To drive infections, a hijacking virus mimics a cell's signaling system

ScienceDaily (Mar. 26, 2012) — New biological research reveals how an invading virus hijacks a cell's workings by imitating a signaling marker to defeat the body's defenses. By manipulating cell signals, the virus destroys a defensive protein designed to inhibit it. This finding, from studies in human cell cultures, may represent a broader targeting strategy used by other viruses, and may lay the scientific groundwork for developing more effective treatments for infectious diseases.

"Learning details of how cells respond to viruses helps us to understand key cellular machinery better," said study leader Matthew D. Weitzman, Ph.D., of the Center for Cellular and Molecular Therapeutics at The Children's Hospital of Philadelphia. "This study tells us how a virus overcomes intrinsic host defenses. In this case the virus mimics signals used during normal DNA repair mechanisms."

The study team, formerly based at the Salk Institute for Biological Studies in La Jolla, Calif., published their current findings online March 8 in Molecular Cell.

Biologists have long known that viruses hijack cellular processes to replicate themselves, while host cells have evolved intrinsic defense systems to resist viral invasion. To replicate, viruses must deliver their own DNA into a cell's nucleus, so a viral infection entails a conflict between two genomes -- the DNA of the host cell versus the foreign DNA of the virus.

Viruses mount their attack by interacting with specific cell proteins as a way of penetrating the cell's defenses. "In this study, we asked how the herpes simplex virus finds the specific proteins that it interacts with," said Weitzman. "By describing the mechanism of this particular interaction between a virus and a cell protein, we have pinpointed key regulators of a cell's processes, and shed light on how a cell regulates its defenses."

This laboratory study focused on herpes simplex virus type-1 (HSV-1), a common human virus that results in recurrent infections alternating with inactive periods. Like other viruses, HSV-1 is known to manipulate cellular processes in order to infect cells, but the specific mechanisms by which it acts on the DNA repair pathway were previously unknown.

Weitzman's study team was studying a viral protein called ICP0 that overcomes host defenses by targeting cellular proteins for destruction. They found that ICP0 exploits phosphorylation, a chemical mark that is often used in cells to promote interactions between proteins, especially as part of the cellular signaling response to DNA damage. In HSV-1 infection, the phosphorylation signal on ICP0 attracts a cellular DNA damage response protein, RNF8, which binds to the false signaling marker and is then degraded. Because RNF8 normally inhibits viral replication, its destruction leaves the cell vulnerable to HSV-1 infection, as the virus takes over the cell's machinery.

The researchers also found that ICP0 exploits the same phosphorylation signal to bind to other cellular proteins in addition to RNF8, a hint that it may play a broader role in defeating antiviral defenses and manipulating cellular machinery. Weitzman will continue to investigate HSV-1 infection in neurons and in animal models. He also plans to extend his research into other viruses, which may act on different pathways than HSV-1 does. "Ultimately," he added, "better knowledge of molecular mechanisms in infection may suggest strategies to interrupt the viral life cycle and treat infections."

The National Institutes of Health, the Salk Institute, the American Cancer Society and the Howard Hughes Medical Institute were among the funders of this research.

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The above story is reprinted from materials provided by Children's Hospital of Philadelphia.

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Mira S. Chaurushiya, Caroline E. Lilley, Aaron Aslanian, Jill Meisenhelder, Daniel C. Scott, Sébastien Landry, Simina Ticau, Chris Boutell, John R. Yates, Brenda A. Schulman, Tony Hunter, Matthew D. Weitzman. Viral E3 Ubiquitin Ligase-Mediated Degradation of a Cellular E3: Viral Mimicry of a Cellular Phosphorylation Mark Targets the RNF8 FHA Domain. Molecular Cell, 2012; DOI: 10.1016/j.molcel.2012.02.004

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Antiviral therapy associated with fewer recurring eye problems from herpes simplex virus

ScienceDaily (Sep. 14, 2010) — Taking oral antiviral medications following infection with the herpes simplex virus may be associated with a reduced risk of recurring eye-related manifestations of the disease, according to a report in the September issue of Archives of Ophthalmology, one of the JAMA/Archives journals.

"Herpes simplex virus (HSV) is a common cause of corneal disease and is the leading infectious cause of corneal blindness among developed nations," the authors write as background information in the article. After the initial exposure to the virus and the resulting systemic infection, herpes simplex establishes a latent infection in sensory nerve structures. Reactivation of this latent infection could lead to initial or recurrent disease in one or both eyes, including inflammation or infection of the cornea, eyelid, membrane inside the eye (conjunctivitis, or pink eye) or middle layer of the eye (uveitis).

Ryan C. Young, B.A., of Mayo Clinic, Rochester, Minn., and colleagues estimated the incidence of HSV eye disease in a community-based cohort, in Olmstead County, Minnesota, from 1976 through 2007. During this time period, 394 patients with ocular HSV were identified, for an annual incidence of 11.8 per 100,000 individuals.

Oral antiviral therapy was prescribed in 175 (44 percent) of these patients, who underwent therapy for an average of 2.8 years (36 percent of the average 7.7 years of follow-up). Patients not taking this prophylactic therapy were 9.4 times more likely to have a recurrence of epithelial keratitis (infection of the top layer of the cornea), 8.4 times more likely to have a recurrence of stromal keratitis (infection of deeper layers of the cornea) and 34.5 times more likely to have a recurrence of blepharitis (eyelid infection) or conjunctivitis than those taking antiviral medications.

A total of 20 patients experienced adverse outcomes, including visual loss and perforation of the cornea; of these, 17 (85 percent) were not taking oral antiviral prophylaxis.

"Overall, this community-based retrospective study demonstrated a stable incidence of HSV eye disease during a recent 32-year period," the authors write. "We found a more dramatic protective effect of oral antiviral prophylaxis on recurrences of ocular HSV than had been described previously."

"The results of this study suggest that oral antiviral prophylaxis should be considered for patients with frequent recurrences of corneal disease," they conclude. "Additionally, we recommend an evaluation of the possible barriers preventing compliance with antiviral prophylaxis and a reassessment of the cost-effectiveness of long-term oral antiviral therapy."

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Ryan C. Young; David O. Hodge; Thomas J. Liesegang; Keith H. Baratz. Incidence, Recurrence, and Outcomes of Herpes Simplex Virus Eye Disease in Olmsted County, Minnesota, 1976-2007: The Effect of Oral Antiviral Prophylaxis. Arch Ophthalmol, 2010; 128 (9): 1178-1183 [link]

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Goodbye cold sores

ScienceDaily (June 27, 2011) — Herpes infections on the lips, in the eyes or on the nose are painful, long-lasting and unpleasant. A new 3D herpes infection model brings hope: active ingredients and new treatments can be reliably tested with this model. Animal tests could soon be a thing of the past.

It burns and itches on your upper lip: a herpes infection is on the advance. Caught early, the number and size blisters can be controlled with virus-controlling salves, but the herpes simplex virus can recur at any time. "About 90 percent of the world's population carry it in them all their lives, once infected, and become sick again in stress situations," explains Dr. Anke Burger-Kentischer of the Fraunhofer Institute for Interfacial Engineering and Biotechnology IGB in Stuttgart. Coming down with a herpes virus is not always without its dangers. In the worst cases the nervous system and the brain become inflamed. The researcher, together with her team and the cell systems department, developed a 3D herpes infection model. This makes it possible for the first time to integrate the complicated dormant stage of the virus into a model of the skin. A patent application has been submitted for the new process.

The expert explains the particularity of the virus: "After the blisters subside, the herpes virus retreats to the nerve cells and rests there. At this stage, only the virus' DNA can be proven." As soon as a human suffers too much stress or is even exposed to too much intense sun, the nerve cell may release the virus. It travels along the neural pathways to sites where it has occurred several times before, and the new infection becomes visible.

To date the skin models used for drug testing and to detect the virus have been very simple and unable to simulate the dormancy state of the virus. "We have integrated a neuronal cell line into the certified skin model of the IGB and are able to detect this latency stage for the first time. Just like in the human nerve cells, the particles of the virus itself cannot be seen; only the presence of its DNA can be proven by means of a PCR (polymerase chain reaction) analysis," explains the expert.

The researcher and her team then exposed the skin model to ultraviolet radiation at wave lengths of 280 to 315 nanometers (UVB). This reactivated the herpes virus, and there was an infection on the skin model. Proof of this reactivation was also possible on a co-culture. For this, the researchers introduced the latently infected neuronal cell line to a carrier with pores. Subsequently the cells were also irradiated with UVB. The virus was reactivated and penetrated these pores, infecting the cutaneous keratinocytes -- the keratinizing cells cultivated previously. To verify the infection, the scientists used a specific antibody that binds to a specific protein on the outer layer of the virus. The coloration of this antibody made it possible to clearly show the infection of the skin cells with the reactivated virus from the nerve cells.

"The 3-D herpes infection model therefore simulates an in-vivo situation exactly. Animal experiments will in the future become largely unnecessary," happily explain Burger-Kentischer and the doctoral candidate, Ina Hogk, who has worked on the development of the model from the beginning.

Research on active ingredients can profit from the 3D herpes infection model of the researchers from IGB, a model that also enables improved study of infection mechanisms. This procedure might also be used to test new medications for shingles, which is also caused by a variant strain of the herpes virus.

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Progress made toward a genital herpes vaccine

ScienceDaily (Jan. 6, 2012) — An investigational vaccine protected some women against infection from one of the two types of herpes simplex viruses that cause genital herpes, according to findings in the New England Journal of Medicine.

The vaccine was partially effective at preventing herpes simplex virus type 1 (HSV-1), but did not protect women from herpes simplex virus type 2 (HSV-2). There were less than half of the cases of genital herpes caused by HSV-1 -- 58 percent fewer -- in women who received the investigational vaccine compared to women who received the control vaccine.

"There is some very good news in our findings. We were partially successful against half of the equation -- protecting women from genital disease caused by HSV-1," said Robert Belshe, M.D., director of the Saint Louis University Center for Vaccine Development and lead author of the study.

"It's a big step along the path to creating an effective vaccine that protects against genital disease caused by herpes infection. It points us in the direction to work toward making a vaccine that works on both herpes simplex viruses."

Both HSV-1 and HSV-2 are members of the herpesvirus family. Typically, HSV-2 causes lesions and blisters in the genital area. HSV-1 generally causes sores in the mouth and lips, although it increasingly has been found to cause genital disease.

There currently is no cure or approved vaccine to prevent genital herpes infection, which affects about 25 percent of women in the United States and is one of the most common communicable diseases. Once inside the body, HSV remains there permanently. The virus can cause severe neurological disease and even death in infants born to women who are infected with HSV and the virus is a risk factor for sexual transmission of HIV.

The clinical trial of an investigational genital herpes vaccine was funded by the National Institute of Allergy and Infectious Diseases (NIAID), which is part of the National Institutes of Health, along with GlaxoSmithKline (GSK), and conducted at 50 sites in the U.S. and Canada.

The study enrolled 8,323 women between ages 18 and 30 who did not have HSV-1 or HSV-2 infection at the start of the study. They were randomly assigned to receive either three doses of the investigational HSV vaccine that was developed by GSK or a hepatitis A vaccine, which was the control.

Participants were followed for 20 months and evaluated carefully for occurrence of genital herpes disease. In addition, all study participants were given blood tests to determine if asymptomatic infection with HSV-1 or HSV-2 occurred during the trial. Researchers found that two or three doses of the investigational vaccine offered significant protection against genital herpes disease caused by HSV-1. However the vaccine did not protect women from genital disease caused by HSV-2.

"We were surprised by these findings," said Belshe, who also is a professor of infectious diseases and immunology at Saint Louis University School of Medicine. "We didn't expect the herpes vaccine to protect against one type of herpes simplex virus and not another. We also found it surprising that HSV-1 was a more common cause of genital disease than was HSV-2."

HSV-1 infection has become an increasingly common cause of genital disease, likely because more couples are engaging in oral sex. HSV-1 and HSV-2 are spread by direct contact -- mouth to mouth, mouth to genitals and genitals to genitals -- even when the infected person shows no symptoms, Belshe added.

Researchers are conducting laboratory tests on serum obtained from study participants as they continue to study why the vaccine protected women from genital disease caused by HSV-1 and not HSV-2.

One hypothesis, Belshe said, is HSV-1 is more easily killed by antibodies than is HSV-2. This means that the vaccine antibodies might work better against HSV-1 and result in protection from HSV-1 but not HSV-2.

Earlier studies of the investigational herpes vaccines showed it protected against genital herpes disease in women who were not infected with HSV-1 or HSV-2, but whose sexual partners were known to have genital herpes. Researchers believe the reason for the different outcome in the most recent clinical trial could be related to the fact that different populations were studied. The women in the earlier studies may have been protected due to immunologic or behavioral factors not present in the later study.

"It's always important to confirm scientific findings in repeated studies, which is why we investigated the vaccine in a large, placebo controlled trial," Belshe said. "Our findings confirmed the validity of the scientific process. You've got to have good scientific evidence that something actually works."

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Robert B. Belshe et al. Efficacy Results of a Trial of a Herpes Simplex Vaccine. New England Journal of Medicine, Jan 5, 2012 DOI: 10.1056/NEJMoa1103151

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Map of herpes virus protein suggests a new drug therapy

ScienceDaily (July 8, 2010) — The mechanism by which a herpes virus invades cells has remained a mystery to scientists seeking to thwart this family of viruses. New research funded by the National Institutes of Health and published online in advance of print in Nature Structural & Molecular Biology reveals the unusual structure of the protein complex that allows a herpes virus to invade cells. This detailed map of a key piece of the herpes virus "cell-entry machinery" gives scientists a new target for antiviral drugs.

"Most viruses need cell-entry proteins called fusogens in order to invade cells. We have known that the herpes virus fusogen does not act alone and that a complex of two other viral cell-entry proteins is always required. We expected that this complex was also a fusogen, but after determining the structure of this key protein complex, we found that it does not resemble other known fusogens," said senior author Ekaterina Heldwein, PhD, assistant professor in the molecular biology and microbiology department at Tufts University School of Medicine.

"This unexpected result leads us to believe that this protein complex is not a fusogen itself but that it regulates the fusogen. We also found that certain antibodies interfere with the ability of this protein complex to bind to the fusogen, evidence that antiviral drugs that target this interaction could prevent viral infection," Heldwein continued. Heldwein is also a member of the biochemistry and molecular microbiology program faculties at the Sackler School of Graduate Biomedical Sciences at Tufts.

"Katya Heldwein's work has resulted in a map of the protein complex needed to trigger herpes virus infection. The NIH Director's New Innovator Awards are designed to support such breakthroughs. This research not only adds to what we know about how herpes viruses infect mammalian cells, but also sets the stage for new therapeutics that restrict herpes virus's access to the cell," said Jeremy M. Berg, PhD, director of the National Institute of General Medical Sciences (NIGMS) at the National Institutes of Health.

"We hope that determining the structure of this essential piece of the herpes virus cell-entry machinery will help us answer some of the many questions about how herpes virus initiates infection. Knowing the structures of cell-entry proteins will help us find the best strategy for interfering with this pervasive family of viruses," said first author Tirumala K. Chowdary, PhD, a postdoctoral associate in the department of molecular biology and microbiology at TUSM and member of Heldwein's lab.

Currently, there is no cure for herpes viruses. Upon infection, the viruses remain in the body for life and can stay inactive for long periods of time. When active, however, different herpes viruses can cause cold sores, blindness, encephalitis, or cancers. More than half of Americans are infected with herpes simplex virus type 1 (HSV-1), which causes cold sores, by the time they reach their 20s. Currently, about one in six Americans is infected with herpes simplex virus type 2 (HSV-2), the virus responsible for genital herpes. Complications of HSV-2, a sexually-transmitted disease, include recurrent painful genital sores, psychological distress, and, if transmitted from mother to child, potentially fatal infections in newborn infants.

Heldwein teamed up with colleagues at University of Pennsylvania and used x-ray crystallography along with cell microscopy techniques to study the structure and function of this cell-entry protein complex in HSV-2. Heldwein is currently developing a molecular movie that illustrates how herpes virus enters the cell.

Additional authors are Tina Cairns, PhD, a research specialist; Doina Atanasiu, a research associate; and Gary Cohen, PhD, professor and chair, all in the department of microbiology at the University of Pennsylvania School of Dental Medicine; and Roselyn Eisenberg, PhD, professor in the department of microbiology at the University of Pennsylvania School of Veterinary Medicine.

This work was funded by the Office of the Director of the National Institutes of Health, through a New Innovator Award in 2007 to Ekaterina Heldwein. The New Innovator Awards, part of the NIH Roadmap for Medical Research initiative, are awarded to support early-career scientists who take innovative -- and potentially transformative -- approaches to major challenges in biomedical research. The work was also funded by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, and the Pew Scholar Program in Biomedical Sciences.

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Tirumala K Chowdary, Tina M Cairns, Doina Atanasiu, Gary H Cohen, Roselyn J Eisenberg, Ekaterina E Heldwein. Crystal structure of the conserved herpesvirus fusion regulator complex gH-gL. Nature Structural & Molecular Biology, 2010; DOI: 10.1038/nsmb.1837

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New way to target viruses could make antiviral drugs more effective

ScienceDaily (July 21, 2010) — Scientists have developed a new way to target viruses which could increase the effectiveness of antiviral drugs.

Instead of attacking the virus itself, the method developed at the University of Edinburgh alters the conditions which viruses need to survive and multiply.

By making the site of infection less hospitable for the virus, the virus becomes less able to mutate and build up resistance to drugs. The researchers were also able to target more than one virus at the same time.

Viruses take up residence in host cells within our body, which produce proteins that enable the virus to multiply and survive.

The study, published in the journal Proceedings of the National Academy of Sciences (PNAS), analysed molecules known as microRNAs, which regulate how much of these proteins are made.

The scientists were able to manipulate the microRNA levels, which enabled them to control a network of proteins and stop viruses from growing.

Most existing antiviral therapies only work against one virus. However, by adapting the virus host environment the researchers were able to target different types of viruses.

It is hoped that the research could lead to new treatments for patients suffering from a range of infections.

Dr Amy Buck, of the University's Centre for Immunity, Infection & Evolution, said: "A problem with current antiviral therapies, which generally target the virus, is that viruses can mutate to become resistant. Since new viral strains emerge frequently, and many infections are difficult to diagnose and treat, it is important to find new ways of targeting infection. Our hope is that we will be able to use host-directed therapies to supplement the natural immune response and disable viruses by taking away what they need to survive."

Scientists studied the herpes family of viruses, which can also cause cancer with the Epstein-Barr virus, and the Semliki Forest virus, which is mainly spread by mosquitoes.

Both viruses have different characteristics. Viruses from the herpes family replicate inside the nuclei of cells, while the Semliki Forest multiplies outside the nucleus of a cell.

Further research has begun to look at how this method could be used to target influenza.

The study was funded by the Wellcome Trust and the Biotechnology and Biological Sciences Research Council.

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Diwakar Santhakumar, Thorsten Forster, Nouf N. Laqtom, Rennos Fragkoudis, Paul Dickinson, Cei Abreu-Goodger, Sergei A. Manakov, Nila Roy Choudhury, Samantha J. Griffiths, Annaleen Vermeulen, Anton J. Enright, Bernadette Dutia, Alain Kohl, Peter Ghazal, and Amy H. Buck. Combined agonist-antagonist genome-wide functional screening identifies broadly active antiviral microRNAs. Proceedings of the National Academy of Sciences, 2010; DOI: 10.1073/pnas.1008861107

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Immunogene therapy combined with standard treatment is safe for patients with brain tumors, study suggests

ScienceDaily (Sep. 6, 2011) — A clinical trial has shown that a form of gene therapy is safe for treating a deadly form of brain cancer, even when combined with radiation therapy.

The phase 1b trial was conducted at the Ohio State University Comprehensive Cancer Center -- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC -- James) and at Methodist at Hospital in Houston, TX.

The novel treatment uses an adenovirus vector called AdV-tk. The vector is taken up by cancer cells where it activates a drug that kills the cells. The vector is applied in the operating room after removing brain tumors such as glioblastoma multiforme, the most common and dangerous form of brain cancer.

The findings, published online in the Journal of Clinical Oncology, suggest that the therapy might also stimulate an immune response against the tumor.

"This is the first time that a gene therapy approach was combined with radiation in patients with newly diagnosed glioblastoma," says first author Dr. E. Antonio Chiocca, professor and chair of neurological surgery and co-director of the Dardinger Center for Neuro-oncology and Neurosciences at Ohio State.

"There had been a concern that combining these two treatments could be too toxic for patients, but this was not the case. We do not know yet if this will improve survival, but these findings are encouraging," he says.

Glioblastomas occur in about 18,500 Americans annually and kill nearly 13,000 of them yearly. Glioblastoma multiforme is the most common and lethal form of the malignancy, with an average survival of 15 months after diagnosis.

The tumors often recur because cancer cells typically migrate into adjacent brain tissue where they can give rise to a recurrent tumor. This study examines an immunogene therapy approach that is designed to kill these undetected cancer cells and prevent recurrence.

This clinical trial involved 10 patients with glioblastoma multiforme and two patients with anaplastic astrocytoma. The procedure works as follows:

After removing the tumor, the neurosurgeon injects the tumor bed with 1 milliliter (1/30th oz) of a solution containing the AdV-tk vector. The vector carries a gene from herpes simplex virus for an enzyme called thymidine kinase (the '-tk' in AdV-tk). Cancer cells infected with the vector begin making the enzyme.Patients then take the anti-herpes virus drug valacyclovir for two weeks.Inside the cancer cells, the herpes thymidine kinase enzyme converts valacyclovir into DNA building blocks that the rapidly growing cancer cells cannot use to make DNA, and this kills them.Radiation therapy begins halfway through the course of valacyclovir. The radiation damages the DNA in the cancer cells, which then try to repair it, using the toxic valacyclovir building blocks.

In addition to improved overall survival, studies revealed a significant rise in the number of T lymphocytes in the tumors. This suggests that the gene therapy stimulated an immune response against the tumor, producing an "immunogene therapy" effect.

Cancer immunogene therapy refers to genetically manipulating cancer cells to stimulate an immune response against a tumor. (Note: This differs from "immunotherapy," which attempts to stimulate the immune system directly against tumor cells.)

"If the results of another recently completed phase 2 efficacy trial are also encouraging, the next step will be to compare this therapy head-to-head with the current standard of care," Chiocca says.

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E. A. Chiocca, L. K. Aguilar, S. D. Bell, B. Kaur, J. Hardcastle, R. Cavaliere, J. McGregor, S. Lo, A. Ray-Chaudhuri, A. Chakravarti, J. Grecula, H. Newton, K. S. Harris, R. G. Grossman, T. W. Trask, D. S. Baskin, C. Monterroso, A. G. Manzanera, E. Aguilar-Cordova, P. Z. New. Phase IB Study of Gene-Mediated Cytotoxic Immunotherapy Adjuvant to Up-Front Surgery and Intensive Timing Radiation for Malignant Glioma. Journal of Clinical Oncology, 2011; DOI: 10.1200/JCO.2011.35.5222

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