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1 edition of Selected abstracts on virus latency and oncogenesis found in the catalog.

Selected abstracts on virus latency and oncogenesis

Selected abstracts on virus latency and oncogenesis

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Published by U.S. Dept. of Health, Education, and Welfare, Public Health Service, National Institutes of Health, National Cancer Institute, National Technical Information Service [distributor in [Bethesda, Md.?], Springfield, Va .
Written in English

    Subjects:
  • Oncogenic viruses -- Abstracts.

  • Edition Notes

    Other titlesVirus latency and oncogenesis.
    StatementDonald H. Gilden and William C. Lawrence.
    GenreAbstracts.
    SeriesOncology overview
    ContributionsGilden, Donald H., Lawrence, William C., National Cancer Institute (U.S.), International Cancer Research Data Bank., Cancer Information Dissemination and Analysis Center on Virology, Immunology, and Biology.
    The Physical Object
    Paginationx, 71 p. ;
    Number of Pages71
    ID Numbers
    Open LibraryOL17549840M

      Regulation of oncogenesis by a critical window of differentiation. Schematic depicts the hypothesis that a critical window of differentiation dictates successful breast oncogenesis. The transgenic iPSC clones give rise to breast ontogeny followed by breast oncogenesis only when undifferentiated and injected orthotopically. Gastric carcinoma is the third leading cause of cancer mortality, with , deaths worldwide. 1 Many gastric carcinomas are associated with infection by Helicobacter pylori and Epstein–Barr virus (EBV). EBV-associated gastric carcinoma (EBVaGC) comprises approximately 10% of all cases of gastric carcinoma. 2 –6 EBV, also called human herpesvirus 4 (HHV-4), is a ubiquitous virus with an.   VIRUS GENES publishes. studies on analysis of virus genes, gene products and functions, regulation of virus gene function, cell biology of virus infection; functional studies of genes and gene families, encoded by eukaryotic, prokaryotic and archaeal viruses, viroids, as well as unconventional and novel infectious agents. MicroRNAs (miRNAs) are small non-coding RNAs important in gene regulation. They are able to regulate mRNA translation through base-pair complementarity. Cellular miRNAs have been involved in the regulation of nearly all cellular pathways, and their deregulation has been associated with several diseases such as cancer. Given the importance of microRNAs to cell homeostasis, it is no surprise.


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Selected abstracts on virus latency and oncogenesis Download PDF EPUB FB2

Author(s): Gilden,Donald H; Lawerence,William C; International Cancer Research Data Bank.; Cancer Information Dissemination and Analysis Center for Virology, Immunology, and Biology.

Title(s): Selected abstracts on virus latency and oncogenesis/ Donald H. INTRODUCTION. Latent infection with Epstein-Barr virus (EBV), a nearly ubiquitous human herpesvirus, is responsible for multiple malignancies in the two types of cells Selected abstracts on virus latency and oncogenesis book it infects: B lymphocytes and epithelial cells ().The mechanism by which EBV leads to transformation depends on both the properties of the host cell and the state of the host immune by:   In this review, we summarize the potential roles and mechanisms of viral and cellular miRNAs in the host–pathogen interactions during infection with selected tumor viruses and HIV, which include (i) repressing viral replication and facilitating latency establishment by targeting viral transcripts, (ii) evading innate and adaptive immune Cited by:   Core tip: Current models for viral driven oncogenesis cannot explain why tumor development in carriers of tumorigenic viruses is a very rare event, occurring decades after virus infection.

Considering that viruses are mutagenic agents per se and human oncogenic viruses additionally establish latent and persistent infections, we attempt here to provide a general Cited by: 8.

A.J. Smith, L.A. Smith, in Progress in Molecular Biology and Translational Science, 4 Conclusion. The study of oncogenic viruses has contributed greatly to the scientific advances made during this molecular age in the field of cancer biology.

They have been the key to unlocking cell cycle function and control. Research with acute transforming retroviruses led to the discovery of reverse. This novel regulatory layer, mediated by microRNAs, has a far-reaching impact on the latency and pathogenesis of viruses, including the mechanism of virus induced cancers.

The molecular role of microRNAs in viral oncogenesis may be diverse, ranging from viral encoded microRNAs to virus encoded suppressors of RNA interference.

Certain fundamental notions concerning virus oncogenesis are reviewed. A brief description of the main morphological features of the more common oncogenic viruses is followed by an account of their mechanism of action and cell and organism factors essentially associated with.

A normal cell is transformed into a cancerous cell when a virus infects and persists in the infected cells. Tumor viruses are either DNA viruses, Selected abstracts on virus latency and oncogenesis book include EBV, Kaposi's sarcoma-associated herpesvirus (KSHV), human papillomavirus (HPV), hepatitis B virus (HBV), and Merkel cell polyomavirus (MCPyV); or RNA viruses such as hepatitis C virus (HCV) and human T-lymphotrophic virus (HTLV-1).

Abstract. The virus was first described years ago as a filterable, transmissible agent that causes disease in plants and animals. A virus is a “submicroscopic and intracellular parasite” that can propagate only inside a living cell.

The obligatory nature of a virus brought a. Abstract. Viral pathogenesis seeks to understand how a virus interacts with its host at multiple levels.

Key questions include the source (an infected human, animal, or insect vector), the transmission mechanism, and how the virus is shed and transmitted. The most likely explanation for the connection between virus latency and tumorigenesis is that productively replicating viruses initiate cell death, which has long been known to virologists as the cytopathic effect (Cai et al.,Enrique et al.,Ann Arvin et al., ).

Small DNA tumor viruses, that is, HPV and MCPyV do not encode. T1 - Marek's disease virus oncogenicity: Molecular mechanisms. AU - Nair, Venugopal K. AU - Kung, Hsing-Jien. PY - /6/ Y1 - /6/ N2 - This chapter discusses the oncogenicity of Marek's disease virus (MDV).

It provides an overview of the roles of MDV genes that are potentially associated with latency/transformation.

In book: Aids-Associated thus limiting immune exposure while allowing persistence of the virus. Once KSHV is reactivated from latency and enters the oncogenesis, both latency and. Abstracts that highlight the most exciting and new developments in the field of virology will be selected for short talks, and other abstracts will be selected as posters.

The evening poster sessions are a prominent and important aspect of this conference providing yet another opportunity for participants to interact and discuss their research. Virus - Virus - Latency: Inapparent infections (those that do not cause specific signs and symptoms) often result after exposure to picornaviruses, influenza viruses, rhinoviruses, herpesviruses, and adenoviruses but less frequently to measles and chickenpox viruses.

In cases of inapparent infection, long-lasting immunity develops, but only to the strain of virus that has the same antigenic. Background Kaposi sarcoma (KS) is associated with human herpesvirus 8 (HHV‐8). The cutaneous immune response in this tumour is not well established and a. The viruses that are involved in human cancer development are Hepatitis B virus (HBV), Hepatitis C virus (HCV), Epstein-Barr virus (EBV), Human papilloma virus (HPV), Kaposi's sarcoma herpes virus.

Viral oncogenesis can be defined as the feature of tumor viruses that induces benign or malignant proliferation of infected cells. Characteristics Tumor viruses constitute a heterogeneous group of viruses, which play a causative role in naturally occurring malignancies, benign tumors and tumors of experimentally infected laboratory animals.

Approximately 12% of all human cancers are caused by oncoviruses. Human viral oncogenesis is complex, and only a small percentage of the infected individuals develop cancer, often many years to.

The latency-associated nuclear antigen (LANA-1) of Human Herpes Virus 8 (HHV-8), alternatively called Kaposi Sarcoma Herpes Virus (KSHV) is constitutively expressed in all HHV-8 infected cells.

LANA-1 accumulates in well-defined foci that co-localize with the viral episomes. Virus latency (or viral 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. Abstract. Molecular biologic studies of Kaposi's sarcoma-associated herpesvirus (KSHV) have identified a number of potential viral oncogenes that may contribute to KSHV-related neoplasia including a D-type cyclin, an ILlike cytokine, and a novel member of the interferon regulatory factor family.

The use of targeted therapies against EBV as stand-alone or adjunctive treatments is being explored. Undifferentiated NPC is characterized by type II EBV latency where latent genes EBER, EBNA1, LMP1, LMP2A, LMP2B, and BARTs are expressed.

EBNA1 protein is essential for stabilization of the viral episome and proliferation of the virus using the host DNA machinery. 27 Latent membrane. Three Epstein–Barr virus latency proteins independently promote genomic instability by inducing DNA damage, inhibiting DNA repair and inactivating cell cycle checkpoints.

Oncog (See the Major Article by Dai et al., on pages –) In this issue of The Journal of Infectious Diseases, Dai et al present data from a series of experiments that provide insights into the pathogenesis of oral Kaposi sarcoma (KS), a virus-induced angioproliferative neoplastic disease and AIDS-defining condition [].KS-associated herpesvirus (KSHV), also known as human herpesvirus 8, was.

Abstract. Viral oncogenes are responsible for oncogenesis resulting from persistent virus infection. Although different human tumor viruses express different viral oncogenes and induce different tumors, their oncoproteins often target similar sets of cellular tumor suppressors or signal pathways to immortalize and/or transform infected cells.

Epstein-Barr virus (EBV) is a human gamma herpes virus that has a lifetime association with the host and can enter into a state of long-term latency in memory B cells [1]. During viral latency. Some viruses are able to cause latent infection.

Latency is characterized by a quiescent or minimally transcriptionally active viral genome with periods of reactivation. Latent viruses include the herpesviruses (cytomegalovirus, Epstein-Barr virus, herpes simplex virus, varicella-zoster virus), human papillomavirus, human retroviruses.

Ethel Cesarman, MD, PhD, Principal InvestigatorOur laboratory is involved in studying the process of viral oncogenesis in human cancer.

We are performing molecular characterization of AIDS-associated lymphomas and Kaposi’s sarcoma, which are frequently associated with infection by EBV (HHV-4) or KSHV (HHV-8), with the goal of identifying molecular targets and developing.

Principles of Virology, the leading virology textbook in use, is an extremely valuable and highly informative presentation of virology at the interface of modern cell biology and immunology. This text utilizes a uniquely rational approach by highlighting common principles and processes across all viruses.

Using a set of representative viruses to illustrate the breadth of viral complexity. A recently emerged common feature among all herpesviruses is the utilization of virally encoded miRNAs as a means to modulate the host cell during latency and primary infection.

In Marek’s disease virus, a B cell–tropic alpha herpesvirus of chickens, viral miRNAs are the primary driver of oncogenesis. About a fifth of all human cancers worldwide are caused by infectious agents. In 12% of cancers, seven different viruses have been causally linked to human oncogenesis: Epstein-Barr virus, hepatitis B virus, human papillomavirus, human T-cell lymphotropic virus, hepatitis C virus, Kaposi's sarcoma herpesvirus, and Merkel cell polyomavirus.

Here, we review the many molecular mechanisms of. The Epstein–Barr virus (EBV) nuclear antigen (EBNA)-1 is the only viral protein expressed in all EBV-carrying malignancies, but its contribution to oncogenesis has remained enigmatic.

We show that EBNA-1 induces chromosomal aberrations, DNA double-strand breaks, and engagement of the DNA damage response (DDR).

These signs of genomic instability are associated with the. Viral Oncogenesis. February ; DOI: /_7. In book: Molecular Pathology of Hematolymphoid Diseases (pp). Abstract. Collectively, viruses are the principal cause of cancers arising in patients with immune dysfunction, including human immunodeficiency virus (HIV)–positive patients.

Kaposi sarcoma (KS) etiologically linked to Kaposi sarcoma–associated herpesvirus (KSHV) continues to be the most common AIDS-associated tumor.

Viruses that infect the nervous system may cause acute, chronic or latent infections. Despite the so-called immunoprivileged status of the nervous system, immunosurveillance plays an important role in the fate of viral infection of the brain.

Herpes simplex virus 1 (HSV-1) persists in the nervous. Viruses, an international, peer-reviewed Open Access journal. Dear Colleagues, Inthe Nobel Prize in Physiology or Medicine was awarded for the discovery of tumor-inducing viruses, since then, tumor viruses studies have guided us to significant findings in cancer research, including the discovery of various oncoproteins, as well as tumor suppressor proteins that regulate the development.

MicroRNAs (miRNAs) are a new class of 18–23 nucleotide long non-coding RNAs that play critical roles in a wide spectrum of biological processes. Recent reports also throw light into the role of microRNAs as critical effectors in the intricate host-pathogen interaction networks.

Evidence suggests that both virus and hosts encode microRNAs. The exclusive dependence of viruses on the host. Nested PCR was performed for each virus on ng of sample DNA using primers and conditions listed in Table -1 and VZV primers were verified previously in studies of DNA from fixed human trigeminal ganglia [].HSV-2 external primers were obtained from published sequences, and nested primers were designed to be within this original –base pair sequence using Primer3 software [].

Abstract. The ability of herpes simplex virus type 2 (HSV-2) to establish latency in and reactivate from sacral dorsal root sensory ganglia is the basis for recurrent genital hepes, The expression of HSV-2 genes in latently infected human sacral ganglia was investigated by in situ hybridization.

The retrovirus human T-cell leukemia virus type 1 (HTLV-1) integrates into the host DNA, achieves persistent infection, and induces human diseases. Here, we demonstrate that viral DNA-capture sequencing (DNA-capture-seq) is useful to characterize HTLV-1 proviruses in naturally virus .The Annual Review of Virology communicates exciting advances in our understanding of viruses of animals, plants, bacteria, archaea, fungi, and protozoa.

Reviews highlight new ideas and directions in basic virology, viral disease mechanisms, virus-host interactions, and cellular and immune responses to virus infection, and reinforce the position of viruses as uniquely powerful probes of.1.

Introduction. Understanding viral oncogenicity is traditionally an endeavour of clinical microbiologists and relies on analysing molecular pathways (for a review, see e.g. []).Here, we adopt an ecological and evolutionary perspective, which has been extensively applied to study infection virulence over the years [] and has even re-emerged as a prism through which to analyse cancer dynamics [].