and transverse tail disks.

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Virus Podoviridae

The Podoviridae are a family of bacteriophages. Unlike the other families of tailed viruses this family has short tails that are non contractile.

There are at least 74 species in this family.
Virology

The viron is nonenveloped with a head-tail structure. There are 9 structural proteins.

The head is ~60 nanometers (nm) in diameter, consists of 72 capsomers and is icosahedral with a T = 7 symmetry. The head protein has a molecular mass of ~38 kiloDaltons and is present in 460 copies per virion.

The tail is non-contractile and has 6 short subterminal fibers. It is thick, rod-shaped and built of stacked disks. The maximum length is ~17 nm.

The double stranded DNA genome is linear ~40-42 kilobases in length and encodes ~55 genes. The guanine + cytosine content is ~50%. It has terminally redundant sequences and is nonpermuted. By weight the genome constitutes ~50% of the viron.

The genome encodes 9 structural proteins, an adenylated transferase B type DNA polymerase and an RNA polymerase. 3 internal proteins constitute the polymerase complex.

2 classes of genes are recognized (early and late). This classification is based on the timing of transcription which is temporally regulated. Genes with related functions are clustered together. Genome replication is bidirectional.

In general these viruses tend to be lytic rather than lysogenic.
Life cycle

Phages are adsorbed using tail first to specific receptors located on the cell wall and then enter host cells after digestion of the cell wall with lysozyme. Virus uncoating occurs in the cytoplasm. The viral DNA remains linear. In latent infections the infecting genome integrates into the host genome. Genome replication occurs by a semi-conservative mechanism. During replication the viral DNA forms concatamers. In lytic cycles the host genome degenerates.

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Virus Malacoherpesviridae

The Malacoherpesviridae are a family of DNA viruses that cause diseases in molluscs.

The family name Malacoherpesviridae is derived from Greek word ‘μαλακός (malacos) meaning ‘soft’ and from Greek word ‘μαλάκιον (malakion) meaning ‘mollusc.

Within this family two species have been described: Ostreid herpesvirus 1 in 2009 and Haliotid herpesvirus 1 in 2010.

Malacoherpesviridae may have the ability to infect across species, a feature not typically observed in vertebrate herpesviruses. This ability appears to be restricted to related mollusc species.

Genera

Ostreavirus Davison et al., 2009

Ostreid herpesvirus 1 Davison et al., 2009 – acronym: OsHV1, common name: Oyster herpesvirus – its host are bivalves (oyster)

Haliotid herpesvirus 1 Savin et al., 2010 – acronym: AbHV-1, common name: abalone herpesvirus, its host are abalone sea snails Haliotis spp. such as Haliotis diversicolor

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