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It's affinity for sensory nerves allows it to target gene therapy to the central nervous system, while it's capacity for cell destruction could be a powerful weapon for selective destruction of cancer cells. An HSV-1 vector could be engineered to express antigens that induce immunity against a variety of infectious agents. De laatste jaren worden wij ook bij de fokkerij van Drentsche Patrijshonden in toenemende mate geconfronteerd met klachten over het niet drachtig worden van teven, het werpen van te kleine nesten en in mindere mate met doodgeboren pups of pups die kort na de geboorte alsnog dood gaan. Using herpesvirus, molecular immunologists from the USC Norris Comprehensive Cancer Center have discovered a cellular process that activates a critical immune defense against pathogens, which could have implications for developing drugs to bolster one’s immunity to infection. Led by Pinghui Feng, associate professor of molecular microbiology and immunology at the Keck School of Medicine of USC, the team found that herpesvirus proteins activate retinoic acid-induced gene I (RIG-I) by removal of an amino group from the glutamine and asparagine amino acids through a process called deamidation.
Prior to this study, it was unclear whether RIG-I — whose activation is central to the body’s innate immune defense response — could be activated by a component other than viral RNA.
The study appear in the April 2 issue of the peer-reviewed scientific journal Molecular Cell.
Other USC authors include Shanping He, Jun Zhao, Shanshan Song, Arlet Minassian, Yu Zhou, Junjie Zhang, Kevin Brulois, Yuqi Wang, Jackson Cabo, Ebrahim Zandi, Chengyu Liang and Jae Jung.
A 3-D reconstruction illustrates immune cells (shown in blue) clearing the brain of plaque deposits (in red). Immune system can wipe brain of Alzheimer’s-related plaqueRemoving the telltale protein reverses memory loss in mice, USC researchers find. Fasting triggers stem cell regeneration of damaged, old immune systemResults in mice are first evidence of natural intervention triggering stem cell-dependent regeneration of organ or system. A Keck Medicine of USC-led team of microbiologists has identified previously unknown interactions between critical proteins in the human immune response system.
There is good evidence that the human immune system can fight cancer, but it needs some help. USC Viterbi, Northrop Grumman establish institute to develop advanced optical materialsThe Northrop Grumman Institute of Nanophotonics and Nanomaterials will explore the properties of tiny structures and materials. Have classical guitar, will travelEver on the go, a USC Thornton musician is well on his way to international success. Adena Bauer co-founded Spark USC, a group that helps students collaborate on entrepreneurial projects and tap into their creativity. USC Viterbi student finds her calling in computer science and businessAdena Bauer co-founded Spark USC, a group that helps students collaborate on entrepreneurial projects and tap into their creativity. Human herpesvirus 6: A herpes virus that apparently lies dormant in many people, human herpesvirus 6 is most likely to cause problems when the immune system is compromised by disease, as in AIDS patients, or by deliberate immune suppression, as in organ transplant patients. Human herpesvirus 6 (HHV-6) o herpesvirus humano 6, tambien conocido antiguamente como human B-lymphotropic virus (HBLV) o virus linfotropico B humano es un virus de la familia Herpesviridae, uno de los 8 (HHV-1 a HHV-8) que infecta a los humanos.
The Epstein–Barr virus (EBV), also called human herpesvirus 4 (HHV-4), is one of eight viruses in the herpes family, and is one of the most common viruses in humans.
This section may contain an excessive amount of intricate detail that may only interest a specific audience.
To enter B cells, viral glycoprotein gp350 binds to cellular receptor CD21 (also known as CR2).[14] Then, viral glycoprotein gp42 interacts with cellular MHC class II molecules. Once EBV enters the cell, the viral capsid dissolves and the viral genome is transported to the cell nucleus. Unlike lytic replication for many other viruses, EBV lytic replication does not inevitably lead to lysis of the host cell because EBV virions are produced by budding from the infected cell.
It is also postulated that a program exists in which all viral protein expression is shut off (Latency 0). Within B cells, all three latency programs are possible.[8] EBV latency within B cells usually progresses from Latency III to Latency II to Latency I.
In primary infection, EBV replicates in oro-pharyngeal epithelial cells and establishes Latency III, II, and I infections in B-lymphocytes.
When EBV infects B cells in vitro, lymphoblastoid cell lines eventually emerge that are capable of indefinite growth. It is postulated that following natural infection with EBV, the virus executes some or all of its repertoire of gene expression programs to establish a persistent infection.
The latent programs reprogram and subvert infected B-lymphocytes to proliferate and bring infected cells to the sites at which the virus presumably persists.
All EBV nuclear proteins are produced by alternative splicing of a transcript starting at either the Cp or Wp promoters at the left end of the genome (in the conventional nomenclature). The initiation codon of the EBNA-LP coding region is created by an alternate splice of the nuclear protein transcript. EBNA-1 protein binds to a replication origin (oriP) within the viral genome and mediates replication and partitioning of the episome during division of the host cell.
LMP-1 is a six-span transmembrane protein that is also essential for EBV-mediated growth transformation.
EBV microRNAs are encoded by two transcripts, one set in the BART gene and one set near the BHRF1 cluster.
The Epstein–Barr virus has been implicated also in disorders related to alpha-synuclein aggregation (e.g. Antibody titers against EBNA1 and EBNA2 in relation to Hodgkin lymphoma and history of infectious mononucleosis.
Mueller NE, Lennette ET, Dupnik K, Birmann BM.SourceDepartment of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.

A role for Epstein Barr virus (EBV) in Hodgkin lymphoma (HL) pathogenesis is supported by the detection of EBV genome in about one-third of HL cases, but is not well defined. An EHV-1 affected filly finally standing, but struggling, even with some help from a sling and her caretakers. Equine herpesvirus-1, also known as EHV-1, has been making headlines for the past few years. EHV-1 is highly contagious to other horses and can cause respiratory disease primarily in juvenile horses, such as nasal discharge, fever and coughing; infection can also result in abortion and neonatal death.
EHV-1 can affect horses of all breeds and ages and is spread via direct contact (nose-to-nose contact), indirect contact (from shared water buckets or tack, as well as from people's hands), and through the air (aerosolized transmission). Though there are many vaccines containing EHV-1 (the rhinopneumonitis vaccine your horse typically gets in his regular vaccine series), there is no vaccine currently on the market that has a label claim for prevention of the neurologic form of the disease.
Most horses have been exposed to and infected by EHV-1 by the time they are 2-year-olds (typically as they are foals in contact with their dams).
Implementing basic biosecurity measures is key to preventing the spread of EHV-1, according to Nicola Pusterla, DVM, PhD, Dipl.
Contracting the neurologic form of EHV-1 is not a death sentence; some horses can recover fully while others have life-long neurologic deficits to which some can adapt.
Veterinarians in the cutting horse industry who were faced with the EHV-1 outbreak stated that recent research into the disease was very helpful in shaping their treatment plans for affected horses. Ryan Quarles is the featured presenter for the Kentucky Equine Networking Association meeting in May.
Seek the advice of a qualified veterinarian before proceeding with any diagnosis, treatment, or therapy.
Zeker grote kennels met veel externe contacten (door show, training of anderszins) lijken hiermee te maken te hebben: het lijkt er soms op dat rond de 50% van deze kennels hier last van heeft. Als een teef niet bevrucht blijkt, dus leeg blijft, als de nesten klein blijven of de pups na de geboorte alsnog sterven, is dat een grote teleurstelling voor elke fokker. This is the first example in which host immune defense is activated by an enzymatic activity, implying that deamidation can be a highly regulated process and reshaping the conventional notion that deamidation is a non-specific process associated with protein decay. The work was supported in part by grants from the National Institutes of Health (DE021445, CA134241), the American Cancer Society (RSG-11-162-01-MPC) and the USC Norris Comprehensive Cancer Center (P30CA014089-34). Physician scientists at the Keck School of Medicine of USC are studying ways to teach the body’s immune system to fight off cancer.
Existen dos subtipos de HHV-6, denominados HHV-6A (el virus linfotropico B humano) y HHV-6B (relacionado con la roseola infantil). In the United States, about half of all five-year-old children and about 90 percent of adults have evidence of previous infection.[9] Infants become susceptible to EBV as soon as maternal antibody protection disappears.
Please help by spinning off or relocating any relevant information, and removing excessive detail that may be against Wikipedia's inclusion policy.
EBV that are made in the B cells have low numbers of gHgLgp42 complexes, because these three-part complexes interact with Human-leukocyte-antigen class II molecules present in B cells in the endoplasmic reticulum and are degraded. The latent EBV genome is circular, so it must linearize in the process of lytic reactivation. Immediate-early lytic gene products include BZLF1 (also known as Zta, EB1, associated with its product gene ZEBRA) and BRLF1 (associated with its product gene Rta).[11] Early lytic gene products have many more functions, such as replication, metabolism, and blockade of antigen processing. EBV can latently persist within B cells and epithelial cells, but different latency programs are possible in the two types of cell.
Each stage of latency uniquely influences B cell behavior.[8] Upon infecting a resting naive B cell, EBV enters Latency III. EBV latent infection of B-lymphocytes is necessary for virus persistence, subsequent replication in epithelial cells, and release of infectious virus into saliva.
The growth transformation of these cell lines is the consequence of viral protein expression. Given the initial absence of host immunity, the lytic cycle produces large amounts of virus to infect other (presumably) B-lymphocytes within the host. Eventually, when host immunity develops, the virus persists by turning off most (or possibly all) of its genes, only occasionally reactivating to produce fresh virions. EBER-particles also induce the production of IL-10, which enhances growth and inhibits cytotoxic T-cells.
Laboratories around the world continue to study the virus and develop new ways to treat the diseases it causes. In 2011, some horses that had attended the National Cutting Horse Association Western National Championship in Ogden, Utah, began showing neurologic signs after leaving the event. The most concerning manifestations of EHV-1 infection are neurologic signs, such as a wobbly gait caused by lack of coordination of the limbs, with the hind limbs often more severely affected, as well as urinary incontinence.
The goal of vaccination is to boost immunity in order to control respiratory disease or abortion resulting from of EHV-1 infection. Often the virus becomes inactive once the horse is infected, but the animal will remain a life-long carrier of the virus. ACVIM, a professor at the Colorado State University College of Veterinary Medicine and Biomedical Sciences, suggests taking daily temperatures while he is away from his home base and then continuing to monitor his temperature for about a week once he returns. According to Pusterla, 5 to 30% of horses that contract EHV-1 will develop EHM; of these EHM cases, 5 to 50% will necessitate euthanasia.
EHV-1 has been among the priorities of research universities and funding agencies for some time, but there is still much to be learned, including how to effectively contain the disease and how to treat horses that have contracted the disease.

Thus far, the impact of treatment under field conditions has not been widely studied in a regimented way that allows veterinarians to determine the efficacy of the various treatments.
To make a contribution towards equine research, please contact the American Association of Equine Practitioners Foundation, the American Quarter Horse Foundation, Grayson Jockey-Club Research Foundation, Morris Animal Foundation, or your favorite veterinary school or research institution. Een belangrijke mogelijke oorzaak van deze problemen is de besmetting van de teef met het Canine Herpesvirus (CHV). The team also identified the first bonafide enzyme that causes protein deamidation in eukaryotes.
La especie fue aislada por primera vez en 1986 a partir de linfocitos de pacientes afectados por desordenes linforreticulares. Many children become infected with EBV, and these infections usually cause no symptoms or are indistinguishable from the other mild, brief illnesses of childhood. In contrast, EBV from epithelial cells are rich in the three-part complexes because these cells do not normally contain HLA class II molecules. During lytic replication, viral DNA polymerase is responsible for copying the viral genome. Early lytic gene products include BNLF2.[11] Finally, late lytic gene products tend to be proteins with structural roles, like VCA, which forms the viral capsid.
The set of proteins and RNAs produced in Latency III transforms the B cell into a proliferating blast (also known as B cell activation).[8][11] Later, the virus restricts its gene expression and enters Latency II.
A balance is eventually struck between occasional viral reactivation and host immune surveillance removing cells that activate viral gene expression. As a result, the two subtypes differ in their transforming capabilities and reactivation ability. Virus particles were identified in the cultured cells, and the results were published in The Lancet in 1964 by Epstein, Bert Achong, and Barr. One popular way of studying EBV in vitro is to use bacterial artificial chromosomes.[41] Epstein–Barr virus can be maintained and manipulated in the laboratory in continual latency (a property shared with Kaposi's sarcoma-associated herpesvirus, another of the eight human herpesviruses).
Proceedings of the National Academy of Sciences of the United States of America 104 (18): 7606–11. This particular outbreak affected the equine industry in multiple states, and lead to fatalities in some horses that developed the neurologic form of EHV-1, called equine herpesvirus myeloencephalopathy (EHM).
These carriers often show no outward signs of infection with EHV-1, though the virus can be reactivated should the horse become stressed, such as during transport, weaning, or intense exercise.
He concedes that while no horse owner will be able to eliminate all risks, everyday precautions should be taken, including washing hands, using a separate pair of boots when visiting other farms, and keeping horses that leave the premises separate from those that live on the farm full-time. Though the incubation period for EHV-1 can be as short as 24 hours, horses begin to show signs typically a few days after exposure. Since there has not been a reliable way to recreate the disease other than in the geriatric horse challenge model, doing challenge studies to determine efficacy of treatment has limitations. Reproduction in whole or in part in any form or medium without written permission of The Horse Media Group LLC is prohibited.
Hoewel niet zo bekend bij hondeneigenaren blijkt maar liefst 40% van de onderzochte Nederlandse honden ooit met het virus in aanraking geweest te zijn. In the United States and other developed countries, many people are not infected with EBV in their childhood years. As a consequence, EBV made from B cells are more infectious to epithelial cells, and EBV made from epithelial cells are more infectious to B cells. The more limited set of proteins and RNAs produced in Latency II induces the B cell to differentiate into a memory B cell.[8][11] Finally, EBV restricts gene expression even further and enters Latency I.
Type 1 is dominant throughout most of the world, but the two types are equally prevalent in Africa.
Cell lines were sent to Werner and Gertrude Henle at the Children's Hospital of Philadelphia who developed serological markers. Although many viruses are assumed to have this property during infection of their natural hosts, there is not an easily managed system for studying this part of the viral lifecycle. Though EHM is not new, more outbreaks are being recognized with more horses seeming to be affected in each outbreak, causing concern among many equine owners.
Once activated, the virus can spread via the aerosol route (even from a seemingly healthy horse). Simply knowing the health status of other horses your horse might come into contact with can minimize the risk of spreading the disease to your horse. Traub-Dargatz notes that the horse might only have mild fever, slight nasal discharge, or a cough (although some horses exhibit no signs of disease) before neurologic signs develop, so careful monitoring is key. Both Traub-Dargatz and Pusterla agree that collection of information from horses with EHM--occurring during EHV-1 outbreaks, as well as from non-affected horses (controls), is necessary to learn more about potential risk factors for the disease.
Vaccinatie van de moederhond tegen CHV lijkt betere bevruchtingsresultaten en minder problemen bij puppy's op te leveren.
Treatment is experimental at this time, but anti-viral drugs or beta interferon may be tried.

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    Was no want to buy medication after that.....the trick is to catch it if you get else im going.
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