Bibliografías temáticas / Viral infection

Literatura académica sobre el tema "Viral infection"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 18 de mayo de 2024

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Artículos de revistas sobre el tema "Viral infection"

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Kumar, Rajiv y Fatemeh Mohammadipanah. "Nanomedicine, Viral Infection and Cytokine Stor". International Journal of Clinical Case Reports and Reviews 8, n.º 4 (30 de septiembre de 2021): 01–03. http://dx.doi.org/10.31579/2690-4861/156.

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Recently, emerged outbreaks of various viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), MERS-CoV, and ZIKA infections, are fatal for human life. These life-threatening infections to public health pointed out as a major cause responsible for initiating severe diseases globally. These viral infections heightened the morbidity rates and thus, it is a deadly fear to human life. Researchers left no stone unturned for searching newer therapeutic targets and remedies to treat these viral infections and outbreaks. Simultaneously, some of the researchers have gained success in the discovery of an efficient treatment and development of an effective vaccine [1]. In view of that, numerous developments have been made for innovating nanotherapies, which can treat viral infection and few of them are written off as nanomedicine, have been become reality.
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Barroso-González, Jonathan, Laura García-Expósito, Isabel Puigdomènech, Laura de Armas-Rillo, José-David Machado, Julià Blanco y Agustín Valenzuela-Fernández. "Viral infection". Communicative & Integrative Biology 4, n.º 4 (julio de 2011): 398–408. http://dx.doi.org/10.4161/cib.16716.

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Bose, Avirup, Debabrata Saha y Naba K. Gupta. "Viral Infection". Archives of Biochemistry and Biophysics 342, n.º 2 (junio de 1997): 362–72. http://dx.doi.org/10.1006/abbi.1997.0138.

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Saha, Debabrata, Shiyong Wu, Avirup Bose, Nabendu Chatterjee, Arup Chakraborty, Madhumita Chatterjee y Naba K. Gupta. "Viral Infection". Archives of Biochemistry and Biophysics 342, n.º 2 (junio de 1997): 373–82. http://dx.doi.org/10.1006/abbi.1997.0139.

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Han, Mingyuan, Charu Rajput, Tomoko Ishikawa, Caitlin Jarman, Julie Lee y Marc Hershenson. "Small Animal Models of Respiratory Viral Infection Related to Asthma". Viruses 10, n.º 12 (1 de diciembre de 2018): 682. http://dx.doi.org/10.3390/v10120682.

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Respiratory viral infections are strongly associated with asthma exacerbations. Rhinovirus is most frequently-detected pathogen; followed by respiratory syncytial virus; metapneumovirus; parainfluenza virus; enterovirus and coronavirus. In addition; viral infection; in combination with genetics; allergen exposure; microbiome and other pathogens; may play a role in asthma development. In particular; asthma development has been linked to wheezing-associated respiratory viral infections in early life. To understand underlying mechanisms of viral-induced airways disease; investigators have studied respiratory viral infections in small animals. This report reviews animal models of human respiratory viral infection employing mice; rats; guinea pigs; hamsters and ferrets. Investigators have modeled asthma exacerbations by infecting mice with allergic airways disease. Asthma development has been modeled by administration of virus to immature animals. Small animal models of respiratory viral infection will identify cell and molecular targets for the treatment of asthma.
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Uluğ, Mehmet. "A viral infection of the hands: Orf". Journal of Microbiology and Infectious Diseases 03, n.º 01 (1 de marzo de 2013): 41–44. http://dx.doi.org/10.5799/ahinjs.02.2013.01.0078.

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Basmaci, Romain, Philippe Bidet y Stéphane Bonacorsi. "Kingella kingae and Viral Infections". Microorganisms 10, n.º 2 (21 de enero de 2022): 230. http://dx.doi.org/10.3390/microorganisms10020230.

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Kingella kingae (K. kingae) is an oropharyngeal commensal agent of toddlers and the primary cause of osteoarticular infections in 6–23-month-old children. Knowing that the oropharynx of young children is the reservoir and the portal of entry of K. kingae, these results suggested that a viral infection may promote K. kingae infection. In this narrative review, we report the current knowledge of the concomitance between K. kingae and viral infections. This hypothesis was first suggested because some authors described that symptoms of viral infections were frequently concomitant with K. kingae infection. Second, specific viral syndromes, such as hand, foot and mouth disease or stomatitis, have been described in children experiencing a K. kingae infection. Moreover, some clusters of K. kingae infection occurring in daycare centers were preceded by viral outbreaks. Third, the major viruses identified in patients during K. kingae infection were human rhinovirus or coxsackievirus, which both belong to the Picornaviridae family and are known to facilitate bacterial infections. Finally, a temporal association was observed between human rhinovirus circulation and K. kingae infection. Although highly probable, the role of viral infection in the K. kingae pathophysiology remains unclear and is based on case description or temporal association. Molecular studies are needed.
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Schabert, Vernon F., Essy Mozaffari, Yi-Chien Lee y Roman Casciano. "Double-Stranded DNA (dsDNA) Viral Infections Among Allogeneic Hematopoietic Cell Transplant (HCT) Recipients in the First Year after Transplant". Blood 126, n.º 23 (3 de diciembre de 2015): 3296. http://dx.doi.org/10.1182/blood.v126.23.3296.3296.

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Abstract Introduction: Double-stranded DNA (dsDNA) viral infections (including cytomegalovirus, adenoviruses, BK virus, and Epstein-Barr virus) can lead to significant morbidity and mortality among immunocompromised patients following allogeneic hematopoietic stem cell transplant (HCT). The lack of a broad-spectrum antiviral with the safety and tolerability to prevent viral infections poses management challenges for patients at risk of multiple dsDNA viral infections. Using a large US insurance claims database, this study describes the incidence of dsDNA viral infections and co-infections among allogeneic HCT recipients. Methods: The MarketScan Research Databases were used to identify commercial and Medicare enrollees with an ICD-9 or CPT procedure code for an allogeneic HCT between 7/1/2009 and 6/30/2014. Eligible patients were required to have 365 days of health plan enrollment prior to HCT, but no minimum enrollment was required post-HCT. Incidence of cytomegalovirus (CMV), adenovirus (AdV), BK virus, Epstein-Barr virus, herpes simplex, varicella zoster, and other dsDNA virus infection was measured from the date of the transplant until one year post-transplant. The rates of infection with two dsDNA viral infections or three or more dsDNA viral infections were assessed, and in-hospital mortality or transfer to hospice services within one year of transplant was reported by the number of observed dsDNA viral infection. Results: We identified 3,035 allogeneic HCT patients (mean age 47.3 years, 56.9% male), including 30.4% (n=924) with at least one dsDNA viral infection within the first year post-transplant. Of these, 69.2% had CMV infection (n=639), 5.4% had AdV infection (n=50), and 10.3% had BK virus infection (n=95). Among patients with a reported dsDNA viral infection, 17.6% (n=163) had more than one dsDNA viral infection, including 14.6% (n=135) with two dsDNA viral infections and 3.0% (n=28) with three or more viral infections. A statistically significant increase in the rate of in-hospital death or transfer to hospice within the first year post-transplant was observed for patients with reported dsDNA viral infection vs those without. Specifically, the rate of in-hospital mortality/transfer to hospice increased from 14.9% (315/2111) for patients without a reported dsDNA viral infection to 19.2% (146/761, p=0.0060) with one dsDNA viral infection, 23.0% (31/135, p=0.0121) for patients with two dsDNA viral infections, and 35.7% (10/28, p=0.0023) for patients with three or more dsDNA viral infections. Conclusions: A substantial proportion of allogeneic HCT recipients with a dsDNA viral infection have two or more dsDNA viral infections. Diagnoses on insurance claims may underestimate true incidence of dsDNA viral infection and co-infection. Mortality risk increases significantly with the number of dsDNA viral infections. Availability of a safe and well-tolerated broad spectrum antiviral for prevention of primary or reactivation infections could potentially reduce the morbidity and mortality associated with dsDNA viral infections and their significant sequelae. Disclosures Schabert: LASER Analytica: Employment. Mozaffari:Chimerix Inc.: Employment, Equity Ownership. Lee:LASER Analytica: Employment. Casciano:LASER Analytica: Employment.
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Cyr, Peggy R. y William Dexter. "Viral Skin Infection". Physician and Sportsmedicine 32, n.º 7 (julio de 2004): 33–38. http://dx.doi.org/10.3810/psm.2004.07.444.

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Dykxhoorn, Derek M. y Judy Lieberman. "Silencing Viral Infection". PLoS Medicine 3, n.º 7 (25 de julio de 2006): e242. http://dx.doi.org/10.1371/journal.pmed.0030242.

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Tesis sobre el tema "Viral infection"

1

Nikin-Beers, Ryan Patrick. "Immunoepidemiological Modeling of Dengue Viral Infection". Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/82924.

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Dengue viral infection is a mosquito-borne disease with four distinct strains, where the interactions between these strains have implications on the severity of the disease outcomes. The two competing hypotheses for the increased severity during secondary infections are antibody dependent enhancement and original antigenic sin. Antibody dependent enhancement suggests that long-lived antibodies from primary infection remain during secondary infection but do not neutralize the virus. Original antigenic sin proposes that T cells specific to primary infection dominate cellular immune responses during secondary infections, but are inefficient at clearing cells infected with non-specific strains. To analyze these hypotheses, we developed within-host mathematical models. In previous work, we predicted a decreased non-neutralizing antibody effect during secondary infection. Since this effect accounts for decreased viral clearance and the virus is in quasi-equilibrium with infected cells, we could be accounting for reduced cell killing and the original antigenic sin hypothesis. To further understand these interactions, we develop a model of T cell responses to primary and secondary dengue virus infections that considers the effect of T cell cross-reactivity in disease enhancement. We fit the models to published patient data and show that the overall infected cell killing is similar in dengue heterologous infections, resulting in dengue fever and dengue hemorrhagic fever. The contribution to overall killing, however, is dominated by non-specific T cell responses during the majority of secondary dengue hemorrhagic fever cases. By contrast, more than half of secondary dengue fever cases have predominant strain-specific T cell responses. These results support the hypothesis that cross-reactive T cell responses occur mainly during severe disease cases of heterologous dengue virus infections. Finally, using the results from our within-host models, we develop a multiscale model of dengue viral infection which couples the within-host virus dynamics to the population level dynamics through a system of partial differential equations. We analytically determine the relationship between the model parameters and the characteristics of the solutions, and find thresholds under which infections persist in the population. Furthermore, we develop and implement a full numerical scheme for our model.
Ph. D.
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2

Nikin-Beers, Ryan Patrick. "Mathematical Modeling of Dengue Viral Infection". Thesis, Virginia Tech, 2014. http://hdl.handle.net/10919/48594.

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In recent years, dengue viral infection has become one of the most widely-spread mosquito-borne diseases in the world, with an estimated 50-100 million cases annually, resulting in 500,000 hospitalizations. Due to the nature of the immune response to each of the four serotypes of dengue virus, secondary infections of dengue put patients at higher risk for more severe infection as opposed to primary infections. The current hypothesis for this phenomenon is antibody-dependent enhancement, where strain-specific antibodies from the primary infection enhance infection by a heterologous serotype. To determine the mechanisms responsible for the increase in disease severity, we develop mathematical models of within-host virus-cell interaction, epidemiological models of virus transmission, and a combination of the within-host and between-host models. The main results of this thesis focus on the within-host model. We model the effects of antibody responses against primary and secondary virus strains. We find that secondary infections lead to a reduction of virus removal. This is slightly different than the current antibody-dependent enhancement hypothesis, which suggests that the rate of virus infectivity is higher during secondary infections due to antibody failure to neutralize the virus. We use the results from the within-host model in an epidemiological multi-scale model. We start by constructing a two-strain SIR model and vary the parameters to account for the effect of antibody-dependent enhancement.
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3

James, Katherine Louise. "Viral genetics of HIV-2 infection". Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:68ba022d-62e4-4cb1-8032-085ea5240b98.

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HIV-2 is a contemporary human retrovirus with the majority of infections localised to West Africa. Both HIV-1 and HIV-2 are able to cause AIDS; however, in contrast to HIV-1 infection, a common outcome following HIV-2 infection (∼ 37% of patients in this study cohort) is long-term non-progression (LTNP), where patients remain aviraemic and asymptomatic in the absence of treatment, often for decades. HIV-1 and HIV-2 both arose following zoonotic transmission of SIVs from non-human primates at around the beginning of the 20th century and when patients develop AIDS caused by HIV-2 infection, it is clinically indistinguishable from AIDS following HIV-1 infection. Whilst the estimated number of HIV-2 infections remains small in the context of the global HIV pandemic (HIV-2 ∼ 2 million, HIV-1 group M ∼75 million), the differences in pathogenicity between these two viruses has been a source of great interest, particularly the features of LTNPs that allow control of viral replication in the absence of anti-retroviral treatment. The studies described in this thesis were carried out using samples collected from a well-characterised longitudinal community cohort in Caió, Guinea-Bissau. Chapter 3 of this thesis presents an investigation into the variation and evolution present in the HIV-2 specific accessory gene vpx. The data showed significantly increased signals of positive selection pressure in vpx in viraemic when compared to non-viraemic patients and also allowed the identification of novel variations at high frequencies (up to 22%) in this cohort that were previously un-described. Chapters 4 and 5 present a novel application of shotgun RNA sequencing (RNA- Seq) to HIV ex vitro and ex vivo samples. Chapter 4 demonstrates the divergence seen in a cultured viral isolate at the level of the whole genome, in the absence of many of the biases typically involved in sequencing of RNA viruses. Chapter 5 further extends this method to show the applicability of using RNA-Seq on primary patient HIV samples for the first time. Analysis of diversity estimates over the whole genome in the context of a low bias sequencing method show a high level of diversity in HIV-2 pol and low diversity in vpx. The aim of this work was to combine traditional and novel sequencing methods to facilitate assessment of the variation and evolution acting on vpx and to generate an accurate picture of the genetic diversity over the whole genome of HIV-2.
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Pruikkonen, H. (Hannele). "Viral infection induced respiratory distress in childhood". Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526207919.

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Abstract Dyspnoea associated with respiratory infection is a common symptom in infancy and early childhood. Inspiratory stridor is the main symptom in cases of croup and expiratory wheezing in cases of bronchiolitis, obstructive bronchitis and acute asthma exacerbations. Dyspnoea associated with respiratory infection is a common cause of emergency department visits and unplanned hospital admissions among infants and preschool children. The assessment of dyspnea associated with acute childhood respiratory infection is largely subjective, and evidence regarding the severity of acute dyspnoea is needed in order to target hospital admissions more accurately. Wheezing associated with respiratory infection in infancy has been recognized as an important predictor of recurrent wheezing and asthma at school age. The aims of this study were to determine the risk factors for croup, to evaluate factors that reliably predict the need for hospitalizing children with acute wheezing and to find out whether respiratory infection with wheezing during infancy has a positive association with the development of asthma during childhood. The work included two register-based surveys and one prospective cohort study. It is concluded that a family history of croup is an exceptionally strong risk factor for croup and its recurrence in childhood. The early phase of bronchiolitis is unstable in infants below 6 months of age. These infants are most likely to need medical interventions in the first 5 days after onset of the disease. A positive respiratory syncytial -virus test result, a fever of more than 38°C and low initial oxygen saturation are predictors of the need for hospitalization and medical interventions. An initial oxygen saturation >93% effectively identifies children aged more than 6 months with mild wheezing, and this limit can be used to avoid unplanned hospital admissions. There is an association between early respiratory syncytial -virus infections and subsequent wheezing and asthma, in that such infections select children who are prone to wheezing and asthma before school age, but the symptoms tend to decrease with time and an early respiratory syncytial -virus infection will not permanently alter bronchial reactivity
Tiivistelmä Hengitysvaikeus on yleinen oire lapsilla virusten aiheuttamien hengitystieinfektioiden yhteydessä. Kurkunpäätulehdukseen liittyy sisäänhengitysvaikeus. Ilmatiehyttulehdukseen, ahtauttavaan keuhkoputkentulehdukseen ja akuuttiin astmakohtaukseen liittyy uloshengitysvaikeus. Hengitystieinfektioihin liittyvä hengitysvaikeus on yksi yleisimmistä syistä päivystyspoliklinikkakäynteihin ja äkillisiin sairaalahoitojaksoihin lapsipotilailla. Hengitystieinfektioiden taudinkulun tuntemisella ja hengitysvaikeuden vaikeusasteen arvioinnilla on tärkeä merkitys näiden potilaiden hoidon toteuttamisessa. Hengitystieinfektioon liittyvää hengitysvaikeutta on pidetty riskitekijänä astman kehittymiselle. Tämän tutkimuksen tarkoituksena oli selvittää kurkunpäätulehduksen riskitekijöitä ja sairaalahoitoon vaikuttavia tekijöitä hengitystieinfektioon liittyvän uloshengitysvaikeuden hoidossa sekä varhaislapsuudessa sairastetun hengitystieinfektion yhteyttä myöhempään astma- ja allergiasairastavuuteen. Tutkimukseen sisältyi kaksi rekisteriaineistoa ja yksi seurantatutkimusaineisto. Tutkimuksessa todettiin, että kurkunpäätulehduksen uusiutuminen on erittäin tavallista ja sisarusten ja vanhempien sairastama kurkunpäätulehdus on merkittävin riskitekijä kurkunpäätulehdukselle ja sen uusiutumiselle. Alle 6 kuukauden ikäisillä lapsilla ilmatiehyttulehduksen taudinkuva on epävakaa ensimmäisen 5 oirepäivän aikana. Kuume, matala happisaturaatioarvo ja respiratory syncytial -virusinfektio ennustavat osastohoidon ja invasiivisten toimenpiteiden tarvetta ilmatiehyttulehduksen yhteydessä. Yli 6 kuukauden ikäisillä lapsilla happisaturaatioarvo > 93 % ennustaa lievää taudinkuvaa hengitystieinfektioon liittyvän uloshengitysvaikeuden hoidossa. Käyttämällä tätä happisaturaatioarvoa raja-arvona, kun arvioidaan sairaalahoidon tarvetta, voidaan merkittävästi ja turvallisesti vähentää sairaalahoidon tarvetta lasten hengitystieinfektioon liittyvän uloshengitysvaikeuden hoidossa. Alle 6 kuukauden iässä sairastettu respiratory syncytial -virusinfektio on riskitekijä varhaislapsuudessa ilmeneville astmaoireille, mutta tämä riski vähenee iän myötä ja 8 vuoden iässä ei ole havaittavissa eroja astma- ja allergiasairastavuudessa, kun verrataan näitä potilaita muun hengitystieinfektion sairastaneisiin potilaisiin ja terveisiin kontrollipotilaisiin
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Howat, Tom James. "Spatial dynamics of in vitro viral infection". Thesis, University of Cambridge, 2007. https://www.repository.cam.ac.uk/handle/1810/252041.

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Despite the importance of the IFNs in viral infections, many questions about the dynamics of IFN production and activity remain unanswered. Addressing these questions forms the first half of this thesis. It begins with an introduction to innate immunity, and a review of existing research. Focus then falls upon a simple experimental system: the in vitro infection of cell monolayers by Herpes simplex virus and the resulting IFN response. A stochastic spatial model of viral infection and consequent IFN production and activity is constructed. Using this model, simulations of infections under varying initial conditions suggest the existence of critical doses, at which the qualitative behaviour of infection changes. Implications for IFN activity in vivo infections are highlighted, as well as potential applications of the model, particularly in within-host modelling. The data used to parameterize this model come from widely used experiments called plaque assays: infection spreads in cell monolayers in vitro, leaving regions of dead cells, known as plaques. The second half of the thesis considers the dynamics of plaque formation and, in particular, the phenomenon of cometing, where in plaques unexpectedly streak across monolayers forming patterns that resemble comets. Several theories behind comet formation have been proposed in the literature, though the underlying mechanism is not understood. A detailed investigation is carried out here: previously voiced hypotheses are tested, and a method for controlling comet formation is developed; cometing is found to be a purely fluid dynamic phenomenon. The thesis concludes with an overview of the results obtained, and a discussion of potential applications and future directions for research.
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Christie, John Michael Landale. "Viral persistence in hepatitis C virus infection". Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268465.

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Zhang, Lei Centre for Vascular Research Faculty of Medicine UNSW. "Understanding viral-immune dynamics in HIV infection". Awarded by:University of New South Wales. Centre for Vascular Research, 2005. http://handle.unsw.edu.au/1959.4/23372.

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The HIV epidemic has caused a health crisis globally. Using mathematical and statistical tools, we have analysed and modelled data from animal models of HIV, HSV and influenza virus, in order to understand the role of neutralising antibodies (nAbs), CD4+ T cells, CTLs and APCs in HIV infection and the implications of this for HIV vaccine design. Our analysis suggests that antibody and CTL responses confer protection at different stages of HIV infection. Passive antibodies confer protection against SHIV89.6PD infection by either neutralising the initial viral inoculum or reducing the acute viral level and growth. Consequently, CD4+ T cell preservation allows the immune system to control long-term disease progression. Therefore, vaccines that elicit high nAb levels during early infection may induce sterilising immunity or delay disease progression. By contrast, we observed that vaccine-elicited CTLs did not proliferate until day 10 following SHIV89.6P infection. More potent CTL-inducing vaccines did not reduce this delay, but further increased it and reduced CTL growth. However, more potent vaccines result in better memory CTL formation, better CD4 preservation and improved disease outcome. HIV vaccine design should aim to reduce the delay in CTL activation. To further understand the pathogenesis of HIV, we investigated the relationship between viral load and CD4+ T cell levels using simple ODE models. Our results demonstrate a positive correlation between peak viral level and the acute CD4+ T cell depletion in SHIV89.6P infection, which demonstrates how reduction of peak viral level significantly preserves CD4+ T cells. Surprisingly, this relationship between virus and CD4+ T cells was reversed in SIVmac239 infection and other CCR5 tropic infections. Future work should focus on understanding this difference between X4 and R5 infections. Regardless of viral infections, antigen presentation is essential for stimulating effective immune responses. Our study on influenza and HSV-1 infections suggests that antigen loading rate of APCs determines the magnitude of antigen presentation and the APC decay is mainly due to the degradation of pMHC, not CTL killing. The slow kinetics of HIV viral growth may be one factor that limits the level of antigen presentation and subsequent CTL response.
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Li, Wei Beck Melinda A. "Nutritionally-induced oxidative stress and viral infection". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,523.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2006.
Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Nutrition." Discipline: Nutrition; Department/School: Public Health.
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Lobbermann, Jens. "Regulation of immunity during viral lung infection". Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.544288.

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Stevens, Kim. "Multiplicity of viral infection in brown algae". Thesis, University of Plymouth, 2014. http://hdl.handle.net/10026.1/3156.

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Brown algae are important primary producers and habitat formers in coastal environments and are believed to have evolved multicellularity independently of the other eukaryotes. The phaeoviruses that infect them form a stable lysogenic relationship with their host via genome integration, but have only been extensively studied in two genera: Ectocarpus and Feldmannia. In this study I aim to improve our understanding of the genetic diversity, host range and distribution of phaeoviruses. Sequencing and phylogenetic analysis of amplified fragments of three core phaeoviral genes (encoding major capsid protein (MCP), DNA polymerase and superfamily III helicase) of phaeovirus infected algae confirmed the suspected phaeoviral identity of viruses infecting E. fasciculatus, F. simplex, Pilayella littoralis, Myriotrichia clavaeformis and Hincksia hincksiae. Furthermore, this approach revealed multiple virus sequence variants within individual strains, and moreover that the variants formed two distinct subgroups. Subgroup A was highly conserved and observed in multiple algal genera, whereas subgroup B was much more diverse, but only found in Feldmannia species. Transcriptome sequencing of an actively infected F. irregularis strain revealed polymorphisms within key viral genes, suggesting that multiple variants were indeed active within this strain. High resolution melt curve (HRM) technology was used to develop a high throughput screening method for detecting phaeoviral MCP as a proxy for detection of phaeoviruses. This technique was also able to assign 88% of those detected to one of the subgroups, based on their differing melting temperature distributions. This was then applied to 1034 Ectocarpus isolates collected from around Europe and South America, and in accordance with previous studies of phaeoviral infection, 43-79% of strains contain virus sequence (depending on species). 17% of the isolates tested even contained sequence from both subgroups. 82 Laminariales strains, close relatives of the Ectocarpales, were also screened because they comprise commercially important kelp species but are not known to be infected by viruses. 10-17% of these tested positive for phaeoviral MCP, which when sequenced formed a separate group within the phaeoviruses. This finding could have a major impact on the kelp farming industry if the viruses are found to affect reproduction as happens in the Ectocarpales. The discovery of two subgroups is contrary to current beliefs that the phaeoviruses are a single monophyletic group, and that each species of alga has its own phaeovirus, casting doubt on the usefulness of the current convention of naming each phaeovirus after its host. It appears that the subgroup B viruses have begun to evolve away from the stable, K-selected subgroup A viruses towards a more r- type strategy with higher mutation and diversification. This study has identified potential mechanisms that may influence this shift, including mutations in a region of the DNA polymerase known to negatively affect DNA replication fidelity, combined with an active integrase and lack of a proofreading exonuclease, along with the observed infection of individuals with both phaeovirusal subgroups. The resulting mutations and recombinations could lead to the diversity observed here, and may provide a suitable model for the study of other emergent virus infections.
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Libros sobre el tema "Viral infection"

1

R, Burton Dennis, ed. Antibodies in viral infection. Berlin: Springer, 2001.

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Burton, Dennis R., ed. Antibodies in Viral Infection. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-662-05783-4.

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Lane, Thomas E., ed. Chemokines and Viral Infection. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/978-3-540-33397-5.

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G, Donders, Stray-Pedersen B y Anteby E, eds. Viral infection in pregnancy. Paris: Elsevier, 2002.

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5

Sherlock, Sheila. Hepatitis C viral infection: An update. Oxford: Blackwell Scientific, 1989.

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Sheila, Sherlock. Hepatitis C viral infection--an update. Oxford: Blackwell Scientific Publications, 1989.

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Pasquier, C., R. Y. Olivier, C. Auclair y Lester Packer, eds. Oxidative Stress, Cell Activation and Viral Infection. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7424-3.

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-M, Andrieu J., Lu Wei, Levy Jean-Paul y Workshop on Viral Quantitation in HIV Infection (1993 : Paris), eds. Workshop on viral quantitation in HIV infection. Philadelphia, PA: Current Science, 1993.

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Raphael, Dolin y Wright Peter F, eds. Viral infections of the respiratory tract. New York: Marcel Dekker, 1999.

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Michael, Glick, ed. Infections, infectious diseases and dentistry. Philadelphia: W.B. Saunders Co., 2003.

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Capítulos de libros sobre el tema "Viral infection"

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Kawamura, Tatsuyoshi. "Viral Infection". En Immunology of the Skin, 295–324. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55855-2_19.

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Davies, Eryl. "Viral Infection". En The Final FFICM Structured Oral Examination Study Guide, 364–67. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003243694-126.

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Widrow, Bernard. "Viral Infection". En Springer Series on Bio- and Neurosystems, 179–87. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-98140-2_17.

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Santoro, M. G. "Viral infection". En Stress-Inducible Cellular Responses, 337–57. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-9088-5_23.

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Tatara, Alexander M. "Viral Infection". En The Infectious Diseases Consult Handbook, 181–211. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-39474-4_8.

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Fahnert, Beatrix y Phoebe Lostroh. "Viral Infection". En Strelkauskas' Microbiology, 295–318. 3a ed. Boca Raton: Garland Science, 2023. http://dx.doi.org/10.1201/9781003191674-16.

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Chen, Feng, Li Li, Yupeng Liu, Wang Fei, Lili Kong, Yinglin Guo, Dan Mu et al. "Viral Infection". En Radiology of Infectious and Inflammatory Diseases - Volume 3, 61–110. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-4614-3_6.

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Kelly, Deirdre A. y C. Y. William Tong. "Neonatal and Pediatric Infection". En Viral Hepatitis, 529–43. Oxford, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118637272.ch39.

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Gooch, Jan W. "Latent Viral Infection". En Encyclopedic Dictionary of Polymers, 903. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14095.

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Gooch, Jan W. "Persistent Viral Infection". En Encyclopedic Dictionary of Polymers, 914. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14463.

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Actas de conferencias sobre el tema "Viral infection"

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Jahn, Kathleen, Desiree Schumann, Michael Tamm, Hans Hirsch, Joerg Halter, Lilian Junker, Werner Strobel, Spasenija Savic y Daiana Stolz. "Respiratory viral infection in immunocompromised patients". En ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4694.

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Li, John Y., Chad R. Morris, Zhi-Qing Qi, Yambasu A. Brewah, Alison A. Humbles, Donna K. Finch, Anthony J. Coyle y Roland Kolbeck. "Viral Infection Modulates Airway Epithelial Responsiveness To Subsequent Bacterial Infection". En 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.a3827.

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Zavitz, CC, GJ Gaschler, CM Bauer, KM Fraser y MR Stampfli. "Chemokine Dysregulation in Heterologous Viral-Bacterial Infection." En American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3254.

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Lin, Yong-Ping y Bo-Jian Zheng. "Inhibitory effect of DNA aptamers binding H5N1 viral nucleoprotein in the viral infection". En XVIth Symposium on Chemistry of Nucleic Acid Components. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2014. http://dx.doi.org/10.1135/css201414413.

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Dida, Lumta, Dhurata Shehu y Thanas Ruci. "The Balkan grape varieties and their viral infection". En The 5th International Virtual Conference on Advanced Scientific Results. Publishing Society, 2017. http://dx.doi.org/10.18638/scieconf.2017.5.1.407.

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Kwak, Hyun Jung, Tae H. Kim, Jang W. Sohn, Ho J. Yoon, Dong H. Shin y Sung S. Park. "The Role Of Viral Infection In COPD Exacerbation". En American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3118.

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Schuh, Andreas, Michael Morimoto, Piotr Kaszuba, Kevin Hammond, Jerry Swan, Krzysztof Krawiec y NL Shasha Jumbe. "Host-directed vibroacoustic biosignature of viral respiratory infection". En 2023 IEEE EMBS International Conference on Biomedical and Health Informatics (BHI). IEEE, 2023. http://dx.doi.org/10.1109/bhi58575.2023.10313464.

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Mozokhina, Anastasia. "Modelling of the Immune Response to Viral Infection". En IOCMA 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/iocma2023-14392.

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LeDuc, Philip R. y Michael J. Betenbaugh. "Implementation of a Pharmocokinetic Approach to a Baculovirus System for Analytic Solutions to Virus and Cell Interactions". En ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0282.

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Abstract The baculovirus, Autographa californica multiple nuclear polyhedrosis virus (AcMNPV), expression system can be employed for a variety of different cellular applications. In recent years, this baculovirus system has been manipulated to serve as a recombinant system for the expression of heterologous proteins and as a possible retrovirus for gene therapy. A quantitative understanding of the cellular mechanics of virus trafficking would be useful in developing viral expression systems, understanding gene therapy and maximizing recombinant protein production. An analytic solution is presented which incorporates a pharmocokinetic system in order to analyze this problem of viral and cellular mechanics. The multiple stages of viral infection systems, specifically for the baculovirus system, include attachment, internalization, endosomal fusion, cytosol transportation, and nuclear accumulation. The effects of the rate parameters are investigated to determine the parameter sensitivity of the viral infection model in relation to accumulation of surface virus, internalized virus and nuclear virus. The concepts from this model can be used to design infection regimens for various cell lines and to analyze the inherent inefficiency of current baculovirus infecting systems. This approach can also be used to determine the effects of the rate-limiting behaviors exhibited by these types of cellular mechanics and can be further implemented to examine other types of infection applications including viral gene therapy [1].
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Krolikowski, K., C. R. Barnett, C. Rodriguez, I. Atandi, P. Pamar, G. Porter, L. N. Segal y S. Brosnahan. "The Proof Is in the Sputum: Untangling Viral Pneumonia From Bacterial Viral Co-infection". En American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4200.

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Informes sobre el tema "Viral infection"

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Meints, Russel H. Mechanisms of Viral Infection in Marine Brown Algae. Fort Belvoir, VA: Defense Technical Information Center, octubre de 1997. http://dx.doi.org/10.21236/ada330610.

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Chejanovsky, Nor, Diana Cox-Foster, Victoria Soroker y Ron Ophir. Honeybee modulation of infection with the Israeli acute paralysis virus, in asymptomatic, acutely infected and CCD colonies. United States Department of Agriculture, diciembre de 2013. http://dx.doi.org/10.32747/2013.7594392.bard.

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Honey bee (Apis mellifera) colony losses pose a severe risk to the food chain. The IAPV (Israeli acute paralysis virus) was correlated with CCD, a particular case of colony collapse. Honey bees severely infected with IAPV show shivering wings that progress to paralysis and subsequent death. Bee viruses, including IAPV, are widely present in honey bee colonies but often there are no pathological symptoms. Infestation of the beehive with Varroa mites or exposure to stress factors leads to significant increase in viral titers and fatal infections. We hypothesized that the honey bee is regulating/controlling IAPV and viral infections in asymptomatic infections and this control is broken through "stress" leading to acute infections and/or CCD. Our aims were: 1. To discover genetic changes in IAPV that may affect tissue tropism in the host, and/or virus infectivity and pathogenicity. 2. To elucidate mechanisms used by the host to regulate/ manage the IAPV-infection in vivo and in vitro. To achieve the above objectives we first studied stress-induced virus activation. Our data indicated that some pesticides, including myclobutanil, chlorothalonil and fluvalinate, result in amplified viral titers when bees are exposed at sub lethal levels by a single feeding. Analysis of the level of immune-related bee genes indicated that CCD-colonies exhibit altered and weaker immune responses than healthy colonies. Given the important role of viral RNA interference (RNAi) in combating viral infections we investigated if CCD-colonies were able to elicit this particular antiviral response. Deep-sequencing analysis of samples from CCD-colonies from US and Israel revealed high frequency of small interfering RNAs (siRNA) perfectly matching IAPV, Kashmir bee virus and Deformed wing virus genomes. Israeli colonies showed high titers of IAPV and a conserved RNAi pattern of targeting the viral genome .Our findings were further supported by analysis of samples from colonies experimentally infected with IAPV. Following for the first time the dynamics of IAPV infection in a group of CCD colonies that we rescued from collapse, we found that IAPV conserves its potential to act as one lethal, infectious factor and that its continuous replication in CCD colonies deeply affects their health and survival. Ours is the first report on the dominant role of IAPV in CCD-colonies outside from the US under natural conditions. We concluded that CCD-colonies do exhibit a regular siRNA response that is specific against predominant viruses associated with colony losses and other immune pathways may account for their weak immune response towards virus infection. Our findings: 1. Reveal that preventive measures should be taken by the beekeepers to avoid insecticide-based stress induction of viral infections as well as to manage CCD colonies as a source of highly infectious viruses such as IAPV. 2. Contribute to identify honey bee mechanisms involved in managing viral infections.
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Wang, Chenxi, John C. Knight y Matthew C. Elder. On Computer Viral Infection and the Effect of Immunization. Fort Belvoir, VA: Defense Technical Information Center, enero de 2005. http://dx.doi.org/10.21236/ada436727.

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Citovsky, Vitaly y Yedidya Gafni. Suppression of RNA Silencing by TYLCV During Viral Infection. United States Department of Agriculture, diciembre de 2009. http://dx.doi.org/10.32747/2009.7592126.bard.

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The Israeli isolate of Tomato yellow leaf curl geminivirus (TYLCV-Is) is a major tomato pathogen, causing extensive (up to 100%) crop losses in Israel and in the south-eastern U.S. (e.g., Georgia, Florida). Surprisingly, however, little is known about the molecular mechanisms of TYLCV-Is interactions with tomato cells. In the current BARD project, we have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing, and showed that V2 interacts with the tomato (L. esculentum) member of the SGS3 (LeSGS3) protein family known to be involved in RNA silencing. This proposal will use our data as a foundation to study one of the most intriguing, yet poorly understood, aspects of TYLCV-Is interactions with its host plants – possible involvement of the host innate immune system, i.e., RNA silencing, in plant defense against TYLCV-Is and the molecular pathway(s) by which TYLCV-Is may counter this defense. Our project sought two objectives: I. Study of the roles of RNA silencing and its suppression by V2 in TYLCV-Is infection of tomato plants. II. Study of the mechanism by which V2 suppresses RNA silencing. Our research towards these goals has produced the following main achievements: • Identification and characterization of TYLCV V2 protein as a suppressor of RNA silencing. (#1 in the list of publications). • Characterization of the V2 protein as a cytoplasmic protein interacting with the plant protein SlSGS3 and localized mainly in specific, not yet identified, bodies. (#2 in the list of publications). • Development of new tools to study subcellular localization of interacting proteins (#3 in the list of publications). • Characterization of TYLCV V2 as a F-BOX protein and its possible role in target protein(s) degradation. • Characterization of TYLCV V2 interaction with a tomato cystein protease that acts as an anti-viral agent. These research findings provided significant insights into (I) the suppression of RNA silencing executed by the TYLCV V2 protein and (II) characterization some parts of the mechanism(s) involved in this suppression. The obtained knowledge will help to develop specific strategies to attenuate TYLCV infection, for example, by blocking the activity of the viral suppressor of gene silencing thus enabling the host cell silencing machinery combat the virus.
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Bates, Paul. Targeted Retroviral Infection of mammary Cells in Viral Receptor Transgenics. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 1998. http://dx.doi.org/10.21236/ada368410.

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Bates, Paul. Targeted Retroviral Infection of Mammary Cells in Viral Receptor Transgenies. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 1997. http://dx.doi.org/10.21236/ada344605.

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Parshin, V. V. y D. A. Lezhnev. Histological data and computed tomography in patients with viral infection. OFERNIO, marzo de 2023. http://dx.doi.org/10.12731/ofernio.2023.25119.

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Banks, H. T., V. A. Bokil, S. Hu, A. Dhar, Bullis K., Bullis R. A., Browdy R. A., Allmutt C. L. y F. C. Modeling Shrimp Biomass and Viral Infection for Production of Biological Countermeasures. Fort Belvoir, VA: Defense Technical Information Center, diciembre de 2005. http://dx.doi.org/10.21236/ada444188.

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Weber, Karrie A., Kelly S. Bender y Yusong Li. Final Technical Report: Viral Infection of Subsurface Microorganisms and Metal/Radionuclide Transport. Office of Scientific and Technical Information (OSTI), septiembre de 2013. http://dx.doi.org/10.2172/1095019.

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Vaughn, James, William M. Balch y James Novotny. Impact of Viral Infection on Absorption and Scattering Properties of Marine Bacteria and Phytoplankton. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 1999. http://dx.doi.org/10.21236/ada630361.

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