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Epstein–Barr virus and the nervous system
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Alexandros C. Tselis, Kumar Rajamani, Pratik Bhattacharya
Epstein–Barr virus is a member of the herpesvirus family. It is a double-stranded DNA virus of length 172 kilobase pairs (kbp) that codes for about 100 proteins. The viral genome is contained in an icosahedral capsid, which is surrounded by an amorphous tegument. This, in turn, is bounded by a viral envelope. The structure of the genome is similar to that of other herpesviruses, with a unique short and a unique long segment separated by a segment of multiple [6–12] tandem repeats of a stretch of 3071 bp. The unique long segment is further broken up into four smaller segments by tandem internal repeats [7]. The number of repeats is conserved in each strain of EBV and can be used for molecular epidemiological tracing [8]. The viral genes form two broad groups, those expressed during latency and those expressed during the lytic cycle (Figure 7.1).
Physiology and Growth
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
In contrast to the lytic cycle of the phage reproduction, the lysogenic cycle assumes formation of a prophage that is either integration of the phage genome into the host bacterium's genome or formation of a circular replicon in the bacterial cytoplasm, while the host cell continues to live and reproduce normally. Although absence of the elements complementary to the RNA phage genome in the host's chromosome (Doi and Spiegelman 1962) and full independence of the phage replication from the DNA synthesis (Cooper and Zinder 1962; Knolle and Kaudewitz 1964) were established at the first steps of the RNA phage studies, the idea of the putative lysogeny persisted.
Epstein-Barr Virus and Nasopharyngeal Carcinoma
Published in D. V. M. Gerd Reznik, Sherman F. Stinson, Nasal Tumors in Animals and Man, 2017
Lee S. Tuckwiller, Ronald Glaser
When EBV replicates, several virus-specific antigens are synthesized which can be detected by IF. These include the early antigen (EA)17 which is compased of at least two components designated diffuse (D) and restricted (R) based on whether the antigen is found localized in the cytoplasm (R component) or found throughout the cell (D component) as well as the ability to retain IF reactivity after methanol fixation.18 It is uncommon for healthy EBV seropositive individuals to have antibodies to EA, but patients with active EBV disease are usually positive. The virus capsid antigen (VCA) is generally found in cells synthesizing virus particles. It is a late virus protein and a structural component of the virus capsid.36 The EBV membrane antigen (MA) is composed of at least two components, termed early (E-MA) and late (L-MA).37 The E-MA is independent of virus DNA synthesis and can be found in some cells not producing virus. The L-MA appears only during the lytic cycle and after initiation of virus DNA synthesis.37 Correlation of high anti-MA titers with the ability to neutralize EBV strongly suggests that MA is incorporated into the virus envelope,38,39 and monoclonal antibody prepared against MA components has been shown to neutralize the virus.40 The presence of the EBV genome in cells is always accompanied by the synthesis of EBNA, a nonhistone DNA-binding protein detected by the anticomplementary IF test, and is probably involved with regulation of the EBV genome and the transformed or latent state.41-43
Emerging therapeutic targets for nasopharyngeal carcinoma: opportunities and challenges
Published in Expert Opinion on Therapeutic Targets, 2020
Valentin Baloche, François-Régis Ferrand, Anna Makowska, Caroline Even, Udo Kontny, Pierre Busson
Like for all herpesviridae, production of EBV viral particles results ipso facto in the death of the infected cell, hence the name of lytic cycle to characterize a state of infection oriented toward production of viral particles. The idea of disrupting viral latency in EBV-positive malignant cells has been in the air for decades (for a review see Oker et al., Intechopen.com, DOI: 10.5772/64738). Initially the idea was to use EBV as a kind of endogenous oncolytic virus but this was not realistic for at least 2 reasons. First, the mechanisms blocking the lytic cycle operate at multiple levels and it is much easier to obtain partial activation of several lytic genes than to achieve viral production in all cells. Next, activation of the lytic cycle is known to favor the release of soluble factors, especially cytokines, with potential oncogenic activity on bystander cells. Therefore, most investigators in the field aim to partial activation of lytic genes in order to induce expression of viral enzymes with the capacity to transform prodrugs in cytotoxic drugs, specifically in malignant cells. The two main candidate enzymes for this function are EBV thymidine kinase (EBV-TK) and EBV protein-kinase (EBV-PK). Another aim of partial lytic induction could be to increase the immunogenicity of malignant cells.
Increased antibody levels to stage-specific Epstein–Barr virus antigens in systemic autoimmune diseases reveal a common pathology
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2019
Louise Sternbæk, Anette H. Draborg, Mark T. Østerlund, Line V. Iversen, Lone Troelsen, Elke Theander, Christoffer T. Nielsen, Søren Jacobsen, Gunnar Houen
One environmental risk factor is infection with EBV, one of eight known human herpesviruses and one of the most common viruses found in humans. EBV infects approximately 95–99% of the world’s population, mostly during childhood [5]. Most primary EBV infections are asymptomatic, and EBV causes a persistent latent infection in memory B cells. The most important signature protein expressed is Epstein–Barr virus nuclear antigen 1 (EBNA1). EBNA1 plays an essential role in the transcription and replication of the viral DNA during the cell cycle, as it is required for replication and maintenance of the episomal EBV genome [6]. Occasionally, the virus switches to a productive infective stage called lytic cycle, by expressing all its genes and starting production of EBV virions [7, 8]. In this process, the virus goes through successive stages of latency and reactivation, denoted latency 0, I, II, III, early lytic, late lytic, envelopment, and release (budding).
A bacteriophage cocktail targeting Escherichia coli reduces E. coli in simulated gut conditions, while preserving a non-targeted representative commensal normal microbiota
Published in Gut Microbes, 2018
Tomasz Cieplak, Nitzan Soffer, Alexander Sulakvelidze, Dennis Sandris Nielsen
Bacteriophages (or “phages” for short) are bacteria-infecting viruses. Lytic phages have potent bactericidal activity against their host bacterial strains. During the lytic cycle the phage infects the cell, using the cell's replication and translation machinery to replicate and then lyses the cell releasing new phage particles into the environment. In cases where overwhelming concentrations of phage are applied “lysis from without” might occur as well.7,8 Phages are also very specific: they only attack their targeted bacterial hosts, and they cannot infect human or other eukaryotic cells. Even within bacterial taxa, and in clear contrast to broad-spectrum antibiotics, phages usually only lyse strains or a subgroup of strains within the bacterial species, making targeted bacterial therapy possible.