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[PMID]: 29519506
[Au] Autor:Liu H; Servan de Almeida R; Gil P; Albina E
[Ad] Address:CIRAD, UMR ASTRE, F-34398 Montpellier, France; ASTRE, Univ Montpellier, CIRAD, INRA, Montpellier, France.
[Ti] Title:Cleavage site of Newcastle disease virus determines viral fitness in persistent infection cells.
[So] Source:Vet Microbiol;216:123-131, 2018 Mar.
[Is] ISSN:1873-2542
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Newcastle disease, caused by infection with virulent strains of Newcastle disease virus (NDV), poses a risk for the poultry industry. The virulence of NDV is mainly determined by the cleavage site of F protein. Lentogenic NDV can become velogenic after passages in SPF chicken brain and air sac based on some strains isolated from water birds, because the proportion of virulent-related strains gradually increases. In contrast, this proportion remains unchanged if NDV is passaged via 10-day-old SPF chicken embryos. This information suggests that environmental conditions rather than mutation affect NDV fitness in quasispecies. However, it is unknown how the environment selects virulent-related strains from a viral population. In this study, velogenic and lentogenic NDV marked by green or red fluorescence were used to establish persistent infection (PI) in BHK-21 cells. Monitoring viruses by different methods, we found that, without competition, persistently infected cells harbored lentogenic and velogenic NDV strains similarly in terms of viral release, viral spread and the period of persistent viral infection. In contrast, under competitive co-infection, velogenic NDV became dominant in quasispecies from the fifth passage of PI cells, which resulted in the progressive disappearance of the lentogenic NDV strain. This domination was concomitant with a short-term reduction in the superinfection exclusion and supernatant interference in PI cells resulting in a velogenic virus rebound. We concluded that virulent-related F protein cleavage site facilitates the spread and replication of NDV in conditions under which cells do not secret trypsin-like proteases and do not inhibit free virus infection, resulting in a gradual increase in virulent strains in quasispecies with the number of passages.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process

  2 / 6622 MEDLINE  
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[PMID]: 29337163
[Au] Autor:Mercier-Darty M; Boutolleau D; Lepeule R; Rodriguez C; Burrel S
[Ad] Address:INSERM U955 Eq18, IMRB, UPEC and AP-HP, Hôpital Universitaire Henri Mondor, Service de Virologie, Créteil, France.
[Ti] Title:Utility of ultra-deep sequencing for detection of varicella-zoster virus antiviral resistance mutations.
[So] Source:Antiviral Res;151:20-23, 2018 Mar.
[Is] ISSN:1872-9096
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:We report the first application of ultra-deep sequencing (UDS) to varicella-zoster virus (VZV) genotypic antiviral testing in a case of acyclovir-resistant VZV infection initially detected by Sanger sequencing within a deeply immunocompromised heart transplant recipient. As added-value compared to Sanger analysis, UDS revealed complex dynamics of viral population under antiviral pressure. Varicella-zoster virus (VZV) is a ubiquitous human herpesvirus affecting populations worldwide. VZV is commonly acquired in youth whose primary infection usually manifests as benign varicella (chickenpox). After the initial infection, the virus establishes lifelong latency in sensory ganglia leading to a risk of subsequent reactivation. Reactivation usually results in the development of localized herpes zoster (HZ) lesions, a painful skin rash commonly known as shingles (Cohen, 2013). The incidence and severity of HZ increase with impaired specific cell-mediated immunity mainly as a result of increasing age, malignancy, immunodeficiency, organ transplantation, or immunosuppressive drug therapy (Cohen, 2013; Koo et al., 2014; Pavlopoulou et al., 2015). In particular, HZ remains a significant cause of morbidity among solid organ transplant (SOT) recipients, especially in patients undergoing heart transplantation (HT) compared with liver, kidney, or lung transplant recipients (Carby et al., 2007; Koo et al., 2014; Pavlopoulou et al., 2015). These particular individuals are at increased risk of primary infection, reactivation followed by dissemination with visceral involvement and associated with bacterial superinfection, and chronic recurrences (Cohen, 2013). VZV infections may also engender debilitating neuralgia among highly immunocompromised patients (Sampathkumar et al., 2009). HT is also associated with the risk of reactivation of other latent viruses belonging to the Herpesviridae family as herpes simplex virus (HSV). Currently licensed drugs to prevent or to cure HSV- or VZV-associated diseases target the viral DNA polymerase (Pol). Acyclovir (ACV) and its prodrug valacyclovir (VACV) are considered as the first-line therapy, whereas foscarnet (FOS) or cidofovir (CDV) constitute alternative options. After primophosphorylation by the viral thymidine kinase (TK), ACV targets the viral DNA polymerase and inhibits the viral genome replication by a chain termination mechanism. According to this mechanism of action, viral mutations conferring resistance to ACV have been mapped both in TK and Pol encoding genes. Viral mutations conferring resistance to FOS and CDV are only detected in Pol gene. VZV ACV-resistance is mostly mediated by TK alterations, consisting in either translational frameshifts, sometimes associated with premature stop codon, or amino acid substitutions. In the remaining cases, amino acid substitutions are detected within Pol (De et al., 2015; Piret and Boivin, 2014). Classically, Sanger sequencing has been recognized as the gold standard for the detection of drug resistance mutations (DRMs) within VZV TK and Pol genes (Perrier et al., 2016; Piret and Boivin, 2014). However, this approach cannot detect minor variants present at a frequency below 20%. Ultra-deep sequencing (UDS) has an enhanced sensitivity compared to Sanger method and allows quantitative evaluation of the viral mutants (Chin et al., 2013). We report here a case of VZV resistant infection in an HT recipient. Our retrospective study aimed at showing the utility of UDS for DRM detection as a complement of Sanger method.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  3 / 6622 MEDLINE  
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[PMID]: 29272534
[Au] Autor:Varo R; Sitoe A; Cossa A; Ordi J; Rozman M; Bassat Q
[Ad] Address:Centro de Investigação em Saúde de Manhiça (CISM), Maputo 1929, Mozambique.
[Ti] Title:Leukoerythroblastosis in a Young Child with Severe Malaria and Superimposed Gram Negative Infection.
[So] Source:J Trop Pediatr;, 2017 Dec 18.
[Is] ISSN:1465-3664
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Leukoerythroblastosis, a non-specific and often short-lasting response of the bone marrow to different diseases such as malignancies or infections, is characterized by the presence in the peripheral blood of immature red and white cells. Methods: We present a case of leukoerythoblastosis occurring in a 24 months old Mozambican girl, in the context of a severe malaria episode and an associated urinary tract infection. Peripheral blood smear was used for diagnosis of malaria and leukoerythroblastosis. Enterobacter cloacae isolation and antibiotic susceptibility testing were performed by conventional microbiology. Results: Peripheral blood smear was positive for Plasmodium falciparum and showed a leukoerythroblastosis with red cell anisopoikilocytosis and left shifted neutrophils. Urine culture confirmed the presence of a multi-resistant E. cloacae. Treatment of underlying conditions resolved the leukoerythroblastic reaction. Conclusions: Leukoerythroblastosis may be related to different infectious diseases and may also appear in the context of severe malaria. Bacterial superinfection needs to be investigated.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/tropej/fmx101

  4 / 6622 MEDLINE  
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[PMID]: 29491180
[Au] Autor:Reeves DB; Magaret AS; Greninger AL; Johnston C; Schiffer JT
[Ad] Address:Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA dreeves@fredhutch.org.
[Ti] Title:Model-based estimation of superinfection prevalence from limited datasets.
[So] Source:J R Soc Interface;15(139), 2018 Feb.
[Is] ISSN:1742-5662
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Humans can be infected sequentially by different strains of the same virus. Estimating the prevalence of so-called 'superinfection' for a particular pathogen is vital because superinfection implies a failure of immunologic memory against a given virus despite past exposure, which may signal challenges for future vaccine development. Increasingly, viral deep sequencing and phylogenetic inference can discriminate distinct strains within a host. Yet, a population-level study may misrepresent the true prevalence of superinfection for several reasons. First, certain infections such as herpes simplex virus (HSV-2) only reactivate single strains, making multiple samples necessary to detect superinfection. Second, the number of samples collected in a study may be fewer than the actual number of independently acquired strains within a single person. Third, detecting strains that are relatively less abundant can be difficult, even for other infections such as HIV-1 where deep sequencing may identify multiple strains simultaneously. Here we develop a model of superinfection inspired by ecology. We define an infected individual's richness as the number of infecting strains and use ecological evenness to quantify the relative strain abundances. The model uses an EM methodology to infer the true prevalence of superinfection from limited clinical datasets. Simulation studies with known true prevalence are used to contrast our EM method to a standard (naive) calculation. While varying richness, evenness and sampling we quantify the accuracy and precision of our method. The EM method outperforms in all cases, particularly when sampling is low, and richness or unevenness is high. Here, sensitivity to our assumptions about clinical data is considered. The simulation studies also provide insight into optimal study designs; estimates of prevalence improve equally by enrolling more participants or gathering more samples per person. Finally, we apply our method to data from published studies of HSV-2 and HIV-1 superinfection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review

  5 / 6622 MEDLINE  
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[PMID]: 29486803
[Au] Autor:Yeh CT; Yeh CS; Chu YD; Chiang YJ
[Ad] Address:Liver Research Center, Chang Gung Memorial Hospital, 5, Fu-Shin Street, Kuei-Shan District, Taoyuan, Taiwan. chautingy@gmail.com.
[Ti] Title:Seroclearance of hepatitis B surface antigen following hepatitis E exacerbation on chronic hepatitis E and B dual infection in a renal transplant recipient: a case report.
[So] Source:J Med Case Rep;12(1):50, 2018 Feb 28.
[Is] ISSN:1752-1947
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Hepatitis E virus infection usually causes an acute and self-resolving hepatitis. In areas where chronic hepatitis B virus infection is prevalent, acute hepatitis E virus superinfection on chronic hepatitis B virus infection occurs sporadically. In recent years, however, chronic hepatitis E virus infection has been recognized in patients under immunosuppressant therapy. To the best of our knowledge, cases involving patients with chronic hepatitis E virus and hepatitis B virus dual infection have never been reported. CASE PRESENTATION: A 47-year-old Taiwanese woman who was a renal transplant recipient with chronic hepatitis B virus infection was under immunosuppressant and antiviral treatment. An episode of hepatitis B exacerbation developed due to withdrawal of antiviral treatment against advice, but the flare subsided following antiviral re-treatments. However, an episode of hepatitis exacerbation developed following removal of the renal graft because of graft failure. During the hepatitis flare, she was still under successful antiviral suppression against hepatitis B virus, while her serum samples were positive for hepatitis E virus RNA. Following the hepatitis flare, seroclearance of hepatitis B virus surface antigen developed. From then on, she was under regular hemodialysis. Five years later, another episode of mild hepatitis exacerbation occurred again with positive serum hepatitis E virus RNA. Tracing back the longitudinal serum samples, serum hepatitis E virus RNA was persistently positive throughout the course. This patient was thus recognized to have chronic hepatitis E virus and hepatitis B virus dual infection with intermittent hepatitis E exacerbations. CONCLUSIONS: In areas where chronic hepatitis B virus infection is prevalent, chronic hepatitis E virus coinfection can occur in organ transplant recipients receiving immunosuppressant. Intermittent hepatitis E exacerbations may develop, interfering with the status of hepatitis B virus infection.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.1186/s13256-018-1586-2

  6 / 6622 MEDLINE  
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[PMID]: 29459261
[Au] Autor:Hill AB
[Ad] Address:Department of Molecular Microbiology and Immunology, Oregon Health and Science University, Portland, OR, United States. Electronic address: hillan@OHSU.edu.
[Ti] Title:The immune response to CMV infection and vaccination in mice, monkeys and humans: recent developments.
[So] Source:Curr Opin Virol;28:161-166, 2018 Feb.
[Is] ISSN:1879-6265
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The immune response to CMV is characterized by extremely large T cell and antibody responses that persist for a lifetime, but do not prevent superinfection with other CMV strains. This makes generation of a vaccine against CMV very difficult, but has facilitated development of CMV-vectored vaccines, which have shown promise in mouse tumor models and in monkey models of infectious disease. The serendipitous use of a mutant rhesus CMV vector for the SIV vaccine elicited extraordinary, CD8 T cell responses restricted by MHCII and non-classical MHCI molecules which apparently provide protection against SIV. CMV-specific CD8 T cell responses in the mouse model are driven by antigen and live out their lives primarily within the intravascular compartment.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:In-Data-Review

  7 / 6622 MEDLINE  
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[PMID]: 29494796
[Au] Autor:Bricks G; Senise JF; Junior HP; Grandi G; Passarini A; Caldeira DB; Junior DC; Moraes HAB; Granato CFH; Filho AC
[Ad] Address:Universidade Federal de São Paulo, Departamento de Medicina, Divisão de Doenças Infecciosas, São Paulo, SP, Brazil. Electronic address: guibricks@gmail.com.
[Ti] Title:Seroprevalence of hepatitis E virus in chronic hepatitis C in Brazil.
[So] Source:Braz J Infect Dis;, 2018 Feb 26.
[Is] ISSN:1678-4391
[Cp] Country of publication:Brazil
[La] Language:eng
[Ab] Abstract:BACKGROUND AND AIMS: Hepatitis E virus infection in patients with underlying chronic liver disease is associated with liver decompensation and increased lethality. The seroprevalence of hepatitis E virus in patients with chronic hepatitis C in Brazil is unknown. This study aims to estimate the seroprevalence of hepatitis E virus in patients with chronic hepatitis C and to describe associated risk factors. METHODS: A total of 618 patients chronically infected with hepatitis C virus from three reference centers of São Paulo, Brazil were included. Presence of anti-HEV IgG was assessed by enzyme-linked immunosorbent assay (WANTAI HEV-IgG ELISA). RESULTS: Out of the 618 patients tested, 10.2% turned out positive for anti-HEV IgG (95% CI 8.0-12.8%). Higher seroprevalence was found independently associated with age over 60 years (OR=2.04; p=0.02) and previous contact with pigs (OR=1.99; p=0.03). CONCLUSIONS: Patients with chronic hepatitis C are under risk of hepatitis E virus superinfection in São Paulo. Contact with pigs is a risk factor for the infection, suggesting a possible zoonosis with oral transmission.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:Publisher

  8 / 6622 MEDLINE  
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[PMID]: 29494584
[Au] Autor:Martínez DY; Verdonck K; Kaye PM; Adaui V; Polman K; Llanos-Cuentas A; Dujardin JC; Boelaert M
[Ad] Address:Instituto de Medicina Tropical Alexander von Humboldt, Universidad Peruana Cayetano Heredia, Lima, Peru.
[Ti] Title:Tegumentary leishmaniasis and coinfections other than HIV.
[So] Source:PLoS Negl Trop Dis;12(3):e0006125, 2018 Mar.
[Is] ISSN:1935-2735
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Tegumentary leishmaniasis (TL) is a disease of skin and/or mucosal tissues caused by Leishmania parasites. TL patients may concurrently carry other pathogens, which may influence the clinical outcome of TL. METHODOLOGY AND PRINCIPAL FINDINGS: This review focuses on the frequency of TL coinfections in human populations, interactions between Leishmania and other pathogens in animal models and human subjects, and implications of TL coinfections for clinical practice. For the purpose of this review, TL is defined as all forms of cutaneous (localised, disseminated, or diffuse) and mucocutaneous leishmaniasis. Human immunodeficiency virus (HIV) coinfection, superinfection with skin bacteria, and skin manifestations of visceral leishmaniasis are not included. We searched MEDLINE and other databases and included 73 records: 21 experimental studies in animals and 52 studies about human subjects (mainly cross-sectional and case studies). Several reports describe the frequency of Trypanosoma cruzi coinfection in TL patients in Argentina (about 41%) and the frequency of helminthiasis in TL patients in Brazil (15% to 88%). Different hypotheses have been explored about mechanisms of interaction between different microorganisms, but no clear answers emerge. Such interactions may involve innate immunity coupled with regulatory networks that affect quality and quantity of acquired immune responses. Diagnostic problems may occur when concurrent infections cause similar lesions (e.g., TL and leprosy), when different pathogens are present in the same lesions (e.g., Leishmania and Sporothrix schenckii), or when similarities between phylogenetically close pathogens affect accuracy of diagnostic tests (e.g., serology for leishmaniasis and Chagas disease). Some coinfections (e.g., helminthiasis) appear to reduce the effectiveness of antileishmanial treatment, and drug combinations may cause cumulative adverse effects. CONCLUSIONS AND SIGNIFICANCE: In patients with TL, coinfection is frequent, it can lead to diagnostic errors and delays, and it can influence the effectiveness and safety of treatment. More research is needed to unravel how coinfections interfere with the pathogenesis of TL.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pntd.0006125

  9 / 6622 MEDLINE  
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[PMID]: 29488662
[Au] Autor:Ko CC; Hatfull GF
[Ad] Address:Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA, 15260.
[Ti] Title:Mycobacteriophage Fruitloop gp52 inactivates Wag31 (DivIVA) to prevent heterotypic superinfection.
[So] Source:Mol Microbiol;, 2018 Feb 28.
[Is] ISSN:1365-2958
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Bacteriophages engage in complex dynamic interactions with their bacterial hosts and with each other. Bacteria have numerous mechanisms to resist phage infection, and phages must co-evolve by overcoming bacterial resistance or by choosing an alternative host. Phages also compete with each other, both during lysogeny by prophage-mediated defense against viral attack, and by superinfection exclusion during lytic replication. Phages are enormously diverse genetically and are replete with small genes of unknown function, many of which are not required for lytic growth, but which may modulate these bacteria-phage and phage-phage dynamics. Using cellular toxicity of phage gene overexpression as an assay, we identified the 93-residue protein gp52 encoded by Cluster F mycobacteriophage Fruitloop. The toxicity of Fruitloop gp52 overexpression results from interaction with and inactivation of Wag31 (DivIVA), an essential Mycobacterium smegmatis protein organizing cell wall biosynthesis at the growing cellular poles. Fruitloop gene 52 is expressed early in lytic growth, and is not required for normal Fruitloop lytic replication, but interferes with Subcluster B2 phages such as Hedgerow and Rosebush. We conclude that Hedgerow and Rosebush are Wag31-dependent phages, and that Fruitloop gp52 confers heterotypic superinfection exclusion by inactivating Wag31. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:Publisher
[do] DOI:10.1111/mmi.13946

  10 / 6622 MEDLINE  
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[PMID]: 29470882
[Au] Autor:Fernández C; Larrubia JR; Avellón A; Martínez NM; Gómez A; Praetorius AG
[Ti] Title:Hepatitis aguda grave por sobreinfección por virus delta: importancia diagnóstica de la biologia molecular. [Severe acute hepatitis by delta virus superinfection: diagnostic significance of molecular biology.]
[So] Source:Acta Gastroenterol Latinoam;46(1):35-37, 2016 Mar.
[Is] ISSN:0300-9033
[Cp] Country of publication:Argentina
[La] Language:spa
[Ab] Abstract:HDV infection may occur within a primary HBV infection (co-infection) or by sub sequent acquisition ofthe virus in patients with chronic hepatitis B (superinfection). Acute HDV infection is rarely diagnosed. Since cero conversion usually takes place about six weeks after viral infection, early diagnosis requires the use of direct diagnostic techniques, such as antigen HD V (HDAg) detection, or genomic amplification by means of molecular biology methods (RT-PCR). Here were port the case of a patient with chronic HBV infection that develops a severe acute hepatitis due to VHD superinfec- tion only detected by molecular biology.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:In-Process


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