scholarly journals Tetranucleotide Profile of Herpesvirus DNA

2020 ◽  
Vol 97 (3) ◽  
pp. 216-226
Author(s):  
Felix P. Filatov ◽  
Alexander V. Shargunov

Introduction. Herpesvirus DNAs (about 90% of the total genomic sequences of the Herpesvirales family presented in GenBank) contain at a minimum concentration one of the two tetranucleotides, CTAG or TCGA. The “underrepresentation” of CTAG was previously observed only in the DNA of some bacteria and phages. The aim of the study was the further analysis of the formal characteristics of herpesvirus DNA, as well as their comparison with the density of the virus/host DNA microhomology and with the genomic macrostructure of herpes viruses.Materials and methods. Twenty strains and isolates of each of the five types of human herpes viruses (HHV1, HHV2, HHV3, HHV4, HHV5), 10 strains of HHV8, 5 strains of HHV6A, 4 strains of HHV6B and 3 strains of HHV7 were analyzed. GenBank tools were used to determine the frequency of tetranucleotides, and human DNA fragments with size matched herpesvirus DNA were used for comparison.Results. Minimum CTAG concentration in DNA of herpes viruses is mainly characteristic of two- and singlesegment genomes with direct or inverted terminal repeats (classes A,D,E), while the minimum TCGA density is characteristic mainly for DNA that is significantly less structured (classes B,C,F). By increasing CTAG density, human herpes viruses form a sequence close to the sequence of increasing the homology density of 20 nt with human DNA, which also correlates with the macrostructure of DNA. A parallel of this minimization with the DNA structure of herpes viruses or with their belonging to one or another subfamily — as well as the context of the “minimal” CpG (that is, TCGA) — is not noted in the literature. Although herpesvirus DNA is quite large (125– 295 Kb), some of them (for example, HHV4, HHV5 and HHV7 DNA) show noticeable deviations from the second DNA parity rule, and can thus serve as a component of the molecular signature.The Discussion suggests possible hypotheses for the origin of some of the observed phenomena.

2015 ◽  
Vol 28 (2) ◽  
pp. 130-137 ◽  
Author(s):  
Yaneth Miranda Brand ◽  
Vicky Constanza Roa-Linares ◽  
Liliana Amparo Betancur-Galvis ◽  
Diego Camilo Durán-García ◽  
Elena Stashenko

Author(s):  
Mamadou Malado Jallow ◽  
Amary Fall ◽  
Serigne Fallou Wade ◽  
Ndeye Sophie Fall ◽  
Davy Kiori ◽  
...  

Herpesviruses are known to cause a diversity of clinical syndromes, ranging from minor cutaneous lesions to life-threatening illnesses, especially in immunocompromised hosts. Here, we investigate retrospectively the contribution of five human herpesviruses, including herpes simplex virus Cytomegalovirus (CMV), the Epstein–Barr virus (EBV), human herpesvirus 6, and varicella zoster virus (VZV) in serum samples collected from measles suspected patients with at least fever and rash. Sera specimens were first tested for serological evidence of measles and rubella virus infection by ELISA, and DNA extracted from an aliquot of each clinical specimen for molecular detection of human herpes viruses by RT-qPCR. A total of 3,358 specimens have been collected and tested for herpes viruses. Nearly half of the overall suspected cases were children younger than 5 years (49.4%). Of the 3,358 sera tested by ELISA, 227 (6.7%) were measles laboratory confirmed and 152 (4.5%) rubella laboratory confirmed. Herpes viruses were detected in 1763 (52.5%), and VZV was the most common with 44.3%, followed by EBV with 10.7%. Coinfections were found in 352 (20%) cases, and the most common co-detections were VZV/EBV or VZV/CMV (169 and 81 cases, respectively). A clear seasonal pattern of VZV, EBV, and CMV identification was observed, with the highest incidence between February and April each year. Results of this investigation provide more insights into cutaneous rash syndrome etiologies in patients sampled in the framework of measles/rubella surveillance in Senegal, which is useful for the guidance of both case definition revision and clinical practice as well as for public health policy.


2020 ◽  
Vol 8 (2) ◽  
pp. e000841
Author(s):  
Simon Jasinski-Bergner ◽  
Ofer Mandelboim ◽  
Barbara Seliger

Several human herpes viruses (HHVs) exert oncogenic potential leading to malignant transformation of infected cells and/or tissues. The molecular processes induced by viral-encoded molecules including microRNAs, peptides, and proteins contributing to immune evasion of the infected host cells are equal to the molecular processes of immune evasion mediated by tumor cells independently of viral infections. Such major immune evasion strategies include (1) the downregulation of proinflammatory cytokines/chemokines as well as the induction of anti-inflammatory cytokines/chemokines, (2) the downregulation of major histocompatibility complex (MHC) class Ia directly as well as indirectly by downregulation of the components involved in the antigen processing, and (3) the downregulation of stress-induced ligands for activating receptors on immune effector cells with NKG2D leading the way. Furthermore, (4) immune modulatory molecules like MHC class Ib molecules and programmed cell death1 ligand 1 can be upregulated on infections with certain herpes viruses. This review article focuses on the known molecular mechanisms of HHVs modulating the above-mentioned possibilities for immune surveillance and even postulates a temporal order linking regular tumor immunology with basic virology and offering putatively novel insights for targeting HHVs.


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