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Academic literature on the topic 'Virus Physiological Phenomena'
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Journal articles on the topic "Virus Physiological Phenomena"
1
Abedon, Stephen T. "Phage Therapy: Eco-Physiological Pharmacology." Scientifica 2014 (2014): 1–29. http://dx.doi.org/10.1155/2014/581639.
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Bacterial virus use as antibacterial agents, in the guise of what is commonly known as phage therapy, is an inherently physiological, ecological, and also pharmacological process. Physiologically we can consider metabolic properties of phage infections of bacteria and variation in those properties as a function of preexisting bacterial states. In addition, there are patient responses to pathogenesis, patient responses to phage infections of pathogens, and also patient responses to phage virions alone. Ecologically, we can consider phage propagation, densities, distribution (within bodies), impact on body-associated microbiota (as ecological communities), and modification of the functioning of body “ecosystems” more generally. These ecological and physiological components in many ways represent different perspectives on otherwise equivalent phenomena. Comparable to drugs, one also can view phages during phage therapy in pharmacological terms. The relatively unique status of phages within the context of phage therapy as essentially replicating antimicrobials can therefore result in a confluence of perspectives, many of which can be useful towards gaining a better mechanistic appreciation of phage therapy, as I consider here. Pharmacology more generally may be viewed as a discipline that lies at an interface between organism-associated phenomena, as considered by physiology, and environmental interactions as considered by ecology.
2
Jauhari, Mujahid Shiroth Rasyid, and Hanif Achmad Rasyid Jauhari. "PHENOMENA OF WORK FROM HOME POLICY IN DEALING WITH THE COVID-19 PANDEMIC." Journal of Public Administration 1, no. 2 (October 30, 2022): 43–52. http://dx.doi.org/10.61317/jc.v1i2.16.
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This scientific paper discusses the phenomenon of public policy, namely the policy of working from home (Work From Home) due to the co-19 pandemic. The author's purpose in choosing this title is because the Covid-19 pandemic is not only about health problems or prolonged transmission of the virus which results in death, but also about service, physiological, communication, psychological problems, and the tendency to overuse gadgets. This policy that has been regulated by the government by working from home (Work From Home) is in order to reduce cases of contracting the Covid-19 virus and can reduce the death rate which continues to grow, other policies regulated by the government also require every citizen to take vaccinations. Of course the work from home policy has advantages and disadvantages in several aspects of life and work. This scientific work seeks to provide an analysis of the Work From Home phenomenon during the Covid-19 pandemic. The Covid-19 pandemic has brought major changes to all levels of society in various aspects, including the socio-cultural aspects. The Covid-19 pandemic forced restrictions on social activities between individuals, giving rise to habits that were different from their previous lives. In other words, this pandemic has given rise to a new societal culture to respond to existing policies of limiting social activities. The results of the author's analysis, the Covid-19 pandemic is still happening today.
3
Voisset, Cécile, Anne Op de Beeck, Pauline Horellou, Marlène Dreux, Thierry Gustot, Gilles Duverlie, François-Loic Cosset, Ngoc Vu-Dac, and Jean Dubuisson. "High-density lipoproteins reduce the neutralizing effect of hepatitis C virus (HCV)-infected patient antibodies by promoting HCV entry." Journal of General Virology 87, no. 9 (September 1, 2006): 2577–81. http://dx.doi.org/10.1099/vir.0.81932-0.
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The neutralizing activity of anti-hepatitis C virus (HCV) antibodies is attenuated by a factor present in human sera, which has been proposed to be high-density lipoproteins (HDLs). HDLs have also been shown to facilitate the entry of HCV pseudoparticles (HCVpp) into target cells. Here, the aim of the study was to determine whether HDL-mediated facilitation of HCVpp and infectious HCV (HCVcc) entry and attenuation of neutralization are two related phenomena. The data indicated that HDLs attenuate neutralization at a constant rate. In addition, as for HDL-mediated facilitation of HCVpp entry, attenuation of neutralization depended on the expression of the scavenger receptor BI (SR-BI) and its selective lipid-uptake function. Finally, kinetic experiments showed that HDL-mediated facilitation of HCVpp entry is more rapid than virus neutralization. Altogether, these observations indicate that HCV is exploiting the physiological activity of SR-BI for promoting its entry into target cells, which consequently also protects the virus against neutralizing antibodies.
4
Sultana, Sonia, and Tawhida Jahan. "Physiological Effects of Pandemic COVID-19 On Children With Autism Spectrum Disorder In Bangladesh." Social Science Review 38, no. 1 (January 28, 2022): 203–16. http://dx.doi.org/10.3329/ssr.v38i1.56531.
Full textAbstract:
Novel Coronavirus (Covid-19) pandemic is considered as the most challenging and life-threatening condition in today’s world. It has been evident that children with autism spectrum disorder (ASD) face double challenge during the pandemic situation due to disrupted routine and unavailability of therapy resulting in some new adopted physiological symptoms that increases the risk of getting infected with corona virus. So, this study aims to find out the nature and causes of the physiological effects of Covid 19 pandemic on children with autism and at the same time suggest taking the proper action regarding these physiological phenomena reducing the of rate of vulnerability. The participants of this study are the parents and the therapists of the children (age range: 5-15 years) with ASD who have been chosen purposefully from Dhaka and Chattogram divisions, Bangladesh. Data has been collected from the participants with the questionnaire and focus group discussion tools through online platform zoom cloud. Results demonstrates that most of the children have an increase in body weight, reduced energy burning, and sleep disturbances since lockdown started that further worsen their hyperactivity suggesting the necessity of acting for the awareness of parents group and thus prevention of covid-19 among children with ASD. Social Science Review, Vol. 38(1), June 2021 Page 203-216
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Stoltz, Kyle, Tatyana Golovkina, and Vera Tarakanova. "Non-classical major histocompatibility factor H2-O counteracts gammaherpesvirus manipulation of the germinal center response." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 126.35. http://dx.doi.org/10.4049/jimmunol.208.supp.126.35.
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Abstract Gammaherpesviruses, such as Epstein Barr virus, infect 95% of adults and form lifelong infection primarily through manipulation of B cells. During primary infection, gammaherpesviruses establish latent infections within B cells and drive robust, polyclonal germinal center (GC) responses, which atypically include B cells specific to both viral and self antigens. Consequently, this humoral response results in production of both autoantibodies, and interestingly, antibodies reactive to antigens of non-human species. While this non-physiological production of antibodies suggests viral manipulation of immune tolerance, the underlying mechanisms driving these phenomena are poorly understood. Utilizing murine gammaherpesvirus 68 (MHV68), a rodent pathogen highly similar to EBV which serves as an animal model of EBV infection, we have discovered that the host factor H2-O (HLA-DO in humans) attenuates MHV68 latency establishment and the MHV68 driven GC response. H2-O acts as an inhibitor of H2-M (HLA-DM), the protein which regulates peptide exchange and thus the repertoire of peptides associated with the MHC-II peptide binding groove. We found that mice deficient in H2-O displayed increased MHV68 latent reservoirs, increased GC response, and a selective increase in dsDNA specific IgG, with no change in virus specific IgG at the peak of latent viral infection. These results show a novel role of H2-O in attenuating the non-physiological, self-directed B cell response driven by MHV68. Furthermore, these studies are the first to demonstrate that fine tuning of MHC-II antigen presentation is sufficient to alter the self-directed B cell differentiation usurped by a ubiquitous viral pathogen during establishment of life-long infection.
6
Morikawa, Yuko, Toshiyuki Goto, Daisuke Yasuoka, Fumitaka Momose, and Tetsuro Matano. "Defect of Human Immunodeficiency Virus Type 2 Gag Assembly in Saccharomyces cerevisiae." Journal of Virology 81, no. 18 (July 3, 2007): 9911–21. http://dx.doi.org/10.1128/jvi.00027-07.
Full textAbstract:
ABSTRACT We have previously shown that the expression of human immunodeficiency virus type 1 (HIV-1) Gag protein in Saccharomyces cerevisiae spheroplasts produces Gag virus-like particles (VLPs) at the plasma membrane, indicating that yeast has all the host factors necessary for HIV-1 Gag assembly. Here we expand the study by using diverse primate lentiviral Gags and show that yeast does not support the production of HIV-2 or simian immunodeficiency virus SIVmac Gag VLPs but allows the production of SIVagm and SIVmnd Gag VLPs. Particle budding was observed at the surfaces of cells expressing SIVagm and SIVmnd Gags, but cells expressing HIV-2 and SIVmac Gags showed only membrane-ruffling structures, although they were accompanied with electron-dense submembrane layers, suggesting arrest at an early stage of particle budding. Comparison of HIV-1 and HIV-2 Gag expression revealed broadly equivalent levels of intracellular Gag expression and Gag N-terminal myristoylation in yeast. Both Gags showed the same membrane-binding ability and were incorporated into lipid raft fractions at a physiological concentration of salt. HIV-2 Gag, however, failed to form a high-order multimer and easily dissociated from the membrane, phenomena which were not observed in higher eukaryotic cells. A series of chimeric Gags between HIV-1 and HIV-2 and Gag mutants with amino acid substitutions revealed that a defined region in helix 2 of HIV-2 MA (located on the membrane-binding surface of MA) affects higher-order Gag assembly and particle production in yeast. Together, these data suggest that yeast may lack a host factor(s) for HIV-2 and SIVmac Gag assembly.
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Desai, Nisarg, Pawel Fedurek, Katie Slocombe, Adam Clark Arcadi, Lisa O'Bryan, Charlotte Uhlenbroek, and Michael Wilson. "Acoustic properties of chimpanzee pant-hoots reflect male mate quality." Journal of the Acoustical Society of America 153, no. 3_supplement (March 1, 2023): A186. http://dx.doi.org/10.1121/10.0018605.
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Sexual selection theory predicts that acoustic structure may provide cues of individual traits correlated with mate quality. Chimpanzee pant-hoots are complex, conspicuous calls that may be products of sexual selection. Insofar as pant-hoots are difficult to produce, requiring individuals to approach their physiological limits of sound production, they may serve as honest signals of physical condition. The highest pitch elements in pant-hoots appear the most difficult elements to produce, as they sometimes exhibit distortions in acoustic structure known as non-linear phenomena (NLP). Producing high pitch vocalizations with fewer NLPs may, thus, signal superior physical condition. We examined whether the proportion of NLPs, the pitch, and noise in these elements of the pant-hoots contain cues of mate quality including age, rank, and a measure of health (infection with the simian immunodeficiency virus, SIVcpz), and if they predict male mating success. Consistent with predictions from sexual selection, we found that (i) the proportion of NLPs was associated with age in a non-linear fashion—specifically, subadult and old males exhibited higher proportions of NLPs compared to males in their prime mating age; (ii) a lower proportion of NLPs predicted higher mating success; and (iii) SIVcpz positive individuals exhibited more noise in their pant-hoots.
8
Fang, Shaozhong, Mi Lin, Muhammad Moaaz Ali, Yiping Zheng, Xiaoyan Yi, Shaojuan Wang, Faxing Chen, and Zhimin Lin. "LhANS-rr1, LhDFR, and LhMYB114 Regulate Anthocyanin Biosynthesis in Flower Buds of Lilium ‘Siberia’." Genes 14, no. 3 (February 23, 2023): 559. http://dx.doi.org/10.3390/genes14030559.
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The bulb formation of Lilium is affected by many physiological and biochemical phenomena, including flower bud differentiation, starch and sucrose accumulation, photoperiod, carbon fixation, plant hormone transduction, etc. The transcriptome analysis of flower buds of Lilium hybrid ‘Siberia’ at different maturity stages showed that floral bud formation is associated with the accumulation of anthocyanins. The results of HPLC-MS showed that cyanidin is the major anthocyanin found in Lilium ‘Siberia’. Transcriptome KEGG enrichment analysis and qRT-PCR validation showed that two genes related to flavonoid biosynthesis (LhANS-rr1 and LhDFR) were significantly up-regulated. The functional analysis of differential genes revealed that LhMYB114 was directly related to anthocyanin accumulation among 19 MYB transcription factors. Furthermore, the qRT-PCR results suggested that their expression patterns were very similar at different developmental stages of the lily bulbs. Virus-induced gene silencing (VIGS) revealed that down-regulation of LhANS-rr1, LhDFR, and LhMYB114 could directly lead to a decrease in anthocyanin accumulation, turning the purple phenotype into a white color. Moreover, this is the first report to reveal that LhMYB114 can regulate anthocyanin accumulation at the mature stage of lily bulbs. The accumulation of anthocyanins is an important sign of lily maturity. Therefore, these findings have laid a solid theoretical foundation for further discussion on lily bulb development in the future.
9
Bogdanova, Simona, Tanya Shivacheva, Tsvetoslav Georgiev, and Petar Petrov. "Pain in COVID-19 and features of pathogenetic molecular mechanisms." Rheumatology (Bulgaria) 30, no. 4 (March 6, 2023): 28–33. http://dx.doi.org/10.35465/30.4.2022.pp28-33.
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Although it has been almost three years since the World Health Organization (WHO) declared a pandemic, COVID-19 is still an unsolved problem, thereby attracting great scientific interest. The disease has a heterogeneous clinical picture with multiple manifestations from different organs and systems. Currently, COVID-19 is perceived as a polysyndromic inflammatory disease involving not only the respiratory system, but also the musculoskeletal system, the cardiovascular system, the skin, the excretory and the nervous system, and is accompanied by a number of hematological, gastrohepatoenterological and endocrine disorders. Various pain phenomena also appear in the clinical presentation of the disease, often as a single manifestation or in combination with symptoms from different organs and systems. The pathogenesis of pain is complex and there is still no consensus on the exact driving mechanisms. Several different signaling pathways play an important role in the generation of pain impulses and perception. They are different for different types of pain. At this stage, the role of angiotensin-converting enzyme 2 (ACE), the renin-angiotensin system (RAC), angiotensin 2 receptors (AT2R), direct neuronal invasion of the virus, the involvement of pro-inflammatory cytokines, hypoxia, the involvement of macrophages, is discussed. as well as the role of overactivity of the immune system, causing the so-called "cytokine storm". Pain is the result of complex biochemical processes influenced to varying degrees by biological, physiological and social factors. Our knowledge at this stage remains scarce and is the subject of many studies on the key pathogenic mechanisms. Therefore, the purpose of this review is to describe the known mechanisms for the occurrence and persistence of pain in patients with COVID-19, as well as to classify the pain phenomena and present its most common localizations. The diagnosis and treatment of COVID-19 and associated pain should be carried out by a multidisciplinary team of specialists, given the heterogeneous clinical presentation of the disease.
10
Petković, Marijana, and Radmila Metlaš. "Cross -Reactivity of the V3-Specific Antibodies with the Human C1q." Zeitschrift für Naturforschung C 56, no. 11-12 (December 1, 2001): 1135–43. http://dx.doi.org/10.1515/znc-2001-11-1235.
Full textAbstract:
Abstract It has been previously shown that the sequence similarity between a portion of the envelope glycoprotein 120 (gp120) from the human immunodeficiency virus type-1 (HIV-1) and several types of human collagen and collagen-like molecules exists. That observation led to the suggestion that the antibodies against the third hypervariable region (V3) of HIV-1 gpl20 (V3-specific antibodies) might have a role in the autoimmune phenomena observed in HIV-infected persons. In this study we have examined the cross-reactivity of the V3-specific anti bodies purified from sera of HIV-infected individuals, sera obtained from the rheumatoid arthritis and systemic lupus erythematosus patients, as well as from the sera of healthy volun teers with the separate chains of a subcomponent of the first component of the human com plement system, C1q. Our results show that the V3-specific antibodies are present in the sera of the HIV-infected individuals, patients suffering of the systemic autoimmune diseases as well as in the sera of healthy volunteers. Whereas these antibodies appeared in the HIV+-sera after antigen challenge, those present in the H IV --sera probably represent the antibod ies that are cross-reactive with the antigen. V3-reactive antibodies can be purified by affinity chromatography and they were highly specific for the V3-peptide. Additionally, they showed cross-reactivity with the separate chains of the human C1q as well as with the chicken colla gen type VI. Possible physiological implications are discussed.
Dissertations / Theses on the topic "Virus Physiological Phenomena"
1
Kaminski, John J. III. "Suppressive Oligodeoxynucleotides Inhibit Cytosolic DNA Sensing Pathways: A Dissertation." eScholarship@UMMS, 2013. https://escholarship.umassmed.edu/gsbs_diss/669.
Full textAbstract:
The innate immune system provides an essential first line of defense against infection. Innate immune cells detect pathogens through several classes of Pattern Recognition Receptors (PRR) allowing rapid response to a broad spectrum of infectious agents. Activated receptors initiate signaling cascades that lead to the production of cytokines, chemokines and type I interferons all of which are vital for controlling pathogen load and coordinating the adaptive immune response. Detection of nucleic acids by the innate immune system has emerged as a mechanism by which infection is recognized. Recognition of DNA is complex, influenced by sequence, structure, covalent modification and subcellular localization.
Interestingly certain synthetic oligodeoxynucleotides comprised of the TTAGGG motif inhibit proinflammatory responses in a variety of disease models. These suppressive oligodeoxynucleotides (sup ODN) have been shown to directly block TLR9 signaling as well as prevent STAT1 and STAT4 phosphorylation. Recently AIM2 has been shown to engage ASC and assemble an inflammasome complex leading to the caspase-1-dependent maturation of IL-1β and IL-18. The AIM2 inflammasome is activated in response to cytosolic dsDNA and plays an important role in controlling replication of murine cytomegalovirus (MCMV). In the second chapter of this thesis, a novel role for the sup ODN A151 in inhibiting cytosolic nucleic acid sensing pathways is described. Treatment of dendritic cells and macrophages with the A151 abrogated type I IFN, TNF-α and ISG induction in response to cytosolic dsDNA. A151 also reduced INF-β and TNF-α induction in BMDC and BMDM responding to the herpesviruses HSV-1 and MCMV but had no effect on the responses to LPS or Sendai virus. In addition, A151 abrogated caspase-1-dependent IL-1β and IL-18 maturation in dendritic cells stimulated with dsDNA and MCMV. Although inhibition of interferon-inducing pathways and inflammasome assembly was dependent on backbone composition, sequence differentially affected these pathways. While A151 more potently suppressed the AIM2 inflammasome, a related construct C151, proved to be a more potent inhibitor of interferon induction. A151 suppressed inflammasome signaling by binding to AIM2 and competing with immune-stimulatory DNA. The interaction of A151 and AIM2 prevented recruitment of the adapter ASC and assembly of the macromolecular inflammasome complex. Collectively, these findings reveal a new route by which suppressive ODNs modulate the immune system and unveil novel applications for suppressive ODNs in the treatment of infectious and autoimmune diseases.
The innate immune response to HSV-1 infection is critical for controlling early viral replication and coordinating the adaptive immune response. The cytokines IL-1β and IL-18 are important effector molecules in the innate response to HSV-1 in vivo. However, the PRRs responsible for the production and maturation of these cytokines have not been fully defined. In the third chapter of this thesis, The TLR2-MyD88 pathway is shown to be essential for the induction of pro-IL-1β transcription in dendritic cells and macrophages responding to HSV-1. The HSV-1 immediate-early protein ICP0 has previously been shown to block TLR2 responses and in keeping with this finding, ICP0 blocked pro-IL-1β expression. Following translation, pro-IL-1β exists as an inactive precursor that must be proteolytically cleaved by a multiprotein complex known as the inflammasome to yield its active form. Inflammasomes are composed of cytoplasmic receptors such as NLRP3 or AIM2, the adapter molecule ASC, and pro-caspase-1. In the present study we found that the NLRP3 inflammasome is important for maturation of IL-1β in macrophages and dendritic cells responding to HSV-1. In contrast the related NLRP12 protein controls IL-1β production in neutrophils. These data indicate that sensing of HSV-1 by TLR2 drives pro-IL-1β transcription and infection activates the inflammasome to mature this cytokine. Moreover, these studies reveal cell type-specific roles for NLRP3 and NLRP12 in inflammasome assembly.
2
Kaminski, John J. III. "Suppressive Oligodeoxynucleotides Inhibit Cytosolic DNA Sensing Pathways: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/669.
Full textAbstract:
The innate immune system provides an essential first line of defense against infection. Innate immune cells detect pathogens through several classes of Pattern Recognition Receptors (PRR) allowing rapid response to a broad spectrum of infectious agents. Activated receptors initiate signaling cascades that lead to the production of cytokines, chemokines and type I interferons all of which are vital for controlling pathogen load and coordinating the adaptive immune response. Detection of nucleic acids by the innate immune system has emerged as a mechanism by which infection is recognized. Recognition of DNA is complex, influenced by sequence, structure, covalent modification and subcellular localization.
Interestingly certain synthetic oligodeoxynucleotides comprised of the TTAGGG motif inhibit proinflammatory responses in a variety of disease models. These suppressive oligodeoxynucleotides (sup ODN) have been shown to directly block TLR9 signaling as well as prevent STAT1 and STAT4 phosphorylation. Recently AIM2 has been shown to engage ASC and assemble an inflammasome complex leading to the caspase-1-dependent maturation of IL-1β and IL-18. The AIM2 inflammasome is activated in response to cytosolic dsDNA and plays an important role in controlling replication of murine cytomegalovirus (MCMV). In the second chapter of this thesis, a novel role for the sup ODN A151 in inhibiting cytosolic nucleic acid sensing pathways is described. Treatment of dendritic cells and macrophages with the A151 abrogated type I IFN, TNF-α and ISG induction in response to cytosolic dsDNA. A151 also reduced INF-β and TNF-α induction in BMDC and BMDM responding to the herpesviruses HSV-1 and MCMV but had no effect on the responses to LPS or Sendai virus. In addition, A151 abrogated caspase-1-dependent IL-1β and IL-18 maturation in dendritic cells stimulated with dsDNA and MCMV. Although inhibition of interferon-inducing pathways and inflammasome assembly was dependent on backbone composition, sequence differentially affected these pathways. While A151 more potently suppressed the AIM2 inflammasome, a related construct C151, proved to be a more potent inhibitor of interferon induction. A151 suppressed inflammasome signaling by binding to AIM2 and competing with immune-stimulatory DNA. The interaction of A151 and AIM2 prevented recruitment of the adapter ASC and assembly of the macromolecular inflammasome complex. Collectively, these findings reveal a new route by which suppressive ODNs modulate the immune system and unveil novel applications for suppressive ODNs in the treatment of infectious and autoimmune diseases.
The innate immune response to HSV-1 infection is critical for controlling early viral replication and coordinating the adaptive immune response. The cytokines IL-1β and IL-18 are important effector molecules in the innate response to HSV-1 in vivo. However, the PRRs responsible for the production and maturation of these cytokines have not been fully defined. In the third chapter of this thesis, The TLR2-MyD88 pathway is shown to be essential for the induction of pro-IL-1β transcription in dendritic cells and macrophages responding to HSV-1. The HSV-1 immediate-early protein ICP0 has previously been shown to block TLR2 responses and in keeping with this finding, ICP0 blocked pro-IL-1β expression. Following translation, pro-IL-1β exists as an inactive precursor that must be proteolytically cleaved by a multiprotein complex known as the inflammasome to yield its active form. Inflammasomes are composed of cytoplasmic receptors such as NLRP3 or AIM2, the adapter molecule ASC, and pro-caspase-1. In the present study we found that the NLRP3 inflammasome is important for maturation of IL-1β in macrophages and dendritic cells responding to HSV-1. In contrast the related NLRP12 protein controls IL-1β production in neutrophils. These data indicate that sensing of HSV-1 by TLR2 drives pro-IL-1β transcription and infection activates the inflammasome to mature this cytokine. Moreover, these studies reveal cell type-specific roles for NLRP3 and NLRP12 in inflammasome assembly.
Books on the topic "Virus Physiological Phenomena"
1
Shors, Teri. Understanding viruses. 2nd ed. Burlington, MA: Jones & Bartlett Learning, 2013.
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3
W, Compans Richard, Helenius Ari, and Oldstone Michael B. A, eds. Cell biology of virus entry, replication, and pathogenesis: Proceedings of a Glaxo-UCLA Symposium held at Taos, New Mexico, February 28-March 5, 1988. New York: A.R. Liss, 1989.
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4
Bailer, Susanne M., and Diana Lieber. Virus-host interactions: Methods and protocols. New York: Humana Press, 2013.
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5
Wah, Chiu, Burnett Roger M, and Garcea Robert L, eds. Structural biology of viruses. New York: Oxford University Press, 1997.
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6
Agbandje-McKenna, Mavis, and McKenna Robert. Structural virology. Cambridge: RSC Publishing, 2011.
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7
Heinz, Feldmann, and Klenk H. D. 1938-, eds. Ebola and Marburg viruses: Molecular and cellular biology. Wymondham, Norfolk, U.K: Horizon Bioscience, 2004.
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8
Michaela, Kendall, Rehfeldt Florian, and SpringerLink (Online service), eds. Adhesion of Cells, Viruses and Nanoparticles. Dordrecht: Springer Science+Business Media B.V., 2011.
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9
M, Hardy Leslie, and Institute of Medicine (U.S.). Committee on Prenatal and Newborn Screening for HIV Infection., eds. HIV screening of pregnant women and newborns. Washington, D.C: National Academy Press, 1991.
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