Tony Minson | |
---|---|
Born | [1] | 8 February 1944
Alma mater | University of Birmingham (BSc) Australian National University (PhD) |
Awards | FMedSci (2002) |
Scientific career | |
Institutions | University of Cambridge University of Birmingham Australian National University |
Thesis | Studies of the biosynthesis of histidine in Neurospora crassa (1968) |
Doctoral students | Tony Kouzarides [2] |
Website | www |
Anthony Charles Minson (born 8 February 1944) [3] is a British virologist known for his work on the biology of herpesviruses, [4] [5] [6] [7] [8] and a university administrator. He was the Senior Pro-Vice-Chancellor of the University of Cambridge from 2003 to 2009. He is an emeritus professor of virology at the university's Department of Pathology and an emeritus fellow of Wolfson College. [9]
Born in Ilford, Essex, Minson was educated at Ilford High School [1] and went on to study microbiology at the University of Birmingham in 1965. His postgraduate work was at the Research School of Biological Sciences of the Australian National University, researching fungal genetics with E. H. Creaser. [10] [11] [12] He gained his PhD in 1968 for work on the biosynthesis of histidine in Neurospora crassa . [13]
By the early 1970s, Minson had returned to the University of Birmingham. [14] In 1976, he took up a position as Senior Research Associate at the University of Cambridge. In the mid-1980s, he became head of the Division of Virology and, in 1991, was appointed professor of virology in the Department of Pathology. [10] He is a fellow of Wolfson College. [11]
Since moving to Cambridge, Minson's research has focused on animal viruses, particularly those of the herpesvirus family, including herpes simplex virus (HSV) and human cytomegalovirus. [15] These large and complex enveloped DNA viruses commonly infect humans, causing a lifelong latent infection. Conditions associated with HSV include cold sores and genital herpes, and both HSV and cytomegalovirus can be life-threatening in immunodeficient people. Much of Minson's research has investigated herpesvirus replication and life cycle, viral pathogenesis and the immune response. His work has contributed to understanding the processes by which HSV fuses with the cell membrane and acquires its envelope. [16] [17] As of 2013, his research focuses on herpesvirus entry, in particular how the viral membrane proteins cooperate to induce fusion, as well as assembly, in particular of the viral membrane proteins. [18]
Minson has also worked in collaboration with Margaret Stanley on another DNA virus, human papillomavirus, which is associated with cervical cancer. [19] His research in the early 1970s was in the field of plant viruses, including tobacco rattle virus and tobacco necrosis virus, in collaboration with Graham Darby and others. [14] [20] Leszek Borysiewicz and Geoffrey L. Smith are among his other research collaborators, [15] [21] and notable students have included Tony Kouzarides. [2] [22]
In the early 1990s, Minson's group was one of several investigating a novel method of attenuating viruses for use in live vaccines. One or more of the genes absolutely required for replication is deleted and the virus is grown in a cell line engineered to express these gene products. The resulting virus can infect normal human cells but should be safe because it cannot replicate in them. [23] [24] [25] Such replication-impaired viruses unite many of the advantages of both live and killed virus vaccines and are much less likely to revert to a more virulent form than earlier methods of attenuation. [25] [26]
Minson and co-workers pioneered a modification of this approach in which the disabled virus is restricted to a single cycle of replication. Using HSV-2, which causes genital herpes, they disabled the virus by deleting the viral gene encoding the membrane protein glycoprotein H (gH). This product is not required until after the viral assembly process, which means that the disabled virus can undergo a single round of replication in normal human cells, but the progeny virus cannot infect new cells. Minson's group called the resulting virus a "disabled infectious single cycle" (DISC) virus; similarly disabled viruses are also termed "single-cycle" viruses. Their work with DISC HSV-2 led to a series of vaccine candidates, which were developed by Cantab Pharmaceuticals. [23] [24] [25] The DISC HSV-2 vaccine was promising in animal models and early clinical trials, appearing safe and well tolerated, and eliciting appropriate immune responses. [24] [25] [27] [28] However, a large phase II trial of the agent as a therapeutic vaccine in people with genital herpes failed to demonstrate any benefit, [24] [27] and further development has concentrated on the DISC HSV-2 vaccine's potential to prevent infection. [27] [29] The single-cycle strategy can be used to generate live vaccines against other viruses, and such a vaccine has recently been successfully developed for the bluetongue virus of sheep. [30] Single-cycle viruses are also widely used as vaccine vectors, carrying genes from other viruses. [31]
In the early 2000s, a collaboration between Minson and Matthew Cooper's group from the University of Cambridge's chemistry department pioneered a novel acoustic technique for detecting viruses. The technique allows a single virus particle to be detected in a sample and has the potential for use as a quick yet sensitive monitor of viral infection. [32] [33] The researchers co-founded the company Akubio in 2001 to exploit the discovery; the company developed biosensors for detecting bacteria and viruses. It was acquired by Inverness Medical Innovations in 2008. [34]
Minson is a long-term member of the International Committee on Taxonomy of Viruses (ICTV) Study Group that defines herpesvirus taxonomy. [35] [36] In 2008, as a result of the group's deliberations on research into herpesvirus genetics, the ICTV promoted the herpesvirus family to an order and split it into three families. [36]
Minson has been highly active in university administration. In 2001–3, he chaired the School of Biological Sciences, one of the six schools of the University of Cambridge. [11] In 2003, he was appointed Pro-Vice-Chancellor of the university, in succession to Malcolm Grant. Minson was the first, and most senior, of a new team of five Pro-Vice-Chancellors, holding particular responsibility for planning and resources. [10] [37] [38] He said of his role: We have a duty to maintain the university's values of scientific enquiry and scholarship whilst embracing the principles of sustainable, achievable reform. [38] He served in this position until 2009, the university's 800th anniversary year. [37] Soon after his appointment, he was thrown into controversy over his strong support for a proposed new primate research centre attached to the university, which was the target of a campaign by animal rights activists. [39] The plans were later abandoned because of escalating costs, due in part to the activism. [40] [41] In 2005, the university launched a major fund-raising campaign to mark the 800th anniversary; the £1 billion target was achieved ahead of schedule in 2010. [42]
Minson has also served on the steering committee of the multidisciplinary Cambridge Infectious Disease group, launched in 2004. [43] [44] In 2010–12, he chaired the syndicate governing Cambridge University Press. [45] Outside the university, he served on the council of the Society for General Microbiology in 1990–94 and 2003–7, and (as of 2012) is the reviews editor of their journal, the Journal of General Virology . [46] [47] He was an officer of the Biotechnology and Biological Sciences Research Council's Institute for Animal Health (now the Pirbright Institute) from 1997–2003. [48] As of 2013, Minson is on the board of the Lister Institute of Preventive Medicine and is a trustee of the Animal Health Trust. [49] [50]
He has drawn attention to the cost of bureaucracy imposed on researchers by government agencies, writing in 2004:
To be against improvement in standards is like being against motherhood, but we should be alert to the dangers of universal codes of practice imposed for administrative tidiness. The fact is that the great scientific leaps of the past 50 years have not been made in laboratories using validated standard operating procedures, well-defined line-management systems, and 6-monthly milestones. [51]
Minson was elected a fellow of the Academy of Medical Sciences in 2002. [52] He was elected an honorary member of the Society for General Microbiology in 2011. [46]
Varicella zoster virus (VZV), also known as human herpesvirus 3 or Human alphaherpesvirus 3 (taxonomically), is one of nine known herpes viruses that can infect humans. It causes chickenpox (varicella) commonly affecting children and young adults, and shingles in adults but rarely in children. As a late complication of VZV infection, Ramsay Hunt syndrome type 2 may develop in rare cases. VZV infections are species-specific to humans. The virus can survive in external environments for a few hours.
HHV Latency Associated Transcript is a length of RNA which accumulates in cells hosting long-term, or latent, Human Herpes Virus (HHV) infections. The LAT RNA is produced by genetic transcription from a certain region of the viral DNA. LAT regulates the viral genome and interferes with the normal activities of the infected host cell.
Herpesviridae is a large family of DNA viruses that cause infections and certain diseases in animals, including humans. The members of this family are also known as herpesviruses. The family name is derived from the Greek word ἕρπειν, referring to spreading cutaneous lesions, usually involving blisters, seen in flares of herpes simplex 1, herpes simplex 2 and herpes zoster (shingles). In 1971, the International Committee on the Taxonomy of Viruses (ICTV) established Herpesvirus as a genus with 23 viruses among four groups. As of 2020, 115 species are recognized, all but one of which are in one of the three subfamilies. Herpesviruses can cause both latent and lytic infections.
Human Herpes Virus (HHV) Infected Cell Polypeptide 0 (ICP0) is a protein, encoded by the DNA of herpes viruses. It is produced by herpes viruses during the earliest stage of infection, when the virus has recently entered the host cell; this stage is known as the immediate-early or α ("alpha") phase of viral gene expression. During these early stages of infection, ICP0 protein is synthesized and transported to the nucleus of the infected host cell. Here, ICP0 promotes transcription from viral genes, disrupts structures in the nucleus known as nuclear dots or promyelocytic leukemia (PML) nuclear bodies, and alters the expression of host and viral genes in combination with a neuron specific protein. At later stages of cellular infection, ICP0 relocates to the cell cytoplasm to be incorporated into new virion particles.
Herpes simplex virus1 and 2, also known by their taxonomic 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 very common and contagious. They can be spread when an infected person begins shedding the virus.
Viral entry is the earliest stage of infection in the viral life cycle, as the virus comes into contact with the host cell and introduces viral material into the cell. The major steps involved in viral entry are shown below. Despite the variation among viruses, there are several shared generalities concerning viral entry.
HHV Capsid Portal Protein, or HSV-1 UL-6 protein, is the protein which forms a cylindrical portal in the capsid of Herpes simplex virus (HSV-1). The protein is commonly referred to as the HSV-1 UL-6 protein because it is the transcription product of Herpes gene UL-6.
Poliovirus receptor-related 2 (PVRL2), also known as nectin-2 and CD112, is a human plasma membrane glycoprotein.
Poliovirus receptor-related 1 (PVRL1), also known as nectin-1 and CD111 (formerly herpesvirus entry mediator C, HVEC) is a human protein of the immunoglobulin superfamily (IgSF), also considered a member of the nectins. It is a membrane protein with three extracellular immunoglobulin domains, a single transmembrane helix and a cytoplasmic tail. The protein can mediate Ca2+-independent cellular adhesion further characterizing it as IgSF cell adhesion molecule (IgSF CAM).
Herpes meningitis is inflammation of the meninges, the protective tissues surrounding the spinal cord and brain, due to infection from viruses of the Herpesviridae family - the most common amongst adults is HSV-2. Symptoms are self-limiting over 2 weeks with severe headache, nausea, vomiting, neck-stiffness, and photophobia. Herpes meningitis can cause Mollaret's meningitis, a form of recurrent meningitis. Lumbar puncture with cerebrospinal fluid results demonstrating aseptic meningitis pattern is necessary for diagnosis and polymerase chain reaction is used to detect viral presence. Although symptoms are self-limiting, treatment with antiviral medication may be recommended to prevent progression to Herpes Meningoencephalitis.
Sarah A. Connolly is an American virologist. She graduated with a PhD from the University of Pennsylvania in 2003 and is notable for her work on Paramyxovirus and Herpes virus.
Herpesvirus glycoprotein B is a viral glycoprotein that is involved in the viral cell entry of Herpes simplex virus (HSV). Herpesviruses have a lipid bilayer, called the envelope, which contains twelve surface glycoproteins. For infectivity to be attained, the double stranded DNA genome of HSV must enter the host cell through means of fusion of its envelope with the cellular membrane or via endocytosis. Other viral glycoproteins involved in the process of viral cell entry include gC, gB, gD, gH, and gL, but only gC, gB, gD, and gH are required for the fusion of the HSV's envelope with the cellular membrane. It can be noted that all herpesviruses have glycoproteins gB, gH, and gL.
Herpes simplex research includes all medical research that attempts to prevent, treat, or cure herpes, as well as fundamental research about the nature of herpes. Examples of particular herpes research include drug development, vaccines and genome editing. HSV-1 and HSV-2 are commonly thought of as oral and genital herpes respectively, but other members in the herpes family include chickenpox (varicella/zoster), cytomegalovirus, and Epstein-Barr virus. There are many more virus members that infect animals other than humans, some of which cause disease in companion animals or have economic impacts in the agriculture industry.
ICP8, the herpes simplex virus type-1 single-strand DNA-binding protein, is one of seven proteins encoded in the viral genome of HSV-1 that is required for HSV-1 DNA replication. It is able to anneal to single-stranded DNA (ssDNA) as well as melt small fragments of double-stranded DNA (dsDNA); its role is to destabilize duplex DNA during initiation of replication. It differs from helicases because it is ATP- and Mg2+-independent. In cells infected with HSV-1, the DNA in those cells become colocalized with ICP8.
David Mahan Knipe is the Higgins Professor of Microbiology and Molecular Genetics in the Department of Microbiology at the Harvard Medical School in Boston, Massachusetts and co-chief editor of the reference book Fields Virology. He returned to the Chair of the Program in Virology at Harvard Medical School in 2019, having previously held the position from 2004 through 2016 and served as interim Co-Chair of the Microbiology and Immunobiology Department from 2016 through 2018.
Roselyn J. Eisenberg is a professor at The University of Pennsylvania and a member of the University's School of Veterinary Medicine and School of Dental Medicine. The majority of Eisenberg's research is focused on the herpes simplex virus and the poxvirus and how they enter into susceptible cells. She also studies glycoproteins, vaccines, virology and microbiology.
Joel D. Baines is an American virologist who is serving as dean of the School of Veterinary Medicine, Louisiana State University (LSU) since 2014.
Gabriella Campadelli-Fiume is a virologist with a primary research focus on herpes simplex virus, fusion and viral entry. She is a retired professor of virology from the University of Bologna, Italy.
Patricia Gail Spear is an American virologist. She is a professor emeritus of microbiology and immunology at Northwestern University in Evanston, Illinois. She is best known for her pioneering work studying the herpes simplex virus. Spear is a past president of the American Society for Virology and an elected member of the National Academy of Sciences.
Jay Clark Brown is an American molecular biologist, microbiologist, virologist, and academic. He is a Professor Emeritus in the Department of microbiology, immunology, and cancer biology at the University of Virginia School of Medicine.
{{cite book}}
: CS1 maint: multiple names: authors list (link){{cite web}}
: CS1 maint: bot: original URL status unknown (link) (accessed 9 January 2013)