Jonathan P. Stoye

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Jonathan Stoye

FRS
Jonathan Stoye Royal Society.jpg
Jonathan Stoye
Born
Jonathan Paul Stoye

1952 (age 7071) [1]
Oxford, England
Education Magdalen College School, Oxford
Alma mater University of Cambridge (BA)
University of Basel (PhD)
Scientific career
Fields Virology
Institutions Francis Crick Institute
Thesis Studies on cellular and genetic factors controlling endogenous retrovirus expression in lymphocytes  (1981)
Website crick.ac.uk/research/a-z-researchers/researchers-p-s/jonathan-stoye

Jonathan Paul Stoye (born 1952) [1] FRS is a virologist at the Francis Crick Institute in London, England. He has made substantial contributions to scientific understanding of the interactions of retroviruses with their hosts. [2]

Contents

Education

Stoye was educated at Magdalen College School, Oxford and Magdalene College, Cambridge, where he was awarded a Bachelor of Arts degree in 1973. [1] He was awarded a PhD from the University of Basel in Switzerland in 1981 for studies on cellular and genetic factors controlling endogenous retrovirus expression in lymphocytes. [1] [3]

Career and research

Stoye has worked with the human immunodeficiency virus (HIV), other primate retroviruses, murine leukaemia viruses and retroviruses of pigs, goats, sheep and other animals. His recent publications describe investigations of host restriction factors such as Fv1,[ citation needed ] TRIM5alpha and other members of the tripartite motif family as well as the lentiviral accessory proteins Vpx and Vpr. [4] [5]

Awards and honours

Stoye was elected a Fellow of the Royal Society in 2017. [6] [7]

Related Research Articles

<span class="mw-page-title-main">Retrovirus</span> Family of viruses

A retrovirus is a type of virus that inserts a DNA copy of its RNA genome into the DNA of a host cell that it invades, thus changing the genome of that cell. After invading a host cell's cytoplasm, the virus uses its own reverse transcriptase enzyme to produce DNA from its RNA genome, the reverse of the usual pattern, thus retro (backwards). The new DNA is then incorporated into the host cell genome by an integrase enzyme, at which point the retroviral DNA is referred to as a provirus. The host cell then treats the viral DNA as part of its own genome, transcribing and translating the viral genes along with the cell's own genes, producing the proteins required to assemble new copies of the virus. Many retroviruses cause serious diseases in humans, other mammals, and birds.

Mouse mammary tumor virus (MMTV) is a milk-transmitted retrovirus like the HTL viruses, HI viruses, and BLV. It belongs to the genus Betaretrovirus. MMTV was formerly known as Bittner virus, and previously the "milk factor", referring to the extra-chromosomal vertical transmission of murine breast cancer by adoptive nursing, demonstrated in 1936, by John Joseph Bittner while working at the Jackson Laboratory in Bar Harbor, Maine. Bittner established the theory that a cancerous agent, or "milk factor", could be transmitted by cancerous mothers to young mice from a virus in their mother's milk. The majority of mammary tumors in mice are caused by mouse mammary tumor virus.

<i>Gammaretrovirus</i> Genus of viruses

Gammaretrovirus is a genus in the Retroviridae family. Example species are the murine leukemia virus and the feline leukemia virus. They cause various sarcomas, leukemias and immune deficiencies in mammals, reptiles and birds.

<span class="mw-page-title-main">Endogenous retrovirus</span> Inherited retrovirus encoded in an organisms genome

Endogenous retroviruses (ERVs) are endogenous viral elements in the genome that closely resemble and can be derived from retroviruses. They are abundant in the genomes of jawed vertebrates, and they comprise up to 5–8% of the human genome.

Virus latency is the ability of a pathogenic virus to lie dormant within a cell, denoted as the lysogenic part of the viral life cycle. A latent viral infection is a type of persistent viral infection which is distinguished from a chronic viral infection. Latency is the phase in certain viruses' life cycles in which, after initial infection, proliferation of virus particles ceases. However, the viral genome is not eradicated. The virus can reactivate and begin producing large amounts of viral progeny without the host becoming reinfected by new outside virus, and stays within the host indefinitely.

<i>Jaagsiekte sheep retrovirus</i> Species of virus

Jaagsiekte sheep retrovirus (JSRV) is a betaretrovirus which is the causative agent of a contagious lung cancer in sheep, called ovine pulmonary adenocarcinoma.

The murine leukemia viruses are retroviruses named for their ability to cause cancer in murine (mouse) hosts. Some MLVs may infect other vertebrates. MLVs include both exogenous and endogenous viruses. Replicating MLVs have a positive sense, single-stranded RNA (ssRNA) genome that replicates through a DNA intermediate via the process of reverse transcription.

Simian foamy virus (SFV) is a species of the genus Spumavirus that belongs to the family of Retroviridae. It has been identified in a wide variety of primates, including prosimians, New World and Old World monkeys, as well as apes, and each species has been shown to harbor a unique (species-specific) strain of SFV, including African green monkeys, baboons, macaques, and chimpanzees. As it is related to the more well-known retrovirus human immunodeficiency virus (HIV), its discovery in primates has led to some speculation that HIV may have been spread to the human species in Africa through contact with blood from apes, monkeys, and other primates, most likely through bushmeat-hunting practices.

Group-specific antigen, or gag, is the polyprotein that contains the core structural proteins of an Ortervirus. It was named as such because scientists used to believe it was antigenic. Now it is known that it makes up the inner shell, not the envelope exposed outside. It makes up all the structural units of viral conformation and provides supportive framework for mature virion.

<span class="mw-page-title-main">Syncytin-1</span> Protein-coding gene in the species Homo sapiens

Syncytin-1 also known as enverin is a protein found in humans and other primates that is encoded by the ERVW-1 gene. Syncytin-1 is a cell-cell fusion protein whose function is best characterized in placental development. The placenta in turn aids in embryo attachment to the uterus and establishment of a nutrient supply.

<span class="mw-page-title-main">ERV3</span> Protein-coding gene in the species Homo sapiens

HERV-R_7q21.2 provirus ancestral envelope (Env) polyprotein is a protein that in humans is encoded by the ERV3 gene.

Avian sarcoma leukosis virus (ASLV) is an endogenous retrovirus that infects and can lead to cancer in chickens; experimentally it can infect other species of birds and mammals. ASLV replicates in chicken embryo fibroblasts, the cells that contribute to the formation of connective tissues. Different forms of the disease exist, including lymphoblastic, erythroblastic, and osteopetrotic.

Koala retrovirus (KoRV) is a retrovirus that is present in many populations of koalas. It has been implicated as the agent of koala immune deficiency syndrome (KIDS), an AIDS-like immunodeficiency that leaves infected koalas more susceptible to infectious disease and cancers. The virus is thought to be a recently introduced exogenous virus that is also integrating into the koala genome. Thus the virus can transmit both horizontally and vertically. The horizontal modes of transmission are not well defined but are thought to require close contact.

Paleovirology is the study of viruses that existed in the past but are now extinct. In general, viruses cannot leave behind physical fossils, therefore indirect evidence is used to reconstruct the past. For example, viruses can cause evolution of their hosts, and the signatures of that evolution can be found and interpreted in the present day. Also, some viral genetic fragments which were integrated into germline cells of an ancient organism have been passed down to our time as viral fossils, or endogenous viral elements (EVEs). EVEs that originate from the integration of retroviruses are known as endogenous retroviruses, or ERVs, and most viral fossils are ERVs. They may preserve genetic code from millions of years ago, hence the "fossil" terminology, although no one has detected a virus in mineral fossils. The most surprising viral fossils originate from non-retroviral DNA and RNA viruses.

An endogenous viral element (EVE) is a DNA sequence derived from a virus, and present within the germline of a non-viral organism. EVEs may be entire viral genomes (proviruses), or fragments of viral genomes. They arise when a viral DNA sequence becomes integrated into the genome of a germ cell that goes on to produce a viable organism. The newly established EVE can be inherited from one generation to the next as an allele in the host species, and may even reach fixation.

Human endogenous retrovirus K (HERV-K) or Human teratocarcinoma-derived virus (HDTV) is a family of human endogenous retroviruses associated with malignant tumors of the testes. Phylogenetically, the HERV-K group belongs to the ERV2 or Class II or Betaretrovirus-like supergroup. Over the past several years, it has been found that this group of ERVs play an important role in embryogenesis, but their expression is silenced in most cell types in healthy adults. The HERV-K family, and particularly its subgroup HML-2, is the youngest and most transcriptionally active group and hence, it is the best studied among other ERVs. Reactivation of it or anomalous expression of HML-2 in adult tissues has been associated with various types of cancer and with neurodegenerative diseases such as amytrophic lateral sclerosis (ALS). Endogenous retrovirus K (HERV-K) is related to mammary tumor virus in mice. It exists in the human and cercopithecoid genomes. Human genome contains hundreds of copies of HERV-K and many of them possess complete open reading frames (ORFs) that are transcribed and translated, especially in early embryogenesis and in malignancies. HERV-K is also found in apes and Old World monkeys. It is uncertain how long ago in primate evolution the full-length HERV-K proviruses which are in the human genome today were created.

Jay A. Levy, M.D. is an AIDS and cancer research physician. He is a professor of medicine with specialties in virology and immunology at the University of California, San Francisco (UCSF).

Human Endogenous Retrovirus-W (HERV-W) is the coding for a protein that would normally be part of the envelope of one family of Human Endogenous Retro-Viruses, or HERVs.

Charles Bangham holds the Chair in Immunology at Imperial College London.

Gibbon-ape leukemia virus (GaLV) is an oncogenic, type C retrovirus that has been isolated from primate neoplasms, including the white-handed gibbon and woolly monkey. The virus was identified as the etiological agent of hematopoietic neoplasms, leukemias, and immune deficiencies within gibbons in 1971, during the epidemic of the late 1960s and early 1970s. Epidemiological research into the origins of GaLV has developed two hypotheses for the virus' emergence. These include cross-species transmission of the retrovirus present within a species of East Asian rodent or bat, and the inoculation or blood transfusion of a MbRV-related virus into captured gibbons populations housed at medical research institutions. The virus was subsequently identified in captive gibbon populations in Thailand, the US and Bermuda.

References

  1. 1 2 3 4 Anon (2017). "Stoye, Dr. Jonathan" . Who's Who (online Oxford University Press  ed.). Oxford: A & C Black. doi:10.1093/ww/9780199540884.013.289292.(Subscription or UK public library membership required.)
  2. "Stoye Research profile". Archived from the original on 6 May 2015.
  3. Stoye, Jonathan Paul (1981). Studies on cellular and genetic factors controlling endogenous retrovirus expression in lymphocytes (PhD thesis). University of Basel. OCLC   166505796.
  4. Jonathan P. Stoye publications indexed by the Scopus bibliographic database. (subscription required)
  5. "Recent publications by Stoye". Archived from the original on 5 September 2017. Retrieved 16 June 2015.
  6. Anon (2017). "Jonathan Stoye". royalsociety.org. London: Royal Society. Archived from the original on 23 May 2017. Retrieved 28 May 2017.
  7. Anon (2005). "Jonathan Stoye". The Lancet . 365 (9462): 839. doi: 10.1016/S0140-6736(05)71029-1 . ISSN   0140-6736. S2CID   54344040.