DOCSLIB.ORG

Possible Relation of Roseolovirus Infection

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Possible Relation of Roseolovirus Infection PROCEEDINGS OF THE LATVIAN ACADEMY OF SCIENCES. Section B, Vol. 70 (2016), No. 4 (703), pp. 205–210. DOI: 10.1515/prolas-2016-0032 POSSIBLE RELATION OF ROSEOLOVIRUS INFECTION WITH FIBROMYALGIA Svetlana Èapenko1,#, Marija Mihailova2, Santa Rasa1, Angelika Krûmiòa3, Zane Zazerska1, Inâra Logina2, and Modra Murovska1 1 Augusts Kirhenðteins Institute of Microbiology and Virology, Rîga Stradiòð University, Râtsupîtes iela 5, Rîga, LV-1067, LATVIA 2 Department of Neurology and Neurosurgery, Rîga Stradiòð University, Dzirciema iela 16, Rîga, LV-1007, LATVIA 3 Depatment of Infectology and Dermatology, Rîga Stradiòð University, Dzirciema iela 16, Rîga, LV-1007, LATVIA # Corresponding author; [email protected] Contributed by Modra Murovska Fibromyalgia (FM) is a chronic widespread pain disorder that impacts 0.5%–7% of the general population worldwide. The aetiology and pathogenesis of the disease are still unknown. Human herpesvirus-6 and -7 belong to the family Herpesviridae, subfamily Betaherpesvirinae, and genus Roseolovirus and are immunomodulating viruses potentially pathogenic to the nervous system. Presence of anti-HHV-6 and -HHV-7 antibodies and viral genomic sequences, viral loads, HHV-6 variant-specificity, and TNF-a level were studied in 41 FM patients and 50 healthy individuals us- ing polymerase chain reactions, restriction endonuclease analysis and ELISA. There was no dif- ference in the presence of anti-HHV-6 and anti-HHV-7 IgG class antibodies between FM patients and control group individuals. Viral sequences were found in 80.5% of FM patients and in 62.0% of controls. Significantly higher rate of concurrent HHV-6 and HHV-7 infection and higher viral loads in peripheral blood were detected in FM patients compared to the control group individuals. Plasma viremia was detected only in FM patients. Significantly higher TNF-a levels were detected in virus positive FM patients. From all positive cases only in two FM patients HHV-6A was re- vealed. Significantly higher detection frequency of concurrent HHV-6 and HHV-7 infection, simul- taneous HHV-6 and HHV-7 activation, higher viral loads and TNF-a expression levels in primary FM patients than in control group individuals indicate the potential involvement of Roseoloviruses in development of this disorder. Key words: fibromyalgia, human herpesvirus-6, human herpesvirus-7, infection, molecular diag- nostic. INTRODUCTION College of Rheumatology (ACR) diagnostic criteria. Ac- cording to these criteria, FM diagnosis may be stated if the Fibromyalgia (FM) is a common, chronic widespread pain patient has chronic widespread pain and 11 or more positive disorder that is estimated to impact 0.5% to 7% of the gen- of a possible 18 tender points on physical examination, fa- eral population worldwide (Balon and Wise, 2015). The tigue, sleep disorders, headaches, memory or concentration epidemiology of FM in Latvia has not been studied in de- problems, mood disturbances, and stiffness. tail. In 2010, ACR FM diagnostic criteria were supplemented Host individuals diagnosed in clinics are young or middle with new details (Hakim et al., 2010; Wolfe et al., 2011) aged; however, population surveys suggest that frequency that include the estimation of the widespread pain index of disease increases with age as well as symptom severity (WPI) and the symptoms of severity (SS) score scale. The and worsening of life quality (Ballantyne et al., 2010; SS scale score is the sum of the severity of three symptoms Branco et al., 2010; Jiao et al., 2014; Balon and Wise, (fatigue, waking unrefreshed, cognitive symptoms) plus the 2015). Females suffer from FM eight times more frequently extent of somatic symptoms in general. than males (Albin et al., 2008). The aetiology and pathogenesis of FM are still unknown. The term fibromyalgia appeared relatively recently, in 1976. This disease is probably of multi-factorial nature, since Diagnosis is clinical and is based on the 1990 American many patients have onset of the clinical phenotype of FM Proc. Latvian Acad. Sci., Section B, Vol. 70 (2016), No. 4. 205 following a specific trigger. There are many open questions may significantly affect the generation and functionality of with few or controversial answers. Such triggers can include effective immune responses (Lusso et al., 2006). Lusso various viral infections, such as hepatitis C (Kozanoglu et (2006) and Atedzoe et al. (1999) have shown that both of al., 2003; Mohammad et al., 2012; Rogal et al., 2015), par- the viruses increase the production of inflammatory cytoki- vovirus B19 (Cassisi et al., 2011), HIV (Kole et al., 2013; nes. Wiffen et al., 2013; Fox and Walker-Bone, 2015), and Ep- stein-Barr virus (Buchwald et al., 1987). 55% of patients The aim of this study was to: 1) examine the presence of identify a “flu-like” or viral infection as a precursor to the HHV-6 and/or HHV-7 genomic sequences in whole periph- onset of symptoms, but the role of viral infection in FM de- eral blood and cell free plasma DNA samples from patients velopment has not been estimated. with FM and practically healthy persons (control group); 2) determine HHV-6 variant-specificity in whole peripheral One of the major theories is that cytokines may have a role blood DNA; 3) compare HHV-6 and HHV-7 load in periph- in both the aetiology of the FM and in the intensity of core eral blood samples from the FM patients and control per- symptoms (Menzies and Lion, 2010). Goldberg (1989) sug- sons; 4) compare pro-inflammatory cytokine TNF-a plasma gests that the viruses might directly invade central nervous level in patients with FM and control group individuals. system or are capable of activating cytokines which may in turn cause severe myalgia, fatigue, and neurocognitive dis- turbances. MATERIALS AND METHODS The study was performed during 2013–2015. Clinical and According to the current state of knowledge the origin of virological (including serology and molecular biology) fea- the pain in FM and variety of FM symptoms are triggered tures were examined in the 41 patients with clinical diag- by peripheral as well as central mechanisms (Sprott, 2011; nose of primary FM and 50 practically healthy persons. The Clauw et al., 2011). primary FM diagnosis was established by a neurologist or Up to date, there are no data on the role of HHV-6 and algologist in the out-patients’ clinic of Pauls Stradiòð Clini- HHV-7 infection in the FM development. Human herpes- cal University Hospital. None of the 41 patients with pri- virus-6 (HHV-6) and -7 (HHV-7) belong to the Herpesviri- mary diagnosed FM were hospitalised in the Neurology and dae family, Betaherpesvirinae subfamily, Roseolovirus ge- Neurosurgery Hospital. According to case and drug history, nus (Berneman et al., 1992) and are ubiquitous (more than 10 of the 41 patients had not received prior medical treat- 90% of adults have antibodies to the viruses) immunomodu- ment; none of the patients had received steroids or statins, lating, and potentially pathogenic to the nervous system. In but pain relief medication only. 2012, the International Committee on Taxonomy of Viruses Diagnosis was setup based on ACR 2010 diagnostic criteria re-classified HHV-6 as separate viruses HHV-6A and for the FM (Widespread pain index (WPI) is equal or more HHV-6B based on biocharacteristics regarding cell tropism than 7, symptom severity scale score (SS) — equal or more and pathological implications (Ablashi et al., 2014). After than 5, duration of symptoms at least three months, and the primary infection, the viruses establish a state of life-long patients do not have a disorder that would otherwise explain subclinical persistence or latency in CNS (Yoshikawa and the pain). In our FM patients group the mean WPI was 12.7 Asano, 2000) and can be reactivated in cases of immuno- ± 3.24 (minimal score 4 and maximal score 18), and mean suppression. HHV-6A, HHV-6B and HHV-7 DNA are of- SS scale score — 8.1 ± 1.4 (minimal score 6 and maximal ten found in brain tissue from healthy individuals (without score 11). Mean duration of symptoms was 7.9 ± 6.2 years. pathological changes in the brain) (Chan et al., 2001; Yao et Exclusion criteria were previously known polyneuropathy, al., 2010). cervical radiculopathy clinical symptoms, diabetes mellitus, HHV-6 infection has been associated with neurologic pa- rheumatoid arthritis, liver diseases, myalgic encephalomye- thologies such as multiple sclerosis (Ablashi et al., 2000; litis/chronic fatigue syndrome, and myocardial infarction. Chapenko et al., 2003; Nora-Krukle et al., 2011), which is Of 41 individuals with FM, 40 were females and one was associated with inflammation, mesial temporal lobe epi- male (mean age 51, range: 24–71) and from 50 control lepsy in the absence of inflammation in brain tissue (Donati group individuals, 40 were females and 10 were males et al., 2003; Fotheringham et al., 2007; Niehusmann et al., (mean age 48, range: 35–78). Peripheral blood samples 2010), myalgic encephalomyelitis/chronic fatigue syndrome from the patients with FM were received from the Neurol- (Ablashi et al., 2000; Chapenko et al., 2006; Bansal et al., ogy and Neurosurgery Department, Rîga Stradiòð Univer- 2012; Chapenko et al., 2012) and with different neurologi- sity. cal complications after allogeneic hematopoietic stem cell transplantation (Bhanushali et al., 2013) and solid organ The study was approved by the Ethics Committee of Rîga transplantations (Chapenko et al., 2009; Massih and Ra- Stradiòð University, and all of the participants gave in- zonable, 2009). The association of HHV-7 infection with formed consent before the examination. these disorders is not sufficiently studied. HHV-6 and HHV-7 serology. Testing for antibodies HHV-6 and HHV-7 infection profoundly modifies the pro- against HHV-6 and HHV-7 in cell free blood plasma sam- file of cytokine and chemokine production, which in turn ples was carried out using HHV-6 IgG ELISA kits (Panbio, 206 Proc.
Load more

Recommended publications
  • Infection Status of Human Parvovirus B19, Cytomegalovirus and Herpes Simplex Virus-1/2 in Women with First-Trimester Spontaneous
    Gao et al. Virology Journal (2018) 15:74 https://doi.org/10.1186/s12985-018-0988-5 RESEARCH Open Access Infection status of human parvovirus B19, cytomegalovirus and herpes simplex Virus- 1/2 in women with first-trimester spontaneous abortions in Chongqing, China Ya-Ling Gao1, Zhan Gao3,4, Miao He3,4* and Pu Liao2* Abstract Background: Infection with Parvovirus B19 (B19V), Cytomegalovirus (CMV) and Herpes Simplex Virus-1/2 (HSV-1/2) may cause fetal loses including spontaneous abortion, intrauterine fetal death and non-immune hydrops fetalis. Few comprehensive studies have investigated first-trimester spontaneous abortions caused by virus infections in Chongqing, China. Our study intends to investigate the infection of B19V, CMV and HSV-1/2 in first-trimester spontaneous abortions and the corresponding immune response. Methods: 100 abortion patients aged from 17 to 47 years were included in our study. The plasma samples (100) were analyzed qualitatively for specific IgG/IgM for B19V, CMV and HSV-1/2 (Virion\Serion, Germany) according to the manufacturer’s recommendations. B19V, CMV and HSV-1/2 DNA were quantification by Real-Time PCR. Results: No specimens were positive for B19V, CMV, and HSV-1/2 DNA. By serology, 30.0%, 95.0%, 92.0% of patients were positive for B19V, CMV and HSV-1/2 IgG respectively, while 2% and 1% for B19V and HSV-1/2 IgM. Conclusion: The low rate of virus DNA and a high proportion of CMV and HSV-1/2 IgG for most major of abortion patients in this study suggest that B19V, CMV and HSV-1/2 may not be the common factor leading to the spontaneous abortion of early pregnancy.
    [Show full text]
  • Hsv1&2 Vzv R-Gene®
    HSV1&2 VZV R-GENE® REAL TIME PCR ASSAYS - ARGENE® TRANSPLANT RANGE The power of true experience HSV1&2 VZV R-GENE® KEY FEATURES CLINICAL CONTEXT 1-5 • Ready-to-use reagents Herpes Simplex Viruses (HSV) 1 and 2 and Varicella-Zoster Complete qualitative and quantitative kit Virus (VZV) are DNA viruses belonging to the Herpesviridae • family. Primary infection is generally limited to the mucous • Simultaneous detection and quantification of membranes and the skin. After primary infection, the virus HSV1 and HSV2 persists in the host by establishing a latent infection. In case • Detection and quantification of VZV of chronic or transient immunosuppression, the virus may Validated on most relevant sample types reactivate to generate recurrent infection. Usually benign, • the infections with these viruses can develop in severe Validated with the major extraction and • clinical forms such as encephalitis, meningitis, retinitis, amplification platforms fulminant hepatitis, bronchopneumonia and neonatal infections. • Designed for low to high throughput analysis Various antivirals have proven their efficacy in treating these pathologies when •Same procedure for all the ARGENE® prescribed early and at appropriate doses. In case of severe infections, it is therefore Transplant kits essential to obtain an early and rapid diagnosis of the infection. TECHNICAL INFORMATION ORDERING INFORMATION HSV1&2 VZV R-GENE® - Ref. 69-014B Parameters HSV1 HSV2 VZV Gene target US7 UL27 gp19 protein CSF, Whole blood, Plasma, BAL, CSF, Whole blood, Plasma, Mucocutaneous
    [Show full text]
  • Clinical Impact of Primary Infection with Roseoloviruses
    Available online at www.sciencedirect.com ScienceDirect Clinical impact of primary infection with roseoloviruses 1 2 1 Brenda L Tesini , Leon G Epstein and Mary T Caserta The roseoloviruses, human herpesvirus-6A -6B and -7 (HHV- infection in different cell types, have the ability to reac- 6A, HHV-6B and HHV-7) cause acute infection, establish tivate, and may be intermittently shed in bodily fluids [3]. latency, and in the case of HHV-6A and HHV-6B, whole virus Unlike other human herpesviruses, HHV-6A and HHV- can integrate into the host chromosome. Primary infection with 6B are also found integrated into the host genome HHV-6B occurs in nearly all children and was first linked to the (ciHHV-6). Integration has been documented in 0.2– clinical syndrome roseola infantum. However, roseolovirus 1% of the general population and along with latency infection results in a spectrum of clinical disease, ranging from has confounded the ability to correlate the presence of asymptomatic infection to acute febrile illnesses with severe viral nucleic acid with active disease [4]. neurologic complications and accounts for a significant portion of healthcare utilization by young children. Recent advances The syndrome known as roseola infantum was reported as have underscored the association of HHV-6B and HHV-7 early as 1809 by Robert Willan in his textbook ‘On primary infection with febrile status epilepticus as well as the cutaneous diseases’ [5]. This clinical entity is also com- role of reactivation of latent infection in encephalitis following monly referred to as exanthem subitum and early pub- cord blood stem cell transplantation.
    [Show full text]
  • Where Do We Stand After Decades of Studying Human Cytomegalovirus?
    microorganisms Review Where do we Stand after Decades of Studying Human Cytomegalovirus? 1, 2, 1 1 Francesca Gugliesi y, Alessandra Coscia y, Gloria Griffante , Ganna Galitska , Selina Pasquero 1, Camilla Albano 1 and Matteo Biolatti 1,* 1 Laboratory of Pathogenesis of Viral Infections, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy; [email protected] (F.G.); gloria.griff[email protected] (G.G.); [email protected] (G.G.); [email protected] (S.P.); [email protected] (C.A.) 2 Complex Structure Neonatology Unit, Department of Public Health and Pediatric Sciences, University of Turin, 10126 Turin, Italy; [email protected] * Correspondence: [email protected] These authors contributed equally to this work. y Received: 19 March 2020; Accepted: 5 May 2020; Published: 8 May 2020 Abstract: Human cytomegalovirus (HCMV), a linear double-stranded DNA betaherpesvirus belonging to the family of Herpesviridae, is characterized by widespread seroprevalence, ranging between 56% and 94%, strictly dependent on the socioeconomic background of the country being considered. Typically, HCMV causes asymptomatic infection in the immunocompetent population, while in immunocompromised individuals or when transmitted vertically from the mother to the fetus it leads to systemic disease with severe complications and high mortality rate. Following primary infection, HCMV establishes a state of latency primarily in myeloid cells, from which it can be reactivated by various inflammatory stimuli. Several studies have shown that HCMV, despite being a DNA virus, is highly prone to genetic variability that strongly influences its replication and dissemination rates as well as cellular tropism. In this scenario, the few currently available drugs for the treatment of HCMV infections are characterized by high toxicity, poor oral bioavailability, and emerging resistance.
    [Show full text]
  • Topics in Viral Immunology Bruce Campell Supervisory Patent Examiner Art Unit 1648 IS THIS METHOD OBVIOUS?
    Topics in Viral Immunology Bruce Campell Supervisory Patent Examiner Art Unit 1648 IS THIS METHOD OBVIOUS? Claim: A method of vaccinating against CPV-1 by… Prior art: A method of vaccinating against CPV-2 by [same method as claimed]. 2 HOW ARE VIRUSES CLASSIFIED? Source: Seventh Report of the International Committee on Taxonomy of Viruses (2000) Edited By M.H.V. van Regenmortel, C.M. Fauquet, D.H.L. Bishop, E.B. Carstens, M.K. Estes, S.M. Lemon, J. Maniloff, M.A. Mayo, D. J. McGeoch, C.R. Pringle, R.B. Wickner Virology Division International Union of Microbiological Sciences 3 TAXONOMY - HOW ARE VIRUSES CLASSIFIED? Example: Potyvirus family (Potyviridae) Example: Herpesvirus family (Herpesviridae) 4 Potyviruses Plant viruses Filamentous particles, 650-900 nm + sense, linear ssRNA genome Genome expressed as polyprotein 5 Potyvirus Taxonomy - Traditional Host range Transmission (fungi, aphids, mites, etc.) Symptoms Particle morphology Serology (antibody cross reactivity) 6 Potyviridae Genera Bymovirus – bipartite genome, fungi Rymovirus – monopartite genome, mites Tritimovirus – monopartite genome, mites, wheat Potyvirus – monopartite genome, aphids Ipomovirus – monopartite genome, whiteflies Macluravirus – monopartite genome, aphids, bulbs 7 Potyvirus Taxonomy - Molecular Polyprotein cleavage sites % similarity of coat protein sequences Genomic sequences – many complete genomic sequences, >200 coat protein sequences now available for comparison 8 Coat Protein Sequence Comparison (RNA) 9 Potyviridae Species Bymovirus – 6 species Rymovirus – 4-5 species Tritimovirus – 2 species Potyvirus – 85 – 173 species Ipomovirus – 1-2 species Macluravirus – 2 species 10 Higher Order Virus Taxonomy Nature of genome: RNA or DNA; ds or ss (+/-); linear, circular (supercoiled?) or segmented (number of segments?) Genome size – 11-383 kb Presence of envelope Morphology: spherical, filamentous, isometric, rod, bacilliform, etc.
    [Show full text]
  • Is the ZIKV Congenital Syndrome and Microcephaly Due to Syndemism with Latent Virus Coinfection?
    viruses Review Is the ZIKV Congenital Syndrome and Microcephaly Due to Syndemism with Latent Virus Coinfection? Solène Grayo Institut Pasteur de Guinée, BP 4416 Conakry, Guinea; [email protected] or [email protected] Abstract: The emergence of the Zika virus (ZIKV) mirrors its evolutionary nature and, thus, its ability to grow in diversity or complexity (i.e., related to genome, host response, environment changes, tropism, and pathogenicity), leading to it recently joining the circle of closed congenital pathogens. The causal relation of ZIKV to microcephaly is still a much-debated issue. The identification of outbreak foci being in certain endemic urban areas characterized by a high-density population emphasizes that mixed infections might spearhead the recent appearance of a wide range of diseases that were initially attributed to ZIKV. Globally, such coinfections may have both positive and negative effects on viral replication, tropism, host response, and the viral genome. In other words, the possibility of coinfection may necessitate revisiting what is considered to be known regarding the pathogenesis and epidemiology of ZIKV diseases. ZIKV viral coinfections are already being reported with other arboviruses (e.g., chikungunya virus (CHIKV) and dengue virus (DENV)) as well as congenital pathogens (e.g., human immunodeficiency virus (HIV) and cytomegalovirus (HCMV)). However, descriptions of human latent viruses and their impacts on ZIKV disease outcomes in hosts are currently lacking. This review proposes to select some interesting human latent viruses (i.e., herpes simplex virus 2 (HSV-2), Epstein–Barr virus (EBV), human herpesvirus 6 (HHV-6), human parvovirus B19 (B19V), and human papillomavirus (HPV)), whose virological features and Citation: Grayo, S.
    [Show full text]
  • Human Herpesvirus-6 and -7 in the Brain Microenvironment of Persons with Neurological Pathology and Healthy People
    International Journal of Molecular Sciences Article Human Herpesvirus-6 and -7 in the Brain Microenvironment of Persons with Neurological Pathology and Healthy People Sandra Skuja 1,* , Simons Svirskis 2 and Modra Murovska 2 1 Institute of Anatomy and Anthropology, R¯ıga Stradin, š University, Kronvalda blvd 9, LV-1010 R¯ıga, Latvia 2 Institute of Microbiology and Virology, R¯ıga Stradin, š University, Ratsup¯ ¯ıtes str. 5, LV-1067 R¯ıga, Latvia; [email protected] (S.S.); [email protected] (M.M.) * Correspondence: [email protected]; Tel.: +371-673-20421 Abstract: During persistent human beta-herpesvirus (HHV) infection, clinical manifestations may not appear. However, the lifelong influence of HHV is often associated with pathological changes in the central nervous system. Herein, we evaluated possible associations between immunoexpression of HHV-6, -7, and cellular immune response across different brain regions. The study aimed to explore HHV-6, -7 infection within the cortical lobes in cases of unspecified encephalopathy (UEP) and nonpathological conditions. We confirmed the presence of viral DNA by nPCR and viral antigens by immunohistochemistry. Overall, we have shown a significant increase (p < 0.001) of HHV antigen expression, especially HHV-7 in the temporal gray matter. Although HHV-infected neurons were found notably in the case of HHV-7, our observations suggest that higher (p < 0.001) cell tropism is associated with glial and endothelial cells in both UEP group and controls. HHV-6, predominantly detected in oligodendrocytes (p < 0.001), and HHV-7, predominantly detected in both astrocytes and oligodendrocytes (p < 0.001), exhibit varying effects on neural homeostasis.
    [Show full text]
  • A Murine Herpesvirus Closely Related to Ubiquitous Human Herpesviruses Causes T-Cell Depletion Swapneel J
    Washington University School of Medicine Digital Commons@Becker Open Access Publications 2017 A murine herpesvirus closely related to ubiquitous human herpesviruses causes T-cell depletion Swapneel J. Patel Washington University School of Medicine Guoyan Zhao Washington University School of Medicine Vinay R. Penna Washington University School of Medicine Eugene Park Washington University School of Medicine Elvin J. Lauron Washington University School of Medicine See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Patel, Swapneel J.; Zhao, Guoyan; Penna, Vinay R.; Park, Eugene; Lauron, Elvin J.; Harvey, Ian B.; Beatty, Wandy L.; Plougastel- Douglas, Beatrice; Poursine-Laurent, Jennifer; Fremont, Daved H.; and Yokoyama, Wayne M., ,"A murine herpesvirus closely related to ubiquitous human herpesviruses causes T-cell depletion." Journal of Virology.91,9. e02463-16. (2017). https://digitalcommons.wustl.edu/open_access_pubs/5607 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Swapneel J. Patel, Guoyan Zhao, Vinay R. Penna, Eugene Park, Elvin J. Lauron, Ian B. Harvey, Wandy L. Beatty, Beatrice Plougastel-Douglas, Jennifer Poursine-Laurent, Daved H. Fremont, and Wayne M. Yokoyama This open access publication is available at Digital Commons@Becker: https://digitalcommons.wustl.edu/open_access_pubs/5607 GENETIC DIVERSITY AND EVOLUTION crossm A Murine Herpesvirus Closely Related to Ubiquitous Human Herpesviruses Causes T-Cell Depletion Downloaded from Swapneel J. Patel,a Guoyan Zhao,b Vinay R.
    [Show full text]
  • Herpes Simplex Virus and Cytomegalovirus Reactivations
    Balc’h et al. Critical Care (2020) 24:530 https://doi.org/10.1186/s13054-020-03252-3 RESEARCH LETTER Open Access Herpes simplex virus and cytomegalovirus reactivations among severe COVID-19 patients Pierre Le Balc’h1,2, Kieran Pinceaux1,2, Charlotte Pronier3, Philippe Seguin4, Jean-Marc Tadié1,2 and Florian Reizine1,2* Dear Editor, cytomegalovirus replication were measured by quantita- The SARS-CoV-2 infection can lead to severe acute tive real-time PCR on tracheal aspirates twice a week for respiratory distress syndrome (ARDS) with prolonged each patient. Herpesviridae reactivation was defined as mechanical ventilation (MV). Patients with coronavirus two consecutive positive HSV or CMV PCR on tracheal disease 2019 (COVID-19) associated ARDS usually met aspirates. The Mann-Whitney rank sum test was used to the diagnosis criteria for sepsis-associated immunosup- compare non-parametric continuous variables, and pression as acquired infections, primarily bacterial and qualitative data were compared using Fisher’s exact test. fungal co-infections [1], are frequently encountered. Statistical significance was defined as P < .05. PRISM ver- Such secondary infections are associated with late mor- sion 8 (GraphPad Software, San Diego, CA, USA) was tality. Herpesviridae reactivation is common in non- used to perform statistical analyses. immunocompromised patients with prolonged MV and could be responsible for increased mortality and longer Results duration of MV in ICU [2, 3]. Although the diagnosis of A total of 38 patients were included. Table 1 shows the Herpesviridae pulmonary infection is challenging and demographic, clinical, and biological characteristics of not consensual in critically ill patients, therapeutic strat- the included patients.
    [Show full text]
  • The Role of Herpes Simplex Virus Type 1 Infection in Demyelination of the Central Nervous System
    International Journal of Molecular Sciences Review The Role of Herpes Simplex Virus Type 1 Infection in Demyelination of the Central Nervous System Raquel Bello-Morales 1,2,* , Sabina Andreu 1,2 and José Antonio López-Guerrero 1,2 1 Departamento de Biología Molecular, Universidad Autónoma de Madrid, Cantoblanco, 28049 Madrid, Spain; [email protected] (S.A.); [email protected] (J.A.L.-G.) 2 Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Cantoblanco, 28049 Madrid, Spain * Correspondence: [email protected] Received: 30 June 2020; Accepted: 15 July 2020; Published: 16 July 2020 Abstract: Herpes simplex type 1 (HSV-1) is a neurotropic virus that infects the peripheral and central nervous systems. After primary infection in epithelial cells, HSV-1 spreads retrogradely to the peripheral nervous system (PNS), where it establishes a latent infection in the trigeminal ganglia (TG). The virus can reactivate from the latent state, traveling anterogradely along the axon and replicating in the local surrounding tissue. Occasionally, HSV-1 may spread trans-synaptically from the TG to the brainstem, from where it may disseminate to higher areas of the central nervous system (CNS). It is not completely understood how HSV-1 reaches the CNS, although the most accepted idea is retrograde transport through the trigeminal or olfactory tracts. Once in the CNS, HSV-1 may induce demyelination, either as a direct trigger or as a risk factor, modulating processes such as remyelination, regulation of endogenous retroviruses, or molecular mimicry. In this review, we describe the current knowledge about the involvement of HSV-1 in demyelination, describing the pathways used by this herpesvirus to spread throughout the CNS and discussing the data that suggest its implication in demyelinating processes.
    [Show full text]
  • Risk Groups: Viruses (C) 1988, American Biological Safety Association
    Rev.: 1.0 Risk Groups: Viruses (c) 1988, American Biological Safety Association BL RG RG RG RG RG LCDC-96 Belgium-97 ID Name Viral group Comments BMBL-93 CDC NIH rDNA-97 EU-96 Australia-95 HP AP (Canada) Annex VIII Flaviviridae/ Flavivirus (Grp 2 Absettarov, TBE 4 4 4 implied 3 3 4 + B Arbovirus) Acute haemorrhagic taxonomy 2, Enterovirus 3 conjunctivitis virus Picornaviridae 2 + different 70 (AHC) Adenovirus 4 Adenoviridae 2 2 (incl animal) 2 2 + (human,all types) 5 Aino X-Arboviruses 6 Akabane X-Arboviruses 7 Alastrim Poxviridae Restricted 4 4, Foot-and- 8 Aphthovirus Picornaviridae 2 mouth disease + viruses 9 Araguari X-Arboviruses (feces of children 10 Astroviridae Astroviridae 2 2 + + and lambs) Avian leukosis virus 11 Viral vector/Animal retrovirus 1 3 (wild strain) + (ALV) 3, (Rous 12 Avian sarcoma virus Viral vector/Animal retrovirus 1 sarcoma virus, + RSV wild strain) 13 Baculovirus Viral vector/Animal virus 1 + Togaviridae/ Alphavirus (Grp 14 Barmah Forest 2 A Arbovirus) 15 Batama X-Arboviruses 16 Batken X-Arboviruses Togaviridae/ Alphavirus (Grp 17 Bebaru virus 2 2 2 2 + A Arbovirus) 18 Bhanja X-Arboviruses 19 Bimbo X-Arboviruses Blood-borne hepatitis 20 viruses not yet Unclassified viruses 2 implied 2 implied 3 (**)D 3 + identified 21 Bluetongue X-Arboviruses 22 Bobaya X-Arboviruses 23 Bobia X-Arboviruses Bovine 24 immunodeficiency Viral vector/Animal retrovirus 3 (wild strain) + virus (BIV) 3, Bovine Bovine leukemia 25 Viral vector/Animal retrovirus 1 lymphosarcoma + virus (BLV) virus wild strain Bovine papilloma Papovavirus/
    [Show full text]
  • Studies of the Epidemiology of Human Herpesvirus 6
    Studies of the Epidemiology of Human Herpesvirus 6 Julie Dawn Fox Submitted for the degree of Doctor of Philosophy University College London ProQuest Number: 10797776 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a com plete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest ProQuest 10797776 Published by ProQuest LLC(2018). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States C ode Microform Edition © ProQuest LLC. ProQuest LLC. 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106- 1346 Acknowledgements. I would like to thank Prof. R. S. Tedder and Prof. J. R. Pattison for giving me the opportunity to study for a PhD within the Department of Medical Microbiology and for supervision and helpful discussion during the course of this project. I would also like to thank other members of the Virology Section for help and encouragement. Thanks are due to Dr M. Contreras (North London Blood Transfusion Centre, London), Dr H. Kangro (St Bartholomew's Hospital, London), Dr H. Holzel (Hospital for Sick Children, London), Dr T. Stammers (The Church Lane Practice, London), Dr M. Hambling (Public Health Laboratory, Leeds) Dr W. Irving (University Hospital, Nottingham) Dr H. Steel (St George's Hospital, London), Dr E. Larson (Clinical Research Centre, London) and Dr P.
    [Show full text]