Beate Sodeik

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Beate Sodeik
Alma mater Heidelberg University
Columbia University Vagelos College of Physicians and Surgeons
University of Bonn
Scientific career
Institutions Hannover Medical School
Yale University
Thesis Das Assembly des Vaccinia-Virus  (1992)

Beate Sodeik is a German cell biologist who is Professor of Medical Sciences at the Hannover Medical School. Her research considers the biology of viral infections, with a particular focus on Herpes simplex virus.

Contents

Early life and education

Sodeik was an undergraduate student in the University of Bonn, where she studied biology. She earned a Diploma in Cell Biology, where she analysed autophagy in Amoeba proteus . [1] After graduating, she received a DAAD scholarship, and moved to the Columbia University Vagelos College of Physicians and Surgeons. [1] During her time at Columbia, Sodeik worked on integrin receptors of human neutrophils. She was a doctoral student in cell biology at the European Molecular Biology Laboratory in Heidelberg University. Her research considered the assembly of the Vaccina virus (cowpox). [2] After earning her doctorate, Sodeik returned to the United States, where she joined Ari Helenius at Yale University. At Yale, Sodeik studied the early phases of Herpes simplex virus. [1]

Research and career

Sodeik was made a Senior Scientist at Hannover Medical School in 1997. She completed her habilitation in the cell biology of DNA viruses and the maturation of Vaccinia . [3] She was eventually promoted to Professor.[ when? ][ citation needed ] Since starting her postdoctoral research, Sodeik has explored the cell biology of Herpes simplex virus. [4] She is interested in virus-host interactions, virus assembly and viral replication. [1]

Selected publications

Related Research Articles

<span class="mw-page-title-main">DNA virus</span> Virus that has DNA as its genetic material

A DNA virus is a virus that has a genome made of deoxyribonucleic acid (DNA) that is replicated by a DNA polymerase. They can be divided between those that have two strands of DNA in their genome, called double-stranded DNA (dsDNA) viruses, and those that have one strand of DNA in their genome, called single-stranded DNA (ssDNA) viruses. dsDNA viruses primarily belong to two realms: Duplodnaviria and Varidnaviria, and ssDNA viruses are almost exclusively assigned to the realm Monodnaviria, which also includes some dsDNA viruses. Additionally, many DNA viruses are unassigned to higher taxa. Reverse transcribing viruses, which have a DNA genome that is replicated through an RNA intermediate by a reverse transcriptase, are classified into the kingdom Pararnavirae in the realm Riboviria.

<span class="mw-page-title-main">Viral protein</span>

A viral protein is both a component and a product of a virus. Viral proteins are grouped according to their functions, and groups of viral proteins include structural proteins, nonstructural proteins, regulatory proteins, and accessory proteins. Viruses are non-living and do not have the means to reproduce on their own, instead depending on their host cell's resources in order to reproduce. Thus, viruses do not code for many of their own viral proteins, and instead use the host cell's machinery to produce the viral proteins they require for replication.

An oncolytic virus is a virus that preferentially infects and kills cancer cells. As the infected cancer cells are destroyed by oncolysis, they release new infectious virus particles or virions to help destroy the remaining tumour. Oncolytic viruses are thought not only to cause direct destruction of the tumour cells, but also to stimulate host anti-tumour immune system responses. Oncolytic viruses also have the ability to affect the tumor micro-environment in multiples ways.

<span class="mw-page-title-main">Virus latency</span> Ability of some viruses to lie dormant within a cell

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>Herpesviridae</i> Family of DNA viruses

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.

<span class="mw-page-title-main">Viral envelope</span> Outermost layer of many types of the infectious agent

A viral envelope is the outermost layer of many types of viruses. It protects the genetic material in their life cycle when traveling between host cells. Not all viruses have envelopes. A viral envelope protein or E protein is a protein in the envelope, which may be acquired by the capsid from an infected host cell.

<span class="mw-page-title-main">Viroplasm</span>

A viroplasm, sometimes called "virus factory" or "virus inclusion", is an inclusion body in a cell where viral replication and assembly occurs. They may be thought of as viral factories in the cell. There are many viroplasms in one infected cell, where they appear dense to electron microscopy. Very little is understood about the mechanism of viroplasm formation.

<span class="mw-page-title-main">Herpes simplex virus</span> Species of virus

Herpes simplex virus1 and 2, also known by their taxonomical 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.

<span class="mw-page-title-main">Viral entry</span> Earliest stage of infection in the viral life cycle

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.

<span class="mw-page-title-main">Gene delivery</span> Introduction of foreign genetic material into host cells

Gene delivery is the process of introducing foreign genetic material, such as DNA or RNA, into host cells. Gene delivery must reach the genome of the host cell to induce gene expression. Successful gene delivery requires the foreign gene delivery to remain stable within the host cell and can either integrate into the genome or replicate independently of it. This requires foreign DNA to be synthesized as part of a vector, which is designed to enter the desired host cell and deliver the transgene to that cell's genome. Vectors utilized as the method for gene delivery can be divided into two categories, recombinant viruses and synthetic vectors.

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.

<span class="mw-page-title-main">Viral tegument</span> Cluster of proteins that lines the space between the envelope and nucleocapsid of all herpesviruses

A viral tegument or tegument, more commonly known as a viral matrix, is a cluster of proteins that lines the space between the envelope and nucleocapsid of all herpesviruses. The tegument generally contains proteins that aid in viral DNA replication and evasion of the immune response, typically with inhibition of signalling in the immune system and activation of interferons. The tegument is usually released shortly after infection into the cytoplasm. These proteins are usually formed within the late phase of the viral infectious cycle, after viral genes have been replicated. Much information regarding viral teguments has been gathered from studying herpes simplex virus.

<span class="mw-page-title-main">Virus</span> Infectious agent that replicates in cells

A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism. Viruses infect all life forms, from animals and plants to microorganisms, including bacteria and archaea. Since Dmitri Ivanovsky's 1892 article describing a non-bacterial pathogen infecting tobacco plants and the discovery of the tobacco mosaic virus by Martinus Beijerinck in 1898, more than 9,000 of the millions of virus species have been described in detail. Viruses are found in almost every ecosystem on Earth and are the most numerous type of biological entity. The study of viruses is known as virology, a subspeciality of microbiology.

Enzo Paoletti was an Italian-American virologist who developed the technology to express foreign antigens in vaccinia and other poxviruses. This advance led to the development of vaccines against multiple disease-causing pathogens.

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.

<span class="mw-page-title-main">Jelly roll fold</span> Type of beta barrel protein domain structure

The jelly roll or Swiss roll fold is a protein fold or supersecondary structure composed of eight beta strands arranged in two four-stranded sheets. The name of the structure was introduced by Jane S. Richardson in 1981, reflecting its resemblance to the jelly or Swiss roll cake. The fold is an elaboration on the Greek key motif and is sometimes considered a form of beta barrel. It is very common in viral proteins, particularly viral capsid proteins. Taken together, the jelly roll and Greek key structures comprise around 30% of the all-beta proteins annotated in the Structural Classification of Proteins (SCOP) database.

HSV epigenetics is the epigenetic modification of herpes simplex virus (HSV) genetic code.

<i>Duplodnaviria</i> Realm of viruses

Duplodnaviria is a realm of viruses that includes all double-stranded DNA viruses that encode the HK97 fold major capsid protein. The HK97 fold major capsid protein is the primary component of the viral capsid, which stores the viral deoxyribonucleic acid (DNA). Viruses in the realm also share a number of other characteristics, such as an icosahedral capsid, an opening in the viral capsid called a portal, a protease enzyme that empties the inside of the capsid prior to DNA packaging, and a terminase enzyme that packages viral DNA into the capsid.

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.

References

  1. 1 2 3 4 "Medizinische Hochschule Hannover : Sodeik lab". www.mhh.de. Retrieved 2021-09-26.
  2. Sodeik, Beate (1992). Das Assembly des Vaccinia-Virus (Thesis) (in German). OCLC   722777102.
  3. Sodeik, Beate (2001). Die Zellbiologie komplexer DNA-Viren die Reifung des Vaccinia-Virus ; der Zelleintritt von Herpes-Simplex-Virus (Thesis) (in German). OCLC   722946902.
  4. Bettina. "Prof. Dr. Beate Sodeik". RESIST. Retrieved 2021-09-26.