Academic literature on the topic 'Influenza B virus'

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Journal articles on the topic "Influenza B virus"

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McCullers, Jonathan A., Sergio Facchini, P. Joan Chesney, and Robert G. Webster. "Influenza B Virus Encephalitis." Clinical Infectious Diseases 28, no. 4 (April 1999): 898–900. http://dx.doi.org/10.1086/515214.

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FRANK, ARTHUR L., LARRY H. TABER, and CHERYL M. PORTER. "INFLUENZA B VIRUS REINFECTION." American Journal of Epidemiology 125, no. 4 (April 1987): 576–86. http://dx.doi.org/10.1093/oxfordjournals.aje.a114571.

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Osterhaus, A. D. "Influenza B Virus in Seals." Science 288, no. 5468 (May 12, 2000): 1051–53. http://dx.doi.org/10.1126/science.288.5468.1051.

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Mao, Steve. "Stressed out by influenza virus." Science 362, no. 6412 (October 18, 2018): 301.2–301. http://dx.doi.org/10.1126/science.362.6412.301-b.

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Nakajima, S., F. Nishikawa, K. Nakamura, H. Nakao, and K. Nakajima. "Reinfection with influenza B virus in children: analysis of the reinfection influenza B viruses." Epidemiology and Infection 113, no. 1 (August 1994): 103–12. http://dx.doi.org/10.1017/s0950268800051517.

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SUMMARYInfluenza B virus reinfection in Japanese children was studied epidemi-ologically during 1979–91 and virologically during 1985–91. During this investigation, there were four epidemics caused by influenza B viruses, each of which accompanied antigenic drift. Between the epidemics in 1987/88 and 1989/90, the viruses changed drastically, both genetically and antigenically. The minimum rate of reinfection with influenza B virus during the whole period was 3–25% depending on the influenza seasons. The antigens of primary and reinfection strains of influenza B virus isolated from 18 children during 1985–90, which covered three epidemic periods, were studied by haemagglutination inhibition tests. The results showed that the viruses isolated in the 1984/85 and 1987/88 influenza seasons, which belonged to the same lineage, were antigenically close, and reinfection occurred with these viruses. The results of amino-acid analysis of the HA1 polypeptide of these viruses corresponded with those of antigenic analysis. There were no specific amino-acid changes shared by the primary infection and reinfection influenza B viruses; the patients were infected with the viruses epidemic at that time.
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Wanitchang, Asawin, Jaraspim Narkpuk, Peera Jaru-ampornpan, Juggagarn Jengarn, and Anan Jongkaewwattana. "Inhibition of influenza A virus replication by influenza B virus nucleoprotein: An insight into interference between influenza A and B viruses." Virology 432, no. 1 (October 2012): 194–203. http://dx.doi.org/10.1016/j.virol.2012.06.016.

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Bodewes, Rogier, Danny Morick, Gerrie de Mutsert, Nynke Osinga, Theo Bestebroer, Stefan van der Vliet, Saskia L. Smits, et al. "Recurring Influenza B Virus Infections in Seals." Emerging Infectious Diseases 19, no. 3 (March 2013): 511–12. http://dx.doi.org/10.3201/eid1903.120965.

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Nogales, Aitor, Irene Rodríguez-Sánchez, Kristen Monte, Deborah J. Lenschow, Daniel R. Perez, and Luis Martínez-Sobrido. "Replication-competent fluorescent-expressing influenza B virus." Virus Research 213 (February 2016): 69–81. http://dx.doi.org/10.1016/j.virusres.2015.11.014.

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&NA;. "Sialidase inhibitors: influenza B virus resistance emerges." Inpharma Weekly &NA;, no. 1582-1583 (April 2007): 14. http://dx.doi.org/10.2165/00128413-200715820-00038.

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Kugelberg, Elisabeth. "Promoting B cell responses to influenza virus." Nature Reviews Immunology 14, no. 5 (April 7, 2014): 283. http://dx.doi.org/10.1038/nri3662.

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Dissertations / Theses on the topic "Influenza B virus"

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Pavan, Carmen M. "Influenza B virus : segment 7 gene expression." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55673.

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Rowley, Kathryn Victoria. "Genetic manipulation of influenza B virus segment 6." Thesis, University of Reading, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314321.

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MAENO, KOICHIRO. "Replication of Influenza B Virus: Biological Functions of Viral Neuraminidase." Nagoya University School of Medicine, 1994. http://hdl.handle.net/2237/15935.

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Tsang, Chi-ho, and 曾志豪. "A multi-probe quantitative PCR assay for genotyping of influenza B virus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49828599.

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Influenza B virus contributes to a significant portion of influenza disease burden in men. It is structurally similar and replicates in the same manner as the influenza A virus, leading to a comparable clinical presentation between the two viral species. Since 1977, influenza B has caused seasonal epidemics around the world together with A/H1N1 and A/H3N2 subtypes, and has a strong affinity to affect children of school age and young adults. In the 1980s, two antigenically distinct lineages of influenza B virus emerged, one being the B/Yamagata lineage and the other known as B/Victoria lineage. The most significant antigenic difference between the two is located in the HA1 domain of the viral hemagglutinin. Host immunity is not shared between the two viral lineages. Therefore, the global prevalence of the two influenza B lineages is closely monitored by the World Health Organization in order to decide which viral lineage to include in the annual trivalent influenza vaccines. Surprisingly, the current methods used in influenza B viral surveillance and lineage discrimination have not seen much technical advancement in nearly 25 years since the emergence of two viral lineages. The current study presents a novel, asymmetric real-time PCR assay which is able to determine the viral lineage in addition to detecting the presence of influenza B virus in clinical specimens. Asymmetric PCR is performed by deliberately limiting the amount of primers in one side of a PCR reaction. This significantly affects the replication efficiency and sensitivity of the PCR reaction, but at the same time facilitates target sequence detection by hybridization probes, due to an increased number of single stranded products in the reaction. Nevertheless, the use of asymmetric PCR has been avoided in the past. The recent introduction of linear-after-the-exponential (LATE) PCR refines the method by adjusting melting temperature of PCR primers so that TmLimiting – TmExcess ≥ 0°C. The modification is shown to raise the efficiency of asymmetric PCR to those of symmetric PCR, as well as allowing more relaxed criteria for PCR primer and probe design. In the current asymmetric assay, pan-influenza B primers and probes targeting Victoria and Yamagata linage specific regions of the influenza B HA were evaluated against a similar symmetric influenza B assay published by the World Health Organization. HA plasmid standards and 155 clinical specimens were tested by both assays, in which the two had intra-assay CV% of less than 5%. Albeit the efficiency and sensitivity of WHO published assay was slightly higher, LATE-PCR based assay performed influenza B detection and genotyping simultaneously with the use of hydrolysis probes. The overall sensitivity/ specificity of the genotyping assay are 96.81%/100% while the WHO recommended assay is at 98.94%/100% for influenza B detection. The LATE-PCR based genotyping assay also successfully genotyped 89 out of 94 clinical specimens. In conclusion, the influenza B genotyping assay evaluated in this study performed favorably and could serve as an alternative to cumbersome viral culture methods to aid in high-throughput global influenza surveillance.
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Microbiology
Master
Master of Medical Sciences
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Huang, Kuan-Ying. "B cell and antibody responses to influenza A virus in human." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:3c24c905-15e2-4547-944e-e1a46a6aacd0.

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Neutralising antibodies and antigen-specific B cells are important for protection against influenza A virus. However, the antigenic evolution of influenza A viruses has made a continuing challenge to the design of vaccine and the public health. The ability to generate cross-reactive response against influenza remains unclear in human. It is important to explore the antibody and B cell repertoire at single cell level. The pandemic H1N1 and seasonal influenza vaccine induced robust antibody response in adults. However, pre- or co-vaccination with the seasonal vaccine led to a significantly reduced antibody response to pandemic H1N1 virus. Whether this interference has impact on subsequent infection rates remains undetermined. There observed substantial cross-reactive antibody response upon vaccination, as measured by HI, MN and B cell ELISpot assays. The antibody recognizing conserved proteins could be the main component of cross-reactivity against influenza A strains and subtypes. A significant expansion of influenza-specific MBC was observed after infection. Crossreactive response was also noted in the MBC response. Importantly, a robust early-phase ASC response was detected in the peripheral blood upon influenza vaccination or infection. The size of ASC response significantly correlated with serum HI, MN and anti-HA IgG titre three weeks after vaccination. The sequence analysis revealed that early-phase ASC accumulated high level of somatic mutations on Ig variable region and affinity maturation, as well as anti-influenza mAb, which suggested their origin from pre-existing MBC. Eight anti-influenza mAb were made from early-phase ASC, including one high-titre virus-neutralising HA1-specific, two other HA1-specific, one cross-reactive HA2-specific, and four cross-reactive NP-specific antibodies, indicating of the broad diversity of ASC repertoire. In conclusion, this study demonstrated the properties of antibody and B cell responses to influenza A virus at serological, cellular and sequence level. The virus-neutralising and cross-reactive mAb derived from ASC could have therapeutic potential and their analysis might direct the vaccine design in the near future.
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Schneider, Jana [Verfasser]. "Charakterisierung nuklearer Funktionen des Nichtstrukturproteins von Influenza-B-Virus / Jana Schneider." Berlin : Freie Universität Berlin, 2009. http://d-nb.info/1023665859/34.

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Boyden, Alexander Wiser. "Influenza A virus induces regulated T cell-driven B cell responses." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/3432.

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Protection from influenza A virus (IAV) challenge requires switched, high affinity Abs derived from long-lived memory B cells and plasma cells. These subsets are generated in germinal centers (GCs), hallmark structures of T helper cell-driven B cell immunity. A full understanding of the acute and persistent GC B cell reaction following respiratory IAV infection is lacking, as is the characterization of IAV-induced T follicular helper (TFH) cells that support GCs. Additionally, it remains unclear as to whether IAV-induced GC B cells are subject to control by regulatory T cells (Tregs). To address this, GC B cell and TFH cell responses were analyzed in mice following pulmonary challenge with IAV. Studies demonstrated that marked GC reactions were induced in lung-draining lymph nodes (dLNs), lung, spleen and nasal-associated lymphoid tissue (NALT), although the magnitude, kinetics, and isotype switching patterns of the response was site-specific, and largely depended on the magnitude of IAV-induced TFH cell populations. TFH cell magnitude peaked prior to that of GC B cells in all tissues, and TFH cells purified from dLNs generated IL-21 and IFN-gamma upon activation, although CD4+CXCR5- T effector cells produced higher levels of all cytokines. IgA+ GC B cells were infrequent in most sites, but composed a significant subset of the switched GC population in NALT. Further, splenectomized mice withstood a lethal recall challenge, suggesting the spleen to be unnecessary for long-term protection. Additionally, GC B cell populations were analyzed at distal time points to assess the understudied, persistent GC B cell response after IAV infection. Our analysis demonstrated that persistent GC B cell populations in mouse lungs directly correlated with infectious dose, pathogenicity of the virus, as well as the presence of long-term CD4+ T cell help. Finally, experiments showed that Tregs contribute to the control of GCs induced in the spleen by IAV challenge. This was demonstrated by a marked increase in the number of total and switched GC B cell numbers when Tregs were either depleted or disrupted in vivo proximal to IAV exposure.
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INOUE, HIROMASA, and ARIFUMI KUNO. "Antigenic Analysis of Influenza B Virus Isolated from the Epidemic in 1973." Nagoya University School of Medicine, 1985. http://hdl.handle.net/2237/17471.

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Wang, Xiaohui, and 王晓辉. "The role of IL-17A in modulating B cell response during influenza virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208035.

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Interleukin-17A (IL-17A)is an important pro-inflammatory cytokine that plays a critical role in host defenses against diverse pathogens. Studies have shown that IL-17Aplays protective role against sub-lethal H1 and H3 subtypes influenza infections, but it is unclear about the role of IL-17A in the highly pathogenic H5N1 and lethal H1N1 influenza virus infection. B cell is an important effector cell type in anti-influenza immunity. Although roles of B cell in influenza infection have been extensively investigated, it is unclear whether and how IL-17AregulatesB cell response during influenza infection. I examined the role of IL-17A against influenza infection by challengingIL-17A knockout (KO) and wild-type (WT) mice with highly pathogenic H5N1 and lethal H1N1 influenza viruses. Following challenge, IL-17AKO mice exhibited significantly lower survival rate, profoundly reduced body weight, more severe tissue damage and higher viral burden in the lung tissues. These evidences suggest that IL-17Aplays a protective role in lethal influenza infection. To study whether IL-17Amodulates B cell response against influenza, I found that both B-1a and B-2 cells were detected in the lung tissue and pulmonary draining lymph node, Mediastinal lymph node (MedLN),as early as 2days post-infection. Meanwhile, B-1a cells predominantly contributed to the early virus-specific IgM in the respiratory tract. However, virus-specific IgM markedly reduced in IL-17A KO mice when compared with WT controls. Adoptive transfer of B-1a cells or B-1a cell-derived antibodies conferred protection in IL-17A KO mice. These results demonstrate that IL-17A plays a critical role in modulating early antibody production of B-1a cells against lethal influenza infection. To further elucidate how IL-17A regulates B-1a cell response, I observed that B-1a cells migrated into MedLN and lung tissues during infection and underwent plasmacytic differentiation with increased antibody production in airways. IL-17A deficiency impaired these processes of B-1a cells, while intra-nasally instillation of IL-17A restored B-1a cell response by promoting both B-1a cell migration and plasmacytic differentiation. By inducing blimp-1 expression in B-1a cells in an NF-κB dependent pathway, IL-17A directly promoted plasmacytic differentiation of B-1a cells both in vivo and in vitro. Furthermore, chromatin immuno-precipitation analysis confirmed that NF-κB directly bound to the promoter of blimp-1 gene and promoted blimp-1 expression in B-1a cells following IL-17A stimulation. To determine the functional significance of IL-17A signaling in modulating B cell response against influenza infection, I first uncovered markedly reduced B cell response, predominantly B-1a cell response in IL-17A KO mice, showing reduced local migration and impaired plasmacytic differentiation in the early stage of infection. Next, intra-nasal administration of IL-17A into IL-17A KO mice significantly restored this B-1a cell response. Moreover, I detected expression of IL-17A receptor in B-1a cells. IL-17A treatment could promote antibody production from B-1a cells by inducing blimp-1 expression in an NF-κB dependent pathway. Taken together, these findings identify a novel role of IL-17A in actingas an immune modulator of B cell response against influenza infection, which will contribute to a fuller understanding of B cell biology and anti-viral response in host defense.
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Pathology
Doctoral
Doctor of Philosophy
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Audsley, Jennifer M., and jennifer audsley@med monash edu au. "Alternative Approaches In The Preparation And Growth Of Influenza B Vaccine Viruses." RMIT University. Applied Sciences, 2008. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080414.141937.

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Influenza B viruses are a significant cause of disease and influenza B antigens are present in all human vaccines. Achieving suitable yields of seed viruses is often difficult for vaccine manufacturers. With influenza A viruses increases in yields have been achieved by the preparation of reassortants between a high-yielding donor strain and an epidemic strain. However, reassortment of influenza B viruses for the preparation of seeds has not been usually undertaken due to the lack suitable donor strains. Such an approach, which formed the basis of this thesis, could improve vaccine yields, lower costs and introduce a further element of predictability to vaccine manufacture. Potential donor strains were prepared from B/Lee/40 (B/Lee) by two approaches involving the selection of stable cold- and high- temperature mutants. Initial passaging was undertaken in specific-pathogen-free (SPF) chicken embryo kidney (CEK) cultures and later passage in SPF embryonated chicken eggs. Both approaches were successful, although a smaller number of viable progeny could be isolated from plaques obtained at 38„aC. Potential donor strains, isolated by selection at either 25 or 38„aC and plaque-purified in SPF CEK cultures, were tested for haemagglutinin and infectious titre, in comparison with the original parental strain by three methods, and for differences in antigenicity by cross-haemagglutination-inhibition tests. Potential donor strains selected at temperatures of 25„aC (C25) and 38„aC (H38) produced haemagglutination titres of 320 units/50ƒÝL and infectivities of 8.57 and 8.39 50% egg infectious doses, respectively, when grown in eggs at the permissive temperature (34„aC). Reassorting experiments using the B/Lee-derived potential donor strains C25 and H38 and the epidemic strain, B/Johannesburg/5/99 (B/Johannesburg), showed that the preparation of reassortant progeny with both epidemic strain HA and NA was difficult. Only 1/24 of the resulting reassortants possessed both the HA and NA of the epidemic strain. None of the reassortant progeny produced in reassorting experiments using C25 and H38 and the epidemic strain B/Panama/45/90 (B/Panama) possessed the desired 6:2 gene constellation (i.e. genes for the two surface antigens of the epidemic strain and the remainder from the donor strain). The infectious titre of selected progeny from the reassortment experiments were determined by three methods and compared with their respective epidemic parents. Yields of several influenza B epidemic strains and potential donor strains were measured after growth in Madin-Darby canine kidney (MDCK) cells prepared in serum-containing (SC) and animal- and human-derived protein-free (AHPF) media. Optimal multiplicities of infection were determined for B/Panama, B/Johannesburg and C25 in MDCK cultures grown in SC medium. A series of experiments were then undertaken to determine the maximum virus yields in MDCK cells grown in SC medium, followed by a further experiment using C25, B/Panama, B/Johannesburg, and selected reassortants after preparation in AHPF medium. Cell culture yields from 5/6 viruses grown in MDCK cells prepared in AHPF medium were higher than in cells prepared in SC medium and approached those obtained in eggs.
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Books on the topic "Influenza B virus"

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Influenza and it's [sic] global public health significance. West Orange, NJ: Thajema Publishers, 2006.

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Kawaoka, Yoshihiro. Influenza Virology: Current Topics. Caister Academic Pr, 2006.

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Alexander, D. J., N. Phin, and M. Zuckerman. Influenza. Edited by I. H. Brown. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0037.

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Influenza is a highly infectious, acute illness which has affected humans and animals since ancient times. Influenza viruses form the Orthomyxoviridae family and are grouped into types A, B, and C on the basis of the antigenic nature of the internal nucleocapsid or the matrix protein. Infl uenza A viruses infect a large variety of animal species, including humans, pigs, horses, sea mammals, and birds, occasionally producing devastating pandemics in humans, such as in 1918 when it has been estimated that between 50–100 million deaths occurred worldwide.There are two important viral surface glycoproteins, the haemagglutinin (HA) and neuraminidase (NA). The HA binds to sialic acid receptors on the membrane of host cells and is the primary antigen against which a host’s antibody response is targeted. The NA cleaves the sialic acid bond attaching new viral particles to the cell membrane of host cells allowing their release. The NA is also the target of the neuraminidase inhibitor class of antiviral agents that include oseltamivir and zanamivir and newer agents such as peramivir. Both these glycoproteins are important antigens for inducing protective immunity in the host and therefore show the greatest variation.Influenza A viruses are classified into 16 antigenically distinct HA (H1–16) and 9 NA subtypes (N1–9). Although viruses of relatively few subtype combinations have been isolated from mammalian species, all subtypes, in most combinations, have been isolated from birds. Each virus possesses one HA and one NA subtype.Last century, the sudden emergence of antigenically different strains in humans, termed antigenic shift, occurred on three occasions, 1918 (H1N1), 1957 (H2N2) and 1968 (H3N2), resulting in pandemics. The frequent epidemics that occur between the pandemics are as a result of gradual antigenic change in the prevalent virus, termed antigenic drift. Epidemics throughout the world occur in the human population due to infection with influenza A viruses, such as H1N1 and H3N2 subtypes, or with influenza B virus. Phylogenetic studies have led to the suggestion that aquatic birds that show no signs of disease could be the source of many influenza A viruses in other species. The 1918 H1N1 pandemic strain is thought to have arisen as a result of spontaneous mutations within an avian H1N1 virus. However, most pandemic strains, such as the 1957 H2N2, 1968 H3N2 and 2009 pandemic H1N1, are considered to have emerged by genetic re-assortment of the segmented RNA genome of the virus, with the avian and human influenza A viruses infecting the same host.Influenza viruses do not pass readily between humans and birds but transmission between humans and other animals has been demonstrated. This has led to the suggestion that the proposed reassortment of human and avian influenza viruses takes place in an intermediate animal with subsequent infection of the human population. Pigs have been considered the leading contender for the role of intermediary because they may serve as hosts for productive infections of both avian and human viruses, and there is good evidence that they have been involved in interspecies transmission of influenza viruses; particularly the spread of H1N1 viruses to humans. Apart from public health measures related to the rapid identification of cases and isolation. The main control measures for influenza virus infections in human populations involves immunization and antiviral prophylaxis or treatment.
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(Editor), Kathleen Stratton, Donna A. Alamario (Editor), Theresa Wizemann (Editor), and Marie C. McCormick (Editor), eds. Immunization Safety Review: Influenza Vaccines and Neurological Complications. National Academies Press, 2004.

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Russi, Mark. Biological Hazards. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0016.

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This chapter describes various biological hazards and their impact on workers and others. A major focus of the chapter is biological hazards in healthcare and laboratory settings, including exposure to bloodborne pathogens and prevention of diseases related to them. Sections deal with sharps injuries, HIV/AIDS, hepatitis B virus, hepatitis C virus, tuberculosis, and other infectious diseases that can be acquired in the work environment via direct contact, droplet or airborne spread, or fecal-oral transmission. In addition, infectious agents spread by animal contact or arthropod vectors in a broad range of settings will be addressed. Newly emerging infectious or re-emerging infections, such as those due to H5N1 and novel H1N1 influenza, Middle Eastern respiratory syndrome (MERS), and Ebola Virus Disease (EVD) as well as agents associated with bioterrorism are discussed.
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Immunization safety review: Hepatitis B vaccine and demyelinating neurological disorders. Washington, D.C: National Academies Press, 2002.

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(Editor), Kathleen Stratton, Donna Almario (Editor), and Marie C. McCormick (Editor), eds. Immunization Safety Review: Hepatitis B Vaccine and Demyelinating Neurological Disorders. National Academies Press, 2002.

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Oldstone, Michael B. A. Viruses, Plagues, and History. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780190056780.001.0001.

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“Viruses, Plagues, & History” focuses on the effects of viral diseases on human history. Written by an eminent internationally respected virologist, it couples the fabric of history with major concepts developed in virology, immunology, vaccination, and accounts by people who first had, saw and acted at the times these events occurred. Much of the preventive and therapeutic progress (vaccines, antiviral drugs) has been made in the last 60 years. Many of those who played commanding roles in the fight to understand, control and eradicate viruses and viral diseases are (were) personally known to the author and several episodes described in this book reflect their input. The book records the amazing accomplishments that led to the control of lethal and disabling viral diseases caused by Smallpox, Yellow Fever, Measles, Polio, Hepatitis A, B and C, and HIV. These six success stories are contrasted with viral infections currently out of control—COVID-19, Ebola virus, Lassa Fever virus, Hantavirus, West Nile virus, and Zika. Influenza, under reasonable containment at present, but with the potential to revert to a world-wide pandemic similar to 1918–1919 where over 50 million people were killed. The new platforms to develop inhibitory and prophylactic vaccines to limit these and other viral diseases is contrasted to the anti-vaccine movement and the false prophets of autism.
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(Editor), Kathleen Stratton, Donna A. Almario (Editor), Theresa M. Wizemann (Editor), and Marie C. McCormick (Editor), eds. Immunization Safety Review: Vaccinations and Sudden Unexpected Death in Infancy. National Academies Press, 2003.

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R, Stratton Kathleen, Alamario Donna A, McCormick Marie C, and Institute of Medicine (U.S.). Immunization Safety Review Committee., eds. Immunization safety review: SV40 contamination of polio vaccine and cancer. Washington, D.C: National Academies Press, 2003.

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Book chapters on the topic "Influenza B virus"

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Palese, Peter, and Makoto Yamashita. "Evolutionary Lineages and Molecular Epidemiology of Influenza A, B, and C Viruses." In Virus Variability, Epidemiology and Control, 119–29. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9271-3_8.

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Bednarska, K., E. Hallmann-Szelińska, K. Kondratiuk, D. Rabczenko, and L. B. Brydak. "Molecular Characteristics of Influenza Virus Type B Lineages Circulating in Poland." In Respiratory Medicine and Science, 1–8. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/5584_2015_200.

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Baumgarth, N., J. Chen, O. C. Herman, G. C. Jager, and L. A. Herzenberg. "The Role of B-1 and B-2 Cells in Immune Protection from Influenza Virus Infection." In Current Topics in Microbiology and Immunology, 163–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_17.

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Byars, Noelene E., Gayle Nakano, Mary Welch, and Anthony C. Allison. "Use of Syntex Adjuvant Formulation to Augment Humoral Responses to Hepatitis B Virus Surface Antigen and to Influenza Virus Hemagglutinin." In Immunological Adjuvants and Vaccines, 145–52. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-0283-5_15.

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Haralambieva, Iana H., Inna G. Ovsyannikova, Richard B. Kennedy, and Gregory A. Poland. "Detection and Quantification of Influenza A/H1N1 Virus-Specific Memory B Cells in Human PBMCs Using ELISpot Assay." In Methods in Molecular Biology, 221–36. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8567-8_19.

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Lamb, Robert A., and Mark A. Williams. "A Genetic Approach to Determining Glycoprotein Topology: The Influenza B Virus NB Glycoprotein has an Extracellular NH2-Terminal Domain Containing two N-linked Carbohydrate Chains." In Modern Trends in Virology, 1–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73745-9_1.

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Ni, Fengyun, and Qinghua Wang. "Recent Progress in Understanding Influenza B Virus Hemagglutinin." In Influenza: Current Research, 41–54. Caister Academic Press, 2016. http://dx.doi.org/10.21775/9781910190432.03.

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Shin, Gee Yen. "Vaccination Schedules." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0062.

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The vaccines included in the current UK Immunisation Schedule offer protection against the following pathogens: A. Viruses ● Measles ● Mumps ● Rubella ● Polio ● Human Papilloma Virus (certain serotypes) ● Rotavirus ● Influenza virus (flu A and B) ● Varicella zoster virus (shingles) ● Hepatitis B virus B. Bacteria ● Corynebacterium diphtheriae (Diphtheria) ● Clostridium tetani (Tetanus) ● Bordetella pertussis (Pertussis) ● Haemophilus influenzae type B (Hib) ● Neisseria meningitidis (Meningococcal disease—certain serotypes) ● Streptococcus pneumoniae (Pneumococcal disease—certain serotypes) The UK Immunisation Schedule has evolved over several decades and reflects changes in vaccine development and commercial availability, national and sometimes international disease epidemiology, and the latest expert opinion. It is designed to offer optimal protection against infectious diseases of childhood to infants and children at the most appropriate age. The most up-to-date information about the UK Immunisation Schedule is available on the online version of the Department of Health publication commonly known as the ‘Green Book’: Immunisation Against Infectious Disease Handbook (see Further reading. Various chapters of the online version are updated at regular intervals; thus, it is very important to refer to the online version of the Green Book on the website for current guidance. Changes to the UK Immunisation Schedule are made on the recommendation of the independent Joint Committee on Vaccines and Immunisation (JCVI). Several of the UK Immunisation Schedule vaccines are combined vaccines: ● Measles, mumps, and rubella (MMR). ● Hexavalent diphtheria, tetanus, acellular pertussis, inactivated polio virus, Haemophilus influenza type b, hepatitis B (DTaP/IPV/Hib/HepB). ● Diphtheria, tetanus, acellular pertussis, inactivated polio, and Haemophilus influenzae (DTaP/IPV/Hib). ● Diphtheria, tetanus, acellular pertussis, inactivated polio (DTaP/IPV). ● Tetanus, diphtheria, and inactivated polio (Td/IPV). ● Inactivated influenza vaccine: influenza A H1N1, H3N2, influenza B. ● Live attenuated intranasal influenza vaccine: influenza A H1N1, H3N2, influenza B. In the UK, vaccines against single pathogens covered by the MMR vaccine are not recommended and not available in the National Health Service (NHS). There has been some limited demand for single-target vaccines, e.g. measles, due to misguided and unfounded concerns about the alleged risks of autism following MMR.
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Gilsdorf, Janet R. "The Flu and Richard Pfeiffer." In Continual Raving, 23–56. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190677312.003.0002.

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For decades, scientists puzzled over which influenza virus was actually responsible for the Russian pandemic. Finally, in 2014, phylogenetic techniques (examining evolutionary patterns of the virus genes) and seroarcheologic techniques (measuring antibodies likely present in people at various points in time) were applied to the question of which virus caused the Russian flu of 1889–1892. Thus, Pfeiffer’s proclamation that his bacillus caused influenza was finally proven wrong. His identification of Bacillus influenzae in the respiratory tract, however, was a major contribution to the scientific understanding of bacterial infections and moved the field of bacteriology forward in allowing other investigators to unearth its full potential as an important human pathogen. Further, in the course of his studies of B. influenzae, Pfeiffer pioneered the field of nutritional requirements of bacteria. Finally, Pfeiffer’s identification of Haemophilus influenzae launched subsequent studies of the causes of bacterial meningitis and initiated in-depth explorations of bacterial meningitis-causing pathogens that ground our concepts of pathogenesis, and guide our management, of the infection.
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Čulić, Srđana. "Viral Infections, Including Influenza and Corona Virus Disease 2019, and Vitamin D: A Mini-Review." In Vitamin D. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96102.

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Recent research about the influence of vitamin D (VD) deficiency on the occurrence of viral infections suggests that children with VD deficiency have attenuated immune response. This, in turn, increases the severity of viral infections, especially those of the respiratory tract, that show a typical seasonality pattern during the winter months. Despite the immunization of children at the global level, outbreaks of influenza do frequently occur. Over the past months, we have witnessed that the explosive pandemic of the corona virus disease 2019 (COVID-19) has caused significant mortality in some countries. Numerous studies have shown that VD deficiency is increasingly prevalent worldwide, and that it is potentially associated with the onset of viral infections. Persons with hypovitaminosis D and subsequent secondary immunodeficiencies ought to be identified and treated, while preventive supplementation of VD should be recommended to the general population to avoid VD deficiency during the winter. In this way, the burden of viral infections on population health and economy could be reduced. This paper also reviews the influence of VD on infections caused by hepatitis B and C viruses, human papillomavirus, Epstein–Barr virus, Human herpes virus 6, herpes simplex virus, and human immunodeficiency virus.
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Conference papers on the topic "Influenza B virus"

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Elbashir, Israa, Heba Al Khatib, and Hadi Yassine. "Replication Dynamics, Pathogenicity, and Evolution of Influenza Viruses in Intestinal Caco-2 Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0166.

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Background: Influenza virus is a major cause of respiratory infections worldwide. Besides the common respiratory symptoms, namouras cases with gastrointestinal symptoms have been reported. Moreover, influenza virus has been detected in feces of up to 20.6 % of influenza-infected patients. Therefore, direct infection of intestinal cells with influenza virus is suspected; however, the mechanism of this infection has not been explored. AIM: To investigate influenza virus replication, cellular responses to infection, and virus evolution following serial infection in human Caucasian colon adenocarcinoma cells (Caco-2 cells). Method: Two influenza A subtypes (A/H3N2 and A/H1N1pdm 09) and one influenza B virus (B/Yamagata) were serially passaged in Caco-2. Quantitative PCR was used to study hormones and cytokines expression following infection. Deep sequencing analysis of viral genome was used to assess the virus evolution. Results: The replication capacity of the three viruses was maintained throughout 12 passages, with H3N2 virus being the fastest in adaptation. The expression of hormone and cytokines in Caco-2 cells was considerably different between the viruses and among the passages, however, a pattern of induction was observed at the late phase of infection. Deep sequencing analysis revealed a few amino acid substitutions in the HA protein of H3N2 and H1N1 viruses, mostly in the antigenic site. Moreover, virus evolution at the quasispecies level based on HA protein revealed that H3N2 and H1N1 harbored more diverse virus populations when compared to IBV, indicating their higher evolution within Caco-2 cells. Conclusion: The findings of this study indicate the possibility of influenza virus replication in intestinal cells. To further explain the gastrointestinal complications of influenza infections in-vivo experiments with different influenza viruses are needed.
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Achyar, Afifatul, Tati Kristianti, and Sony Suhandono. "Fusion Strategy of Influenza A-H5N1 Virus M2e Epitope DNA Sequence to Hepatitis B Virus HBsAg-S Gene." In International Conference on Biology, Sciences and Education (ICoBioSE 2019). Paris, France: Atlantis Press, 2020. http://dx.doi.org/10.2991/absr.k.200807.067.

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Hendriks, Rudi W., Roel Klein Wolterink, Menno van Nimwegen, Laurens Kil, Henk C. Hoogsteden, Guus F. Rimmelzwaan, and Corine H. Geurts van Kessel. "Aberrant B Cell Activation And Germinal Center Formation Upon Pulmonary Influenza Virus Infection In Mice Deficient For Bruton’s Tyrosine Kinase." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1385.

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Liu, Changwen, Shengtao Li, Zehong Zou, and Ailin Tao. "Comparison of HA, NA amino acid sequences of novel influenza virus A/H1N1 and prediction of related B cell epitopes." In 2010 Sixth International Conference on Natural Computation (ICNC). IEEE, 2010. http://dx.doi.org/10.1109/icnc.2010.5582631.

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MORENO, MARCELO. "SARS-COV-2 infection in a family nucleus resident in the city of João Pessoa/PB, Brazil." In I South Florida Congress of Development. CONGRESS PROCEEDINGS I South Florida Congress of Development - 2021, 2021. http://dx.doi.org/10.47172/sfcdv2021-0011.

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The SARS-COV-2 virus was responsible for the Covid-19 pandemic, starting its first infections in Wuhan, China. The present work aims to analyze the clinical case of a family nucleus resident (resident) of the city of Joao Pessoa/PB - Brazil affected (affected) by Covid-19. The family consists of three people: a 23-year-old woman (Patient A), a one-year-old child (Patient B) and a 31-year-old man (Patient C). The systematized analysis of the report of symptoms over the days, diagnosis and medical (medical) diagnosis, interpretation of computed tomography (CT), in addition to performing bibliographic searches for the basis of the work, framing the symptoms of the patients according to the groups proposed by Sudre et al. (2020) for Covid-19. Patient A was in group 2 (similar to influenza, with fever) and presented pulmonary alterations on her CT. Patient B presented mild symptoms of the disease. Patient C, on the other hand, was included in group 3 (gastrointestinal symptoms) and did not present pulmonary alterations on his CT.
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Cosgriff, T. M., P. G. Canonico, L. Hodgson, D. Parrish, T. Chapman, J. W. Huggins, Z.-J. Gong, L.-B. Xiang, and C.-H. Hsiang. "RIBAVIRIN: STUDIES OF THE EFFECTS OF THE ANTIVIRAL DRUG ON PLATELET FUNCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644545.

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Ribavirin is a broad-spectrum antiviral drug which is presently undergoing testing in patients with AIDS-related complex. It has also been shown to have activity against respiratory syncytial virus, Sicilian sandfly fever virus, influenza A and B viruses, as well as several hemorrhagic fever viruses. It has proved effective in clinical trials in Lassa fever and shows promise as therapy for hemorrhagic fever with renal syndrome. Because platelet dysfunction may contribute significantly to hemostatic impairment in viral hemorrhagic fever, the effects of ribavirin on platelet function were measured in rhesus monkeys after daily injections of 100 mg/kg IM for 14 days. Drug administration led to a significant increase in platelet count associated with megakaryocyte hyperplasia but had no effect on aggregation of platelet-rich plasma (PRP) in response to either collagen (1.6 μg/ml) or ADP (10 μM/ml). Aggregation in whole blood was also unaffected. Addition of ribavirin to human PRP in concentrations up to 0.5 mg/ml had no effect on aggregation in response to collagen, ADP, or epinephrine (5 μg/ml). Preliminary data from Chinese patients treated with ribavirin for hemorrhagic fever with renal syndrome also reveal no evidence of drug-induced platelet dysfunction as indicated by normal aggregation and release reactions to collagen (3 μg/ml) and ADP (10 μM/ml). Bone marrow studies of megakaryocyte number and ploidy are presently underway to further characterize drug-associated thrombocytosis
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Paixão, Vitória da, Juliana De Melo Batista Dos Santos, Ewin Barbosa Almeida, Tamaris Roseira Dos Reis Pavão, and André Luis Lacerda Bachi. "A SUPLEMENTAÇÃO COM L-GLUTAMINA MODULA O PERFIL DE CITOCINAS NA MUCOSA DAS VIAS AÉREAS EM RESPOSTA À VACINAÇÃO CONTRA O VIRUS INFLUENZA EM IDOSOS." In II Congresso Brasileiro de Ciências Biológicas On-line. Revista Multidisciplinar de Educação e Meio Ambiente, 2021. http://dx.doi.org/10.51189/rema/1291.

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Introdução: A glutamina tem mostrado ser capaz de melhorar imunidade. Contudo, sua ação na resposta imune das vias aéreas superiores em idosos necessita de esclarecimentos. Objetivo: Deste modo, nosso objetivo foi avaliar o efeito da suplementação de L-glutamina na resposta inflamatória presente na mucosa das vias aéreas de idosos vacinados contra o vírus Influenza. Material e métodos: Foram coletas amostras de saliva de 83 idosos fisicamente ativos, em dois momentos, antes (pré) e após 30 dias (pós) a vacinação para o vírus Influenza e também suplementação com L-glutamina (Gln, n=42) ou placebo (PL, n=41). Resultados: No grupo Gln foram observados maiores níveis salivares de interleucina (IL) -17 pós-vacinação em comparação aos valores encontrados pré-vacinação e no grupo PL pós-vacinação. Além disso, maiores níveis salivares de IL-6 e IL-10 foram vistos pós-vacinação no grupo Gln, em contrapartida aos menores níveis de IL-37 pós-vacinação, em ambos os grupos, em relação aos valores anteriores. Já os níveis de TNF-α permaneceram inalterados. Em ambos os grupos, tanto pré como pós-vacinação, foram encontradas correlações positivas entre IL-6 e IL-10, além da IL-17 com a IL-6 ou com a IL-10 no grupo Gln pós-vacinação. Uma correlação negativa entre IL-37 e IL-10 foi encontrada pré e pós-vacinação no grupo PL. Conclusão: A suplementação de Gln modula a resposta da imunidade da mucosa, aumentando não só a resposta Th2, que induz a diferenciação de células B imaturas em plasmócitos secretores de IgA, como também o perfil Th17, que tem como característica aumentar a proteção da mucosa por também poder induzir a produção e liberação de IgAs. Diante dos nossos dados, podemos sugerir que a suplementação com glutamina modula a resposta inflamatória da mucosa das vias aéreas e isto pode impactar na melhoria da resposta à vacinação contra o vírus Influenza em idosos.
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Ribeiro, Camilla, Katrini Martinelli, Vinícius Mello, Natália Dias, Oscar Araújo, Lia Ximenez, and Vanessa Paula. "Genetic variability of hepatitis B virus: influence on the course of infection in patients with acute and chronic hepatitis B." In International Symposium on Immunobiological. Instituto de Tecnologia em Imunobiológicos, 2021. http://dx.doi.org/10.35259/isi.2021_46590.

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Kaptelova, V. V., A. S. Speranskaya, A. E. Samoilov, A. V. Valdokhina, V. P. Bulanenko, E. V. Korneenko, O. Y. Shipulina, and V. G. Akimkin. "MUTATIONS IN THE GENOMES OF SARS-COV-2 FROM CLINICAL SAMPLES OBTAINED IN LATE MARCH-EARLY APRIL FROM PATIENTS IN MOSCOW." In Molecular Diagnostics and Biosafety. Federal Budget Institute of Science 'Central Research Institute for Epidemiology', 2020. http://dx.doi.org/10.36233/978-5-9900432-9-9-147.

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Many papers suggested that D614G mutation in the viral spike (S) protein SARS-CoV-2 can influence the ability of virus transmission. In recent work [1], it was shown D614G influences the rate of disease transmission only in combination with the P323L mutation in the viral polymerase. We have sequenced 28 full genomes of SARS-CoV-2, obtained from clinical material from patients of different ages. The analyzed isolates belong to clades B.1 (GH) and B1.1 (GR). Combinations of mutations P323L and D614G were found in all genomes. These differences can be explained by sampling: the samples for the sequencing of the whole genome were selected with high viral load, it can be related to the rate of viral replication in intra-host. That, in turn, can be dependent on the presence of P323L/D614G mutations in the virus genome.
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Di Giamberardino, Paolo, Flavia Forconi, Daniela Iacoviello, Erika Pezzella, and Alessandra Pizzuti. "The influence of the choice of the cost index on the effectiveness of optimal resources allocation strategies for Hepatitis B Virus treatment." In 2019 18th European Control Conference (ECC). IEEE, 2019. http://dx.doi.org/10.23919/ecc.2019.8795613.

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