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1

Van Loveren, H. "Host resistance models." Human & Experimental Toxicology 14, no. 1 (January 1995): 137–40. http://dx.doi.org/10.1177/096032719501400134.

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2

Dixon, G. R. "Interactions of soil nutrient environment, pathogenesis and host resistance." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S87—S94. http://dx.doi.org/10.17221/10326-pps.

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Host plants and soil borne pathogens that attack them exist within an ecological matrix populated by numerous microbial species that may influence the access of pathogenesis. These events are moderated by physical and chemical components of the soil. The impact of inorganic and organic nutrients on pathogenesis and the development of host resistance are discussed in this review using two host – pathogen combinations as examples. Calcium, boron, nitrogen and pH have been demonstrated to affect the processes of resting spore germination, host invasion and colonisation in the Plasmodiophora brassicae-Brassica combination that results in clubroot disease. Organic nutrients that have associated biostimulant properties have been demonstrated to influence the development of Pythium ultimum-Brassica combination that results in damping-off disease. This latter combination is affected by the presence of antagonistic microbial flora as demonstrated by increased ATP, extra-cellular enzyme and siderophore production. In both examples there are indications of the manner by which host resistance to pathogenesis may be enhanced by changes to the nutrient status surrounding host plants. These effects are discussed in relation to the development of integrated control strategies that permit disease control with minimal environmental impact.
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3

Pink, D. A. C., and P. Hand. "Plant resistance and strategies for breeding resistant varieties." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S9—S14. http://dx.doi.org/10.17221/10310-pps.

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An explanation of the ‘boom-bust’ cycle of resistance breeding was provided by the gene-for-gene relationship between a pathogen and its host. Despite this understanding, most R genes continued to be deployed singly and resistance has been ephemeral. The reasons for breeding ‘single R gene’ varieties are discussed. Alternative strategies for the deployment of R genes and the use of quantitative race non-specific resistance have been advocated in order to obtain durable resistance. The feasibility of both of these approaches is discussed taking into account the impact of technologies such as plant transformation and marker-assisted selection. A change in focus from durability of the plant phenotype to that of the crop phenotype is advocated.
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4

ALLEN, J. R. "Host resistance to ectoparasites." Revue Scientifique et Technique de l'OIE 13, no. 4 (December 1, 1994): 1287–303. http://dx.doi.org/10.20506/rst.13.4.824.

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5

Yancey, Michael K. "HOST DEFENSES AND BACTERIAL RESISTANCE." Obstetrics and Gynecology Clinics of North America 19, no. 3 (September 1992): 413–34. http://dx.doi.org/10.1016/s0889-8545(21)00364-8.

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6

Loria, Roger M. "Neurosteroids and Host Immune Resistance." Advances in Neuroimmune Biology 5, no. 1 (2014): 33–42. http://dx.doi.org/10.3233/nib-140084.

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7

Buu, N., F. Sánchez, and E. Schurr. "The Bcg Host-Resistance Gene." Clinical Infectious Diseases 31, Supplement_3 (September 1, 2000): S81—S85. http://dx.doi.org/10.1086/314067.

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8

Burleson, Gary R., and Florence G. Burleson. "Influenza virus host resistance model." Methods 41, no. 1 (January 2007): 31–37. http://dx.doi.org/10.1016/j.ymeth.2006.09.007.

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9

Giga, D. P. "Host plant resistance to insects." Crop Protection 15, no. 5 (August 1996): 488–90. http://dx.doi.org/10.1016/0261-2194(96)84751-x.

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10

Ponpipom, Mitree M., William K. Hagmann, Laura A. O'Grady, Jesse J. Jackson, David D. Wood, and Hans J. Zweerink. "Glycolipids as host resistance stimulators." Journal of Medicinal Chemistry 33, no. 2 (February 1990): 861–67. http://dx.doi.org/10.1021/jm00164a062.

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11

Bandaranayake, Thilinie, and Albert C. Shaw. "Host Resistance and Immune Aging." Clinics in Geriatric Medicine 32, no. 3 (August 2016): 415–32. http://dx.doi.org/10.1016/j.cger.2016.02.007.

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12

Ablin, Richard J., and John M. Bartkus. "Diethylstilbestrol Effects on Host Resistance." Journal of Leukocyte Biology 37, no. 4 (April 1985): 473–74. http://dx.doi.org/10.1002/jlb.37.4.473.

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13

Gammelgård, E., M. L. Mohan, R. A. Andersson, and J. P. T. Valkonen. "Host gene expression at an early stage of virus resistance induction." Plant Protection Science 38, SI 2 - 6th Conf EFPP 2002 (December 31, 2017): 502–3. http://dx.doi.org/10.17221/10535-pps.

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Suppression subtractive hybridization (SSH) was carried out to detect genes differentially expressed in plants expressing resistance to systemic infection with Potato virus A (PVA), genus Potyvirus. Differential screening has up to now revealed 19 putative differentially expressed genes. Nothern blot hybridization has confirmed the differential expression of seven genes. Three of them were only induced by the virus, but four genes were also wound-induced.
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14

Gorter, F. A., A. R. Hall, A. Buckling, and P. D. Scanlan. "Parasite host range and the evolution of host resistance." Journal of Evolutionary Biology 28, no. 5 (April 23, 2015): 1119–30. http://dx.doi.org/10.1111/jeb.12639.

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15

Chand, Himani. "HOST-PLANT RESISTANCE IN PEST MANAGEMENT." Tropical Agrobiodiversity 2, no. 2 (July 21, 2021): 54–58. http://dx.doi.org/10.26480/trab.02.2021.54.58.

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Host Plant Resistance (HPR) is an effective, economical and eco-friendly method introduced for pest management. The concept of HPR has been emphasized mainly in order to reduce the use of pesticides as it provides opportunities to improve research and extension documentation to assist producers. It can also be taken as an effective tool for sustainable agriculture also focusing over the creation of organic farming where very low doses of pesticides are said to be applied if we can focus over this technology. But still in Nepal, the limitation of germplasm availability and development of biotype that can overcome resistance compared to the developed and other developing countries creates disadvantageous situations to completely depend upon this technology right now. Much interest in biotechnology relative to developing insect-resistant plants is in methods known collectively as genetic transformation, rDNA methods, or genetic engineering. These methods enable transfer of a resistance gene that could not be transferred by traditional sexual hybridization. NARC and Government need to prioritize moreover to the entomological research from onwards by increasing manpower in this sector and developing improved resistant and also regarding storage and multiplication of those germplasms.
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16

Baliddawa, C. W. "Insect behaviour and host plant resistance." International Journal of Tropical Insect Science 6, no. 03 (June 1985): 337–40. http://dx.doi.org/10.1017/s1742758400004604.

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17

Wolowicka, Laura, Hanna Bartkowiak, and Ryszard Gorny. "Host Resistance in Patients after Resuscitation." Prehospital and Disaster Medicine 1, no. 3 (1985): 219–23. http://dx.doi.org/10.1017/s1049023x00065687.

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There has recently been a steady increase in the number of patients treated in intensive care units (ICUs) and requiring resuscitation. This number has risen from 1 to 3% in patients after cardiac arrest (19) and from 7 to 13% in those with severe injuries (18). The immune system investigations, introduced more and more widely in intensive care medicine for prophylactic, therapeutic and prognostic reasons, did not, in principle, concern the cases of post-resuscitation disease after cardiac arrest. Only a few reports have been published on this subject (11).The aims of our investigations were the analysis of selected humoral and cellular factors in patients after cardiac arrest in comparison to those with multiple injuries, evaluation of the host resisctance against infection and of prognostic values of some immunological indices.Examinations were carried out in 50 patients, treated in an ICU of 15 beds, from 1981 to 1982, and in 20 healthy volunteers. The patients were divided into two main groups (Fig. 1): The first group consisted of 25 patients after cardiac arrest, age 47±12. The second group consisted of 25 patients after severe multiple injuries, age 42±18 y; they corresponded to an abbreviated injury scale (AIS) of 4–6 (8). 56% of the patients with cardiac arrest could not be resuscitated. In 64% of the trauma patients treatment was unsuccessful. Infection complications, influencing recovery were observed in 10 (40%) after cardiac arrest and in 12 (48%) after trauma. The cardiopulmonary-cerebral resuscitation methods used were standard (16).
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18

Berlinger, M. J. "Host plant resistance to Bemisia tabaci." Agriculture, Ecosystems & Environment 17, no. 1-2 (August 1986): 69–82. http://dx.doi.org/10.1016/0167-8809(86)90028-9.

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19

Ben-Yehuda, Arie, and Marc E. Weksler. "Host Resistance and The Immune System." Clinics in Geriatric Medicine 8, no. 4 (November 1992): 701–12. http://dx.doi.org/10.1016/s0749-0690(18)30438-5.

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20

Newkirk, Marianna M. "Rheumatoid Factors: Host Resistance or Autoimmunity?" Clinical Immunology 104, no. 1 (July 2002): 1–13. http://dx.doi.org/10.1006/clim.2002.5210.

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21

Kang, Eugene, Alanna Crouse, Lucie Chevallier, Stéphanie M. Pontier, Ashwag Alzahrani, Navoun Silué, François-Xavier Campbell-Valois, Xavier Montagutelli, Samantha Gruenheid, and Danielle Malo. "Enterobacteria and host resistance to infection." Mammalian Genome 29, no. 7-8 (May 21, 2018): 558–76. http://dx.doi.org/10.1007/s00335-018-9749-4.

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22

de Castro, J. J., and R. M. Newson. "Host resistance in cattle tick control." Parasitology Today 9, no. 1 (January 1993): 13–17. http://dx.doi.org/10.1016/0169-4758(93)90154-8.

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23

Koskella, Britt, Derek M. Lin, Angus Buckling, and John N. Thompson. "The costs of evolving resistance in heterogeneous parasite environments." Proceedings of the Royal Society B: Biological Sciences 279, no. 1735 (December 14, 2011): 1896–903. http://dx.doi.org/10.1098/rspb.2011.2259.

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The evolution of host resistance to parasites, shaped by associated fitness costs, is crucial for epidemiology and maintenance of genetic diversity. Selection imposed by multiple parasites could be a particularly strong constraint, as hosts either accumulate costs of multiple specific resistances or evolve a more costly general resistance mechanism. We used experimental evolution to test how parasite heterogeneity influences the evolution of host resistance. We show that bacterial host populations evolved specific resistance to local bacteriophage parasites, regardless of whether they were in single or multiple-phage environments, and that hosts evolving with multiple phages were no more resistant to novel phages than those evolving with single phages. However, hosts from multiple-phage environments paid a higher cost, in terms of population growth in the absence of phage, for their evolved specific resistances than those from single-phage environments. Given that in nature host populations face selection pressures from multiple parasite strains and species, our results suggest that costs may be even more critical in shaping the evolution of resistance than previously thought. Furthermore, our results highlight that a better understanding of resistance costs under combined control strategies could lead to a more ‘evolution-resistant’ treatment of disease.
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24

Escudero-Martinez, Carmen, Daniel J. Leybourne, and Jorunn I. B. Bos. "Plant resistance in different cell layers affects aphid probing and feeding behaviour during non-host and poor-host interactions." Bulletin of Entomological Research 111, no. 1 (June 16, 2020): 31–38. http://dx.doi.org/10.1017/s0007485320000231.

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AbstractAphids are phloem-feeding insects that cause economic losses to crops globally. Whilst aphid interactions with susceptible plants and partially resistant genotypes have been well characterized, the interactions between aphids and non-host species are not well understood. Unravelling these non-host interactions can identify the mechanisms which contribute to plant resistance. Using contrasting aphid-host plant systems, including the broad host range pest Myzus persicae (host: Arabidopsis; poor-host: barley) and the cereal pest Rhopalosiphum padi (host: barley; non-host: Arabidopsis), we conducted a range of physiological experiments and compared aphid settling and probing behaviour on a host plant vs either a non-host or poor-host. In choice experiments, we observed that around 10% of aphids selected a non-host or poor-host plant species after 24 h. Using the Electrical Penetration Graph technique, we showed that feeding and probing behaviours differ during non-host and poor-host interactions when compared with a host interaction. In the Arabidopsis non-host interaction with the cereal pest R. padi aphids were unable to reach and feed on the phloem, with resistance likely residing in the mesophyll cell layer. In the barley poor-host interaction with M. persicae, resistance is likely phloem-based as phloem ingestion was reduced compared with the host interaction. Overall, our data suggest that plant resistance to aphids in non-host and poor-host interactions with these aphid species likely resides in different plant cell layers. Future work will take into account specific cell layers where resistances are based to dissect the underlying mechanisms and gain a better understanding of how we may improve crop resistance to aphids.
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25

RUDDAT, I., E. TIETZE, D. ZIEHM, and L. KREIENBROCK. "Associations between host characteristics and antimicrobial resistance ofSalmonellaTyphimurium." Epidemiology and Infection 142, no. 10 (December 3, 2013): 2085–95. http://dx.doi.org/10.1017/s0950268813003026.

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SUMMARYA collection ofSalmonellaTyphimurium isolates obtained from sporadic salmonellosis cases in humans from Lower Saxony, Germany between June 2008 and May 2010 was used to perform an exploratory risk-factor analysis on antimicrobial resistance (AMR) using comprehensive host information on sociodemographic attributes, medical history, food habits and animal contact. Multivariate resistance profiles of minimum inhibitory concentrations for 13 antimicrobial agents were analysed using a non-parametric approach with multifactorial models adjusted for phage types. Statistically significant associations were observed for consumption of antimicrobial agents, region type and three factors on egg-purchasing behaviour, indicating that besides antimicrobial use the proximity to other community members, health consciousness and other lifestyle-related attributes may play a role in the dissemination of resistances. Furthermore, a statistically significant increase in AMR from the first study year to the second year was observed.
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26

Koskella, Britt. "Resistance gained, resistance lost: An explanation for host–parasite coexistence." PLOS Biology 16, no. 9 (September 24, 2018): e3000013. http://dx.doi.org/10.1371/journal.pbio.3000013.

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27

Carlsson-Granér, Ulla, and Peter H. Thrall. "Host resistance and pathogen infectivity in host populations with varying connectivity." Evolution 69, no. 4 (April 2015): 926–38. http://dx.doi.org/10.1111/evo.12631.

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28

Eleftheriou, Andreas. "Relationships among host microbiota, parasite resistance or tolerance, and host fitness." Conservation Biology 34, no. 6 (September 18, 2020): 1327–28. http://dx.doi.org/10.1111/cobi.13582.

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29

Taggar, Gaurav Kumar, and Ranjit Singh Gill. "Host plant resistance in Vigna sp. towards whitefly, Bemisia tabaci (Gennadius): a review." Entomologia Generalis 36, no. 1 (July 1, 2016): 1–24. http://dx.doi.org/10.1127/entomologia/2016/0184.

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30

Burdon, J. J., and P. H. Thrall. "Resistance variation in natural plant populations." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S145—S150. http://dx.doi.org/10.17221/10342-pps.

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The general outcomes of long-term trajectories of coevolutionary interactions between specific hosts and pathogens are<br />set by the interaction of their life histories. However, within those outcomes the speed of co-evolutionary responses and<br />the extent of their expression in the resistance/virulence structure of wild plant and pathogen populations respectively,<br />are highly variable characters changing from place-to-place and time-to-time as a result of the interaction of host and<br />pathogen with the physical environment. As a consequence, understanding of the role of diseases in the evolution of their<br />hosts requires approaches that simultaneously deal with host and pathogen structures over multiple populations within a<br />metapopulation framework.
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31

Mazé-Guilmo, Elise, Géraldine Loot, David J. Páez, Thierry Lefèvre, and Simon Blanchet. "Heritable variation in host tolerance and resistance inferred from a wild host–parasite system." Proceedings of the Royal Society B: Biological Sciences 281, no. 1779 (March 22, 2014): 20132567. http://dx.doi.org/10.1098/rspb.2013.2567.

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Hosts have evolved two distinct defence strategies against parasites: resistance (which prevents infection or limit parasite growth) and tolerance (which alleviates the fitness consequences of infection). However, heritable variation in resistance and tolerance and the genetic correlation between these two traits have rarely been characterized in wild host populations. Here, we estimate these parameters for both traits in Leuciscus burdigalensis , a freshwater fish parasitized by Tracheliastes polycolpus . We used a genetic database to construct a full-sib pedigree in a wild L. burdigalensis population. We then used univariate animal models to estimate inclusive heritability (i.e. all forms of genetic and non-genetic inheritance) in resistance and tolerance. Finally, we assessed the genetic correlation between these two traits using a bivariate animal model. We found significant heritability for resistance ( H = 17.6%; 95% CI: 7.2–32.2%) and tolerance ( H = 18.8%; 95% CI: 4.4–36.1%), whereas we found no evidence for the existence of a genetic correlation between these traits. Furthermore, we confirm that resistance and tolerance are strongly affected by environmental effects. Our results demonstrate that (i) heritable variation exists for parasite resistance and tolerance in wild host populations, and (ii) these traits can evolve independently in populations.
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32

Mou, Beiquan, and Yong-Biao Liu. "Host Plant Resistance to Leafminers in Lettuce." Journal of the American Society for Horticultural Science 129, no. 3 (May 2004): 383–88. http://dx.doi.org/10.21273/jashs.129.3.0383.

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Leafminer (Liriomyza spp.) is a major insect pest of many important agricultural crops including lettuce (Lactuca sativa L.). The goals of this study were to evaluate lettuce genotypes for resistance to leafminers and to estimate the heritabilities of leafminer-resistant traits in the field, to examine the association among different resistant traits, and to study the mechanism of leafminer resistance in lettuce. Seventy-eight lettuce accessions and 232 F2 plants of crosses were evaluated for leafminer stings and the production of pupae and flies in the field in 2001 and 2002, and resistant genotypes were subjected to no-choice test. Wild species (Lactuca serriola L., L. saligna L., and L. virosa L.) had significantly fewer stings than cultivated lettuces. Among cultivated lettuces, sting densities were lowest on leaf lettuce and highest on romaine types. The sting results from the field were highly correlated with the results from insect cages (r = 0.770 and 0.756 for 2001 and 2002 tests, respectively), suggesting that a cage test can be used to screen for resistance in the field. Broad-sense heritability estimates for stings per unit leaf area in the field were 81.6% and 67.4% for 2001 and 2002 tests, respectively. The number of pupae produced per plant or per leaf was moderately correlated with sting density but was not correlated with leaf weight. Results suggest that both antixenosis and antibiosis exist in lettuce germplasm and resistant genotypes from choice tests remain resistant under no-choice conditions. These findings suggest that genetic improvement of cultivated lettuce for leafminer resistance is feasible.
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33

Arya, Anshul, and K. P. S. Kushwaha. "Management of Lentil Wilt through Host Resistance." International Journal of Current Microbiology and Applied Sciences 8, no. 03 (March 10, 2019): 438–44. http://dx.doi.org/10.20546/ijcmas.2019.803.055.

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34

Rodgers, Kathleen, Shiquan Xiong, Theresa Espinoza, Norma Roda, Sonia Maldonado, and Gere S. diZerega. "Angiotensin II Increases Host Resistance to Peritonitis." Clinical Diagnostic Laboratory Immunology 7, no. 4 (July 1, 2000): 635–40. http://dx.doi.org/10.1128/cdli.7.4.635-640.2000.

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ABSTRACT Studies by other laboratories have shown that angiotensin II (AII) can affect the function of cells which comprise the immune system. In the present study, the effect of AII on the function of peritoneal macrophages and peripheral blood monocytes was assessed. In vitro exposure (4 h prior to assay) of peritoneal macrophages from mice and rats to AII increased the percentage of cells that phagocytosed opsonized yeast and the number of yeast per macrophage. Furthermore, AII increased the respiratory burst capacity of peritoneal macrophages from mice and rats and peripheral blood mononuclear cells from humans. Because of these observations, the effect of AII on host resistance to bacterial infection was assessed. Intraperitoneal administration of AII was shown to increase host resistance (reduced abscess formation) in an animal model of bacterial peritonitis. Studies were then conducted to assess whether parenteral administration of AII, a clinically relevant route, could affect peritoneal host resistance in a manner similar to that observed after peritoneal administration. These studies showed that subcutaneous administration of AII throughout the postinfection interval increased the level of host resistance to bacterial peritonitis. Furthermore, in a study which compared AII and Neupogen, an agent approved for use for the reduction of febrile neutropenia after myeloablative therapy, daily subcutaneous administration of AII reduced abscess size and incidence, whereas Neupogen did not have any therapeutic benefit in this model. These data suggest that AII may be of therapeutic benefit as an immunomodulatory agent.
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35

Shlaes, D. M., B. Binczewski, and L. B. Rice. "Emerging Antimicrobial Resistance and the Immunocompromised Host." Clinical Infectious Diseases 17, Supplement_2 (November 1, 1993): S527—S536. http://dx.doi.org/10.1093/clinids/17.supplement_2.s527.

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36

WOLFE, M. S. "Integration of host resistance and fungicide use." EPPO Bulletin 15, no. 4 (December 1985): 563–70. http://dx.doi.org/10.1111/j.1365-2338.1985.tb00269.x.

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37

PÉREZ-DE-LUQUE, A., S. FONDEVILLA, B. PÉREZ-VICH, R. ALY, S. THOIRON, P. SIMIER, M. A. CASTILLEJO, et al. "UnderstandingOrobancheandPhelipanche-host plant interactions and developing resistance." Weed Research 49 (November 2009): 8–22. http://dx.doi.org/10.1111/j.1365-3180.2009.00738.x.

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38

Moll, Heidrun. "Dendritic cells and host resistance to infection." Cellular Microbiology 5, no. 8 (August 2003): 493–500. http://dx.doi.org/10.1046/j.1462-5822.2003.00291.x.

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39

Mira, Marcelo Távora. "Genetic host resistance and susceptibility to leprosy." Microbes and Infection 8, no. 4 (April 2006): 1124–31. http://dx.doi.org/10.1016/j.micinf.2005.10.024.

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40

Beck, Melinda A., and Colette C. Matthews. "Micronutrients and host resistance to viral infection." Proceedings of the Nutrition Society 59, no. 4 (November 2000): 581–85. http://dx.doi.org/10.1017/s0029665100000823.

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Previous work in our laboratory demonstrated that a virus could undergo rapid mutation in a host deficient in Se, leading to a normally avirulent virus acquiring virulence due to genome changes. Once these mutations occur, even a host with adequate Se-nutriture is susceptible to the newly virulent virus. What influence does the deficiency in Se have on the immune response of the host? Infection with myocarditic strains of coxsackievirus induces an inflammatory response in the cardiac tissue. It is this immune response that induces the heart damage, rather than direct viral effects on the heart tissue. Chemokines are chemo-attractant molecules that are secreted during an infection in order to attract immune cells to the site of the injury, and have been found to be important for the development of coxsackievirus-induced myocarditis. We found that a deficiency in Se influences the expression of mRNA for the chemokine monocyte chemo-attractant protein-1, which may have implications for the development of myocarditis in the Se-deficient host. Expression of mRNA for interferon-γ was also greatly decreased in the Se-deficient animal. Thus, a deficiency in Se can have profound effects on the host as well as on the virus itself. How the alteration of the immune response of the Se-deficient animal affects the development of the virulent genotype remains to be answered.
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41

Cory, Jenny S. "Evolution of host resistance to insect pathogens." Current Opinion in Insect Science 21 (June 2017): 54–59. http://dx.doi.org/10.1016/j.cois.2017.04.008.

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42

Malo, Danielle, and Emil Skamene. "Genetic control of host resistance to infection." Trends in Genetics 10, no. 10 (October 1994): 365–71. http://dx.doi.org/10.1016/0168-9525(94)90133-3.

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43

Koprivnjak, Tomaz, and Andreas Peschel. "Bacterial resistance mechanisms against host defense peptides." Cellular and Molecular Life Sciences 68, no. 13 (May 11, 2011): 2243–54. http://dx.doi.org/10.1007/s00018-011-0716-4.

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44

Fox, Jeffrey L. "Exploring Antibiotic Resistance Uncovers Host-Pathogen Quirks." Microbe Magazine 8, no. 9 (September 1, 2013): 348. http://dx.doi.org/10.1128/microbe.8.348.1.

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45

Lipka, Ulrike, Rene Fuchs, and Volker Lipka. "Arabidopsis non-host resistance to powdery mildews." Current Opinion in Plant Biology 11, no. 4 (August 2008): 404–11. http://dx.doi.org/10.1016/j.pbi.2008.04.004.

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46

Martinez-Martinez, L. "Interaction of plasmid and host quinolone resistance." Journal of Antimicrobial Chemotherapy 51, no. 4 (February 25, 2003): 1037–39. http://dx.doi.org/10.1093/jac/dkg157.

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47

Qiu, Hongyu, Zack Li, Rhonda KuoLee, Greg Harris, Xiaoling Gao, Hongbin Yan, H. Howard Xu, and Wangxue Chen. "Host resistance to intranasalAcinetobacter baumanniireinfection in mice." Pathogens and Disease 74, no. 5 (May 17, 2016): ftw048. http://dx.doi.org/10.1093/femspd/ftw048.

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48

Dobson, M. "Vaccines, malaria, and a host of resistance." BMJ 313, no. 7049 (July 13, 1996): 67–68. http://dx.doi.org/10.1136/bmj.313.7049.67.

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49

Suzuki, Yasuhiro. "Host Resistance in the Brain againstToxoplasma gondii." Journal of Infectious Diseases 185, s1 (February 15, 2002): S58—S65. http://dx.doi.org/10.1086/337999.

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50

Burleson, Gary R. "Models of respiratory immunotoxicology and host resistance." Immunopharmacology 48, no. 3 (July 2000): 315–18. http://dx.doi.org/10.1016/s0162-3109(00)00231-9.

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