Classification of interferonopathies.
\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
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The most important advances in the pathophysiology and treatment of gastrointestinal disorders are discussed including; gastroesophageal reflux disease (GERD), peptic ulcer disease, irritable bowel disease (IBD), NSAIDs-induced gastroenteropathy and pancreatitis. Special focus was addressed to microbial aspects in the gut including recent achievements in the understanding of function of probiotic bacteria, their interaction with gastrointestinal epithelium and usefulness in the treatment of human disorders. 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He was a postdoctoral NIH fellow at University of California and Gastroenterology VA Medical Center, Irvine and Long Beach, CA, USA and at Gastroenterology Clinics at Erlangen-Nuremberg and Munster in Germany. 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\r\n\tOrganic synthesis has always been one of the central topics of research for the scientific community in the academic laboratories and industrial world. Many striking journal articles and remarkable reviews and books have been published in the past year describing the practicability and applications of the subject demonstrating the importance of organic synthesis. In the present book, we will be putting together the topics in organic synthesis which may include but not limited to, (1) the basic terms and concepts, (2) various organic reactions including reduction, oxidation, addition, elimination, rearrangements, and cycloadditions, (3) Total Synthesis of Natural products, (4) transition metal catalysts, organocatalysts, enzymes and biotransformations, (5) applications in medicinal chemistry and drug design and development, (6) purification methods and characterization techniques, etc. To set a limit and to increase the scope of the book, author(s) are encouraged to send the chapters that include selected examples with practical applications and good yielding reactions reported within the past decade. Older topics with significant findings or their essence to prepare the foundation may be included in the chapter are welcomed as well.
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Deore was born in India. He received a Master’s degree in organic chemistry from Pune University in 2007. In the same year, he qualified with the SET and CSIR-NET (JRF) and joined in the group of Prof. Narshinha P. Argade for the doctoral studies in National Chemical Laboratory, India. In 2014, he awarded with a Ph. D. in Chemistry and was a recipient of the 2nd prize in “2014 Eli Lilly and Company Asia Outstanding Thesis Awards”. In July 2014 he moved to Canada and joined as a postdoctoral researcher in the group of Prof. Richard Manderville at the University of Guelph, Canada. Presently, Dr. Deore is working on the collaborative project between the University of Guelph and Aterica health Inc., and providing consulting to the company. 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From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Although rice production in the world has increased markedly in the past decades, it is still insufficient to cope with the ever-increasing global demands (Sasaki et al. 2000). This is not an easy task in view of the fact that the land available for cultivation is decreasing year by year, especially in Asia where 90 percent of the world’s rice is produced and consumed (Khush 1997; Fischer et al. 2005). Meanwhile, since rice is grown worldwide and under a wide range of agro-climatic conditions, its productivity is affected by many abiotic and biotic stresses. Major biotic stresses including insect pests, such as brown planthopper (Nilaparvata lugens Stål), green rice leafhopper (Nephotettix cincticeps), and stem borer (Chilo suppressalis); and diseases, such as sheath blight, bacterial leaf blight, tungro virus; and abiotic stresses including salinity, acidity, drought, cold, and iron toxicity severely affect rice production.
During domestication process from wild species to cultivated rice, selecting desirable-agronomic traits to keep achieving high yield allows many genes to be either directly selected or filtered out, resulting in a significant reduction of genetic diversity in rice gene pool (Brar et al. 2003). Sun et al (2001) revealed that the number of alleles in cultivated rice had been reduced by 50-60% compared to wild rice. Thus, it is necessary to broaden the gene pool in rice breeding from diverse sources, especially from wild rice.
In the genus of Oryza, there are two cultivated species and more than 20 wild species. Both of the cultivated species, O. sativa and O. glaberrima, are diploid (2n = 24) and have the AA genome. Wild species have evolved in a wide range of environments over millions of years (Stebbins 1981). The wild species have either 2n = 24 or 2n = 48 chromosomes, and seven genomes (AA, BB, CC, BBCC, CCDD, EE, and FF) have so far been designated for 17 species (Vaughan 1994; Brar et al. 1997). Common wild rice (Oryza rufipogon Griff.), due to its long-term growth in the wild conditions, possesses numerous advantages such as genetic diversity, excellent agronomic traits, and resistance against various biotic and abiotic stresses, proved to be an important resource for genetic improvement of rice (Song et al. 2005). Dongxiang wild rice (O. rufipogon Griff.) is in the northern most habitats among O. rufipogon populations to be discovered in the world (Chen et al. 2008; Xie et al. 2010; Figure 1), and displays strong tolerance to low temperature (Figure 2). It is for certain that many valuable traits exist in the wild rice species, but the most challenges to us are how to explore the valuable genes from wild rice and effectively transfer them into the cultivated rice for diversifying genetic basis of cultivated rice. Recently, many genes and QTLs have been mined from the wild rice, which functions include disease and insect resistances, abiotic stress tolerances, high yield, and so on. In this chapter, we will summarize current research progresses in mining elite genes and QTLs from wild rice for cultivar improvement in breeding programs.
Dongxiang wild rice (Oryza rufipogon Griff.) is a common wild rice located at 28°14′N latitude and 116°30′E longitude in Dongxiang county, Jiangxi province, China, which is considered to be the northernmost region in the world where O. rufipogon is found.
Dongxiang wild rice can survive under freezing conditions.
Rice diseases such as blast, bacterial blight and sheath blight are major obstacles for achieving optimal yields. To complement conventional breeding method, molecular or transgenic method represents an increasingly important approach for genetic improvement of disease resistance and reduction of pesticide usage. During the past two decades, a wide variety of genes and mechanisms involved in rice defense response have been identified and elucidated. However, most of the cloned genes confer high level of race specific resistance in a gene-for-gene manner, and the resistance is effective against one or a few related races or strains of the pathogens. The resistance is effective for only few years because the pathogen race or strain keeps changing for survival in nature. Therefore, there is an urgent need to broaden the rice gene pool from diverse resources, of which the wild rice is an ideal option.
Rice blast, caused by pathogen Xanthomonas oryzae pv. oryzae, is considered as a major disease of rice because of its wide distribution and destructiveness under favorable conditions. Rice blast causes lesion symptoms on leaves, stems, peduncles, panicles, seeds, and even roots. The potential threat for cropping failure makes this disease ranked among the most devastating diseases in rice. It is reported that the rice blast disease can lead to lose one million hectares annually in China alone (Savary et al. 2000; Khush et al. 2009). Exploitation of resistance gene resources for rice breeding is one of the most important ways to control the disease.
Oryza minuta J. S. Presl ex C. B. Presl is a tetraploid wild rice, highly resistant to rice blast. By genetic analysis, Amante-Bordeos et al (1992) found that the disease resistance was controlled by a single dominant gene, named Pi9. Subsequently, Liu et al (2002) mapped Pi9 in an approximately 100-kb region on chromosome 6, tightly linked with RFLP markers R2132 and RG6. Finally, this broad-spectrum rice blast resistance gene was cloned using a map-based cloning strategy. It turns out that Pi9 encodes a nucleotide-binding site-leucine-rich repeat protein, as a member of a multi-gene family in rice (Qu et al. 2006).
Jeung et al (2007) identified a new gene in the introgression line IR65482-4-136-2-2 that has inherited the resistance gene from an EE genome wild Oryza species, O. australiensis (Acc. 100882). Genetic and molecular analysis localized a major resistance gene, Pi40(t), on the short arm of chromosome 6, within 70-Kb chromosomal region narrowed by two molecular markers RM3330 and S2539. Pi40(t) was validated using the most virulent isolates identified in Korea and the Philippines, suggesting a broad resistance spectrum.
Li et al (2009) evaluated blast resistance for 21 progenies from crossing with common wild rice, and obtained three stably resistance progenies. Preliminary analysis showed that the rice blast resistance was controlled by dominant genes. Geng et al (2008) cloned rice blast resistance gene Pi-ta+ from Jinghong erect type of common wild rice. The Pi-ta+ coding region shares 99.86% and 98.78% of homologous identity with Japanese waxy cultivar Yashiro-mochi and Yuanjiang type of common wild rice, respectively in the corresponding regions. There are four nucleotides difference in the coding region and six in intron of the cloned Pi-ta+ gene, compared with Pi-ta from Yashiro-mochi. The allele in the Jinghong Pi-ta+ gene is very rare in nature, because there is an alanine rather than a serine at position 918 within the predicted amino acid sequence of Pi-ta+. The Pi-ta+ allele can display disease resistance in response to blast pathogens in rice plant cells.
Bacterial blight is caused by Xanthomonas oryzae pv. oryzae. Yield losses due to bacterial blight are variable, heavily dependent on the cultivar used and the environment. In Japan, yield losses ranged typically between 20% and 30% after distribution of high-yielding dwarf varieties (Mew et al. 1993). Among tropical climates, yield losses up to 75% were reported in Indonesia, India, and the Philippines (Nino-Liu et al. 2006). It is of great importance to explore elite bacterial blight resistance genes in rice. By now, a total of 35 related genes have been reported, and nine of which were from wild rice, i.e. Xa21(t), Xa23(t), Xa27(t), Xa29(t), Xa30(t), Xa32(t), xa32(t), Xa35(t) and Xa36(t).
In 1977, Dr. S. Devadath found that a strain of Oryza barthii from Mali is resistant to all the races of bacterial blight in India. Then, Khush et al (1989) found that this strain is akin to O. longistaminata, thus crossed it with IR24, which is susceptible to six races of bacterial blight in Philippines. The F1 was resistant to the six races, thereby showing that the resistance of O. longistaminata was dominant. They designated this gene as Xa21(t). By developing nearly isogenic lines of Xa21(t), Ronald et al (1992) mapped locus Xa21(t) to a region larger than 270 kb on chromosome 11. By positional cloning, Song et al (1995) isolated Xa21(t). The sequence of the predicted protein, which carries both a leucine-rich repeat motif and a serine-threonine kinase-like domain, suggests a role in cell surface recognition of a pathogen ligand and subsequent activation of an intracellular defense response. Furthermore, they demonstrated that the transgenic rice plants carrying the cloned Xa21(t) gene display high levels of resistance to the pathogen.
Xa23(t) was first detected from O. rufipogon by Zhang (2005), showing resistance to race 6 of bacterial blight in the Philippines. Wang et al (2005) constructed a F2 population of JG30/CBB23 for molecule mapping of the Xa23(t) in rice. Based on their previous mapping of Xa23(t) gene, 12 EST markers from Rice Genome Program (RGP) database were surveyed in the susceptible F2 plants and two markers, C189 and CP02662, were found to flank Xa23(t) gene, with genetic distance of 0.8 cM and 1.3 cM, respectively.
Jin et al (2007) identified a rice bacterial blight resistance germplasm (Y238) from the wild rice species Oryza rufipogon, and then they transferred the resistance locus into the cultivated rice to breed near isogenic line. By molecular mapping, the gene Xa30(t) was mapped on the long arm of rice chromosome 11. Linkage analysis revealed that four molecular markers RM1341, V88, C189 and 03STS located on the same side of Xa30(t), with genetic distances of 11.4 cM, 11.4 cM, 4.4 cM and 2.0 cM to the candidate gene, respectively.
Gu et al (2004) performed disease evaluation to a Xa27(t) near-isogenic line, IRBB27 with 35 Xanthomonas oryzae pv. oryzae strains collected from 11 countries. The Xa27(t) gene conferred a high level of resistance to 27 strains and moderate resistance to three strains. Resistance of the Xa27(t) gene was developmentally regulated in IRBB27 and showed semi-dominant or a dosage effect in the cv. CO39 genetic background. Molecular mapping located Xa27(t) within a genetic interval of 0.052 cM, flanked by markers M964 and M1197 and co-segregated with markers M631, M1230, and M449.
Guo et al (2010) transferred a new rice bacterial blight resistance gene Xa35(t) from the wild rice species Oryza minuta (Acc. No. 101133) into Oryza sativa L. (IR24). Through genetic analysis and identification of resistance spectrum, Xa35(t) showed a high level of resistance to PXO61, PXO112 and PXO339, but was susceptible to PXO86 and PXO99 after inoculation with the five strains of Xanthomonas oryzae pv. oryzae. With SSR marker analysis, the Xa35(t) locus was mapped to a 1.80 cM region. This locus was co-segregated with marker RM144, and was 0.7 cM from marker RM6293 on one side and 1.1 cM from marker RM7654 on the other side on rice chromosome 11.
Xa29(t), which was detected from the wild rice Oryza officinalis, has a high resistance to bacterial blight. By molecular mapping, the Xa29(t) gene was mapped within a 1.3 cM region flanked by RFLP markers C904 and R596 on chromosome 1 (Tan et al. 2004). Xa32(t), a bacterial blight resistance gene from Oryzae ustraliensis, was resistant to Xanthmonas oryzae pv. oryzae strains P1 (PXO61), P4 (PXO71), P5 (PXO112), P6 (PXO99), P7 (PXO145), P8 (PXO280), P9 (PXO339), and KX085, but susceptible to P2 (PXO86) and P3 (PXO79). Xa32(t) was mapped within a 2.0 cM interval flanked by two SSR markers RM2064 and RM6293 on the long arm of rice chromosome 11 (Zheng et al. 2009). Miao et al (2010) detected that the rice germplasm C4059 harbored a bacterial blight resistance gene, and designated it tentatively as Xa36(t). By analyzing the mapping populations, the gene Xa36(t) was mapped within a length of 4.5 cM flanked by RM224 and RM2136 on the long arm of rice chromosome 11.
Bacterial leaf streak (BLS) is caused by Xanthomonas oryzae pv. Oryzicola in rice. BLS occurs in Asia and West Africa, and yield losses are up to 30 percent. The symptoms of BLS include translucent interveinal streaks extending to orange lesions which may kill the leaf. Yellowish bacterial exudates may be seen. Bacteria may enter through small wounds on the leaf surface, including insect damage. Plants are susceptible at all stages, but infection is most damaging at the tillering stage. BLS is often prevalent in the rainy season. In order to determine if the resistance genes to the BLS disease were from Guangxi wild rice in China, Huang et al (2008) screened 1655 accessions of Guangxi Oryza rufipogon Griss, and identified 57 (1.87%) accessions to be resistant. In another screening, 15 (48.4%) out of 31 accessions of O. officinalis Wall. ex Watt were resistant.
Sheath blight disease, caused by a soilborne necrotrophic fungus Rhizoctonia solani Kühn, is one of the most important diseases in cultivated rice. This disease was first reported in Japan in 1910 and subsequently discovered worldwide (Rush et al. 1992). At present, rice sheath blight widely occurs in most rice-growing areas, including temperate, tropical and subtropical regions in diverse rice production systems (Lee et al. 1983). Sheath blight disease causes approximately 50% yield reduction in test plots of susceptible cultivars (Savary et al. 1996). To identify resistant germplasm to sheath blight disease, Prasad et al (2008) reported seven Oryza spp. accessions as moderately resistant, three were O. nivara accessions (IRGC104705, IRGC100898, and IRGC104443), O. barthii (IRGC100223), O. meridionalis (IRGC105306), O. nivara/O. sativa (IRGC100943), and O. officinalis (IRGC105979). Greater effort should be paid to search sheath blight resistant germplasm from wild rice and to transfer the resistant genes into the cultivated rice in the future.
Insects are serious constraints to rice production. In Asia alone, yield loss due to insects has been estimated at about 25% (Savary et al. 2000). Insects not only damage the plant by feeding on its tissue, but also are vectors of devastating rice viruses in many cases. All portions of the plant, from panicle to root, are possibly attacked by various insects. And all growth stages of the rice plant, from the seedling to mature stages, are vulnerable. Even after harvest, the grain in store might face the attack from insects (Cramer et al. 1967). Because the resistance sources in cultivated rice are limited, it is important to keep exploring resistant germplasm from wild rice species for cultivar improvements.
Brown planthopper (BPH) is a destructive insect pest to rice in Asian countries where most rice is produced in the world, including China, India, the Philippines, Japan, Korea, Vietnam, etc (Khush 1984). BPH directly damages the plant phloem by using its piercing-sucking mouthparts, resulting in “hopper burn” in the most serious cases. Furthermore, it is also a vector for rice grassy stunt virus and ragged stunt virus, which may cause further yield losses in many Asian countries (Chelliah et al. 1993). Identification and incorporation of new BPH resistance genes from wild rice into modern cultivars are important breeding strategies to control the damage caused by the BPH.
Ishii et al (1994) found an introgression line from wild species Oryza australiensis resistant to three biotypes of BPH, and named the gene Bph10(t). RFLP analysis resulted in a linkage of the gene Bph10(t) with RG457 on chromosome 12 at a distance of 3.68 +/- 1.29 cM. A BPH biotype-4 resistance gene Bph13(t) was identified from Oryza officinalis Wall. Using RILs where parents “IR50” (cultivar which is susceptible to BPH Biotype-4) and “IR54745-2-21-12-17-6” (a line with Oryza\n\t\t\t\tofficinalis-derived resistance to BPH biotype-4) are included, Bph13(t) was located on chromosome 3, linked with a RAPD marker AJ09b with the distance of 1.3 cM (Renganayaki et al. 2002).
Later, Jena et al (2006) identified a major BPH resistance gene Bph18(t) from an introgression line (IR65482-7-216-1-2) with wild species Oryza australiensis. Genetic analysis concluded that Bph18(t) is a dominant gene located within a 0.843 Mb physical interval flanked by markers R10289S and RM6869 on the long arm of chromosome 12, where three BAC clones are present.,. Subsequently, Jena et al (2010) successful cloned the Bph18(t) gene. Bph14 is a BPH resistance gene at seedling and maturity stages. Du et al (2009) cloned Bph14 gene to encode a coiled-coil, nucleotide-binding, and leucine-rich repeat (CC-NB-LRR) protein. Sequence comparison indicates that Bph14 carries a unique LRR domain that might function in recognizing the BPH insect invasion and activating the defense response. Bph14 is predominantly expressed in vascular bundles, the site of BPH feeding. Expression of Bph14 activates the salicylic acid signaling pathway and induces callose deposition in phloem cells and trypsin inhibitor production after BPH infestation, thus reducing the BPH feeding to yield low growth rate and longevity of BPH insects.
Rahman et al (2009) conducted a genetic analysis of BPH resistance using an F2 population derived from a cross between an introgression line, IR71033-121-15 from Oryza minuta (Accession number 101141) and a susceptible Korean japonica variety, Junambyeo. Two major QTLs were identified for BPH resistance. One was mapped to 193.4 kb region located on the short arm of chromosome 4, and the other was mapped to a 194.0 kb region on the long arm of chromosome 12.
Abiotic stresses including high salinity, drought and flood, high and low temperatures are largely limiting productivity of rice crops in large areas of the world. According to Hossain (1996), abiotic stresses affect rice cultivation more than the biotic stresses. Improving the resistance to abiotic stresses will increase agricultural productivity and extend cultivatable areas of rice. There is, therefore, a strong demand for rice cultivars resistant to abiotic stresses.
Based on physiological studies on stress responses, recent progress in plant molecular biology has enabled discovery of many genes involved in stress tolerance. These genes include functional genes which protect the cell (e.g., enzymes for generating protective metabolites and proteins), and regulatory genes which regulate stress response (e.g., transcription factors and protein kinases). Wild rice is the ancestor of cultivated rice, having been an important gene pool due to its survival ability in wild conditions and suffering from natural selection. Therefore, it is of great significance to study genetic basis of abiotic stress resistance as well as to explore new related genes in wild rice.
Cold stress is a common problem for rice cultivation, and is a significant factor affecting global food production since cold stress can cause poor germination, slow growth, withering, and anthers injury on rice plants (Andaya et al. 2007). Annually, about 15 million hectares of rice in the world suffered from cold damage (Zhang et al. 2005). In south Asia, about 7 million hectares cannot be planted timely because of the low temperature stress (Sthapit et al. 1998). Consequently, development of rice cultivars with cold tolerance is recognized as one of the important breeding objectives.
Various methods have been adapted to improve rice resistance to low temperature stress (Bertin et al. 1997; Takesawa et al. 2002). With increasing emphasis on F1 hybrid rice production in public institutions and private breeding companies, lots of landraces with diversified genetic background continue to decrease, which makes the genetic base of parental materials become more and more narrower. As a result, development of cultivars for strong cold tolerance becomes increasingly difficult using intra-variation. There is thus an urgent need to study the cold-tolerance character and excavate related genes in wild rice to broaden rice gene pool for developing cold tolerance cultivars.
Genetic analysis of cold tolerance at seedling and/or booting stage has resulted in the identification of many QTLs (Lou et al. 2007; Zeng et al. 2009). Zheng et al (2011) constructed chromosome segment substitution line (CSSL) populations using two core accessions of common wild rice (DP15 and DP30) as donor parents and cultivar 9311 as recipient parent. Thus, they identified cold tolerance QTLs effective at the seedling stage. Two donor lines, DP15 and DP30, are different in the number, location and effect of QTLs for cold tolerance. A total of 19 cold tolerance QTLs were detected, and clustered on chromosome 3 and chromosome 8. The survival rates ranged 8 – 74% after cold treatment among the CSSLs. A major QTL qSCT-3-1 was mapped between SSR markers RM15031 and RM3400, near the centromere of chromosome 3 on the long arm with a distance of 1.8 cM.
Dongxiang wild rice can winter over successful in Wuhan, Hubei province, China, where the lowest temperature can be down to -12C in winter (Liu et al. 2003). In order to transfer cold tolerance gene from Dongxiang wild rice, we have developed introgression lines (ILs) through a backcrossing and single-seed descent program using an elite indica restoring cultivar Xieqingzao B (O. sativa L.) as recipient and Dongxiang wild rice as donor parent (Jian et al. 2011). Analyzing the introgression lines found that the IL5243 and IL5335 were the best for cold tolerant ability (Chen et al. 2013). Genetic analysis using SSR markers further confirmed that a part of alien DNA has been transferred from the common wild rice into IL5243 and IL5335. Therefore, IL5243 and IL5335 might be excellent bridging germplasm for breeding programs to improve cultivar tolerance to cold stress.
Soil salinity is one of the major agricultural problems affecting crop productivity worldwide (Rozema et al. 2008). Of the cereals, rice is one of the most salt-sensitive crops (Shelden et al. 2013). The effects of salinity on rice have been reported to reduce seed germination (Hakim et al. 2010), decrease growth and survival of seedlings (Lutts et al. 1995), damage the structure of chloroplasts (Yamane et al. 2008), reduce photosynthesis (Moradi et al. 2007) and inhibit seed set and grain yield (Asch et al. 2000). Improving evaluation methodologies to identify genetic sources and excavating responsible genes for improving cultivar salt resistance is of continuing importance in rice. Oryza coaretata is an Asian wild rice species, occurring mostly in the coastal areas of India. This species is highly resistant to salt because of survival ability in the coastal environments. O. coarctata has some special unicellular hairs (trichomes) on the adaxial surface of leaves. The hairs efficiently maintain a low concentration of toxic salts in the plant tissue (Bal et al. 1986).
Phosphorus is one of essential nutritive elements for rice growth and development (Abel et al. 2002). The phosphorus content may be too little in the soil to be able to meet the needs of rice growth. It has been estimated that 5.7 billion hectares of land are deficient in phosphorus worldwide. Phosphorus deficiency is considered as one of the greatest limitations in agricultural production (Schachtman et al. 1998; Lynch et al. 2008).
Chen et al (2011) identified the low-phosphorus resistance ability of Dongxiang wild rice at the seedling stage by using the cultivated low-phosphorus sensitive varieties as the control. The results showed that Dongxiang wild rice has strong low-phosphorus resistance ability. And then, they developed BILs by using Dongxiang wild rice as donor parent and the low-phosphorus sensitive variety Xieqingzao B as recurrent parent. By analyzing the morphological indices, they found that the low-phosphorus resistance lines under low-phosphorus stress had higher values of relative leaf age, relative plant height, relative shoot dry mass, and relative soluble content, but low values of relative yellow leaf number and relative malondialdehyde content, suggesting that the low-phosphorus resistance capability of the low-phosphorus resistance lines was mainly attributed to the high phosphorus utilization efficiency of the lines, namely, low-phosphorus resistance lines had stronger capability in synthesizing dry mass with per unit phosphorus uptake (Chen et al. 2011).
Because of global climate warming and increasing scarcity of water resource, drought stress and water scarcity have severely impacted the security of rice production (Farooq et al. 2009). At least 23 million hectares of rice area in Asia are estimated to be drought-prone (Pandey et al. 2005). To date, however, the major challenge for research communities is the relatively limited progress achieved in developing high yielding rice cultivars with drought resistance (Rabello et al. 2008). Therefore, the improvement of drought resistance in newly developed cultivars, for the wide adaptability across rice-growing ecologies, has become a major priority in rice breeding programs. Accordingly, identifying genes from new germplasm resources such as wild rice has become extremely important for drought resistance, which will lay the foundation for utilization of drought resistance gene and genetic improvement of drought resistance (Xie et al. 2004).
Our group has already carried out preliminary experiments for many years on characterization of Dongxiang wild rice for genetic differentiation and conservation, and utilization (Xie et al. 2010). We proved that Dongxiang wild rice has strong drought resistance (Figure 3). Subsequently, Hu et al (2013) constructed BIL population using Indica restorer line R974 (Oryza sativa L.) and Dongxiang wild rice. Using a mixed inheritance model for both major genes and minor genes, they found that the inheritance of drought-resistance at seedling stage was controlled by two independent genes plus polygenes. Therefore, Dongxiang wild rice could be precious resource for genetic improvement of drought resistance in cultivar development.
Dongxiang wild rice has strong drought resistance.
In general, wild rice has smaller seeds and other undesirable traits compared to cultivars, and thus appears not to be appropriate for a donor to enhance yield in cultivars. However, molecular studies have demonstrated that phenotypically poor wild rice contains some genes important for improving cultivar yield (Tanksley et al. 1996). Some wild-QTL alleles are favorable for some traits, but may be associated with deleterious effects on other traits. The positive QTLs from O. rufipogon may be potentially useful for breeding high yield cultivar if the disadvantage linkage drag could be broken through careful selection. In addition, other potentially beneficial QTLs for yield-related traits are often linked to the QTLs conferring negative traits. For example, gpp1.1 with yield increasing effect is closely linked with a negative QTL to increase plant height because this QTL is closely linked to sd1 locus (Cho et al. 2003). Brondani et al (2002) detected specific marker regions to strongly associate with multiple yield-related traits including panicle number, spikelets per panicle, seed set percentage, 100-grain weight, grain yield per plant, filled grain number per panicle and grain yield per panicle.
By using a BC2F5 population derived from the cross between Zhenshan 97 and a wild rice, Wu et al (2012) identified a QTL region flanked by SSR marker RM481 and RM2 on chromosome 7. This QTL has pleiotropic effects on heading date, spikelets per panicle, and grain yield per plant. The alleles from wild rice have increasing effects on these phenotypic traits contributable to grain yield.
Fu et al (2010) developed an advanced backcross population by using an accession of common wild rice collected from Yuanjiang County, Yunnan Province, China, as the donor and an elite cultivar 9311 as the recurrent parent. From this population, several QTLs originating from O. rufipogon display beneficial effects for yield-related traits in the 9311 genetic background. In addition, five QTLs controlling yield and its components are newly identified, and they are potentially novel alleles in Yuanjiang common wild rice. Three regions underling significant QTLs for several yield-related traits are detected on chromosome 1 (RM212-RM5362), 7 (RM125-RM1135) and 12 (RM7003-RM277).
Xiao et al (1998) identified two yield-enhancing QTLs, yld1.1 and yld2.1, from O. rufipogon using BC2 populations. QTLs yld1.1 and yld2.1 have been transferred to the elite restorer lines Ce64-7, 9311 and Minghui63 by marker-assisted selection (MAS), and they are confirmed to produce significant yield-enhancing effects in field tests. Xie et al (2006) fine mapped a yield-enhancing QTL cluster using a BC3F4 population derived from a cross between the Korean japonica cultivar Hwaseongbyeo and O. rufipogon. The cluster contained seven QTLs for 1000-grain weight, spikelets per panicle, grains per panicle, panicle length, spikelet density, heading date and plant height. The alleles from the low-yielding O. rufipogon parent are beneficial in the Hwaseongbyeo background.
As the wild relatives and ancestor of cultivated rice, wild rice carries various characteristics resistant to biotic and abiotic stresses, beneficial agronomic traits, and abundant genetic diversity, which have been lost in the cultivated rice due to breeding activities (Sakai et al. 2010). Thus, it is an extremely important resource for improving important traits in cultivated rice (Xie et al. 2004). However, loss of wild rice genetic diversity was sped up by increasing deterioration of original habitat. For example, the Dongxiang wild rice was sharply reduced from nine populations in nine isolated areas in 1978 to three in 1995 (Hu et al. 2011). The dramatic reduction makes the unique gene pool endangered. Therefore, it is necessary to accelerate a rational conservation for effective utilization of these survived genetic resources.
Breeders have long recognized the intrinsic value of wild rice for improving the traits of modern cultivars. The most successful examples to utilize wild rice in the history of rice breeding include the use of Oryza nivara genes to provide long-lasting resistance to grassy stunt virus (Plucknett et al. 1987), and the use of O. spontanea as a source of wild abortive cytoplasmic male sterility, which has made a cornerstone for today’s hybrid rice (Li et al. 1988). However, despite these successes, it is still difficult to utilize wild rice for the improvement of quantitatively inherited traits. Great progress of molecular markers and maps makes it possible to identify individual QTL associated with elite traits from wild rice, which will help transfer the valuable QTLs into modern cultivars to improve their qualities (Tanksley et al. 1996).
Nowadays, QTL studies for mining favorable genes from wild rice species are receiving more and more attentions in global rice community. Several studies have successfully identified and introduced the QTL enhancing alleles from wild rice for yield-related traits into high-yielding elite cultivars (He et al. 2006; Deng et al. 2007; Tan et al. 2008). In addition, some QTLs related to rice quality traits were also detected using wild rice introgression lines (Hao et al. 2006; Garcia-Oliveira et al. 2009). Molecular mapping of these good genes will help discover and make full use of the elite resources of wild species to broaden the genetic base of modern cultivars. However, only a few genes have been cloned from wild rice, and the mechanism for those excellent traits from wild rice are far from being clarified. Cloning more genes from wild rice should be emphasized in the future, which will help make full use of these elite resources more effectively.
In summary, as a rare germplasm resource, wild rice is of great significance to our agricultural heritage and biodiversity protection. Research reveals that wild rice not only has many elite genes which have lost in cultivated rice, but also maintains a greater genetic diversity than cultivated rice. We should use the wild rice to broaden genetic diversity of cultivated rice, by which new cultivars could withstand biotic and abiotic stresses. This is of great significance to assure both high yield and quality in rice production.
Type I interferonopathies are congenital genetic disorder of the interferon (IFN) system, characterized by certain clinical symptoms resulting from the overproduction of IFNα [1, 2, 3]. In our opinion, the term interferonopathy means a general pathology of the interferon system, congenital or acquired, which includes the following types of disorders of the IFN system: deficiency; paralysis of the IFN system; inadequate response on viruses, bacteria, and mutated tumor cells; and overproduction of type I IFN. Interferons are the cornerstone of immune defense against viral infections and are also involved in the regulation of immune responses. Currently there are isolated type I, II, and III interferons in accordance with their ability to interact with the three types of receptors. Type I interferons include IFNα/IFNβ; type II interferons, IFNγ; and type III interferons, interferon-like cytokines (IL-29, IL-28A, IL-28B) [4].
\nThe main role of type I interferons is to control viral infection. The synthesis and secretion of type I IFN is activated when our immune cells come in contact with viruses. Type I IFN is synthesized by epithelial cells, many cells of the immune system, including plasmacytoid dendritic cells (pDC) that recognize foreign or auto nucleic acids. Although both epithelial and pDC synthesize type I IFN simultaneously in different tissues, pDC-derived type I IFN actually exerts various immune responses through its cognate receptors on target cells. This results in modulation of diverse processes such as antigen presentation and activation of adaptive immunological process involving B and T cells [5]. For the synthesis of interferons in the body, cell activation is necessary. Toll-like receptors (TLRs); RIG-like receptors (RLRs), RIG-I; melanoma differentiation-associated protein 5 (MDA5); and cyclic GMP-AMP synthase (cGAS) participate in the recognition of foreign and host nucleic acid sites [6]. The main inducers of the synthesis of type I interferons are double-stranded and single-stranded RNA of viruses, as well as bacterial DNA [7]. RIG-like receptors recognize both single- and double-stranded viral RNAs, whereas cGAS (cyclic GMP-AMP synthase), in contrast, recognizes double-stranded DNA and RNA: DNA duplexes are formed during the replication of retroviruses and catalyze the synthesis of cGMP-AMP, which is the main agonist of the adapter protein—STING. After binding RNA, RIG-I and MDA5 bind the mitochondrial antiviral-signaling (MAVS) adapter protein. Both STING and MAVS stimulate downstream signaling cascades that include multiple kinases and finally lead to phosphorylation of IRF3 and induction of interferon synthesis [8]. Then type I IFN binds to the corresponding IFNAR receptors located on the cell membrane, which leads to the activation of Tyk2 and Jak1 kinases, which undergo phosphorylation and activate signal transduction and transcription activation proteins (STAT1 and STAT2). As a result, a heterotrimeric complex is formed, known as IFN-stimulating gene factor-3 (ISGF3), which includes IFN regulatory factor 9 (IRF9). Janus kinase (Jak) activation is negatively regulated by IFNα-inducible proteins SOCS1 and SOCS3. The binding of ISGF3 promotes interferon-stimulated genes (ISGs), which leads to their transcriptional activation and the collective actions of hundreds of ISGs, resulting in the production of a large number of induced IFN, which inhibits both viral replication and the spread of viruses. Rapid type I IFN secretion and then rapid synthesis induce activity of congenital and adaptive immunity cells by activation of pro-inflammatory cytokines that activate cellular and humoral antiviral immune response [9] (\nFigure 1\n).
\nMolecular mechanisms of the induction of type I and III interferon synthesis. PAMPs: dsRNA, double-stranded RNA; ssRNA, single-stranded RNA. Nucleic acid sensors: cGAS, cyclic GMP-AMP synthase; MDA5, melanoma differentiation-associated protein 5; RIG-I, RIG-I-like receptor dsRNA helicase enzyme. Adaptor proteins: TIRAP, toll-interleukin 1 receptor (TIR) domain-containing adaptor protein; MAVS, mitochondrial antiviral-signaling protein; STAT, signal transducer and activator of transcription. Nuclear factors: IRF, IFN regulatory factor; NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells; IFNAR, IFNα receptor; ISGs, interferon-stimulated genes; Tyk, tyrosine kinase; Jak, Janus kinase.
During acute viral infection, IFN level is significantly elevated, and more than 70% of cells acquire antiviral status, i.e., they are protected against virus penetration and are able to efficiently neutralize them. Type I IFN has several very important positive effects: direct and indirect antiviral effect, protective antiviral effect, antitumor effect, and immunomodulatory effect. At the same time, it was shown that increased production of IFN can lead to negative consequences similar to autoimmune reactions.
\nThe information presented by several authors about interferon system pathologies is vast and diverse but is not well-systematized. All known defects of IFN system, including type I and II IFN, whether congenital or acquired, including various disorders (deficiency; inadequate response to contact with viruses, bacteria, and mutated or tumor cells; IFN system paralysis; IFN overexpression), are pathologies of IFN system. All those defects of IFN system are collectively known as interferonopathies. There is an urgent need to create a classification of congenital and acquired disorders of the IFN system. We believe that the classification of IFN pathology would help in determining the correct approaches to the differentiated choice of adequate treatment tactics.
\nBased on our own and others’ experience, we have developed the interferonopathies classification as per the following table [1, 2, 3, 10, 11, 12, 13, 14, 15] (\nTable 1\n).
\nRecently several studies have presented genetic and molecular disorders accompanying rare Mendelian diseases that are associated with type I IFN overexpression resulting from defects in intracellular nucleic acid metabolism, DNAse deficiency, or defects in sensor nucleic acid recognition. Genetic disorders—Mendelian diseases (Aicardi-Goutières syndrome, familial chilblain lupus, spondyenchondromatosis, proteasome-associated autoinflammatory syndrome, Singleton-Merten syndrome)—resulting in inadequately high type I IFN overexpression accompanied by a certain range of clinical disorders are called type I interferonopathies. Interferonopathies have rare pathology; their occurrence varies from 1:10,000 to 1:1,000,000 people. According to the literature, the most common syndrome is Aicardi-Goutières [16]. The frequency of some recently described genetic disorders (e.g., PRAAS2) cannot be counted [17]. Such disorders cause a great number of own nucleic acids in cell cytoplasm to appear. It results in active DNA recognition and pathological overexpression of type I IFN which launch autoimmunity hyperactivation, thus leading to autoimmune inflammation affecting the central and peripheral nervous system. It also results to skin and vessel damage (vasculitis), lung damage, etc. Therefore rapid and efficient immune reaction to alien nucleic acids is positive when it causes type I IFN activation during pathogen invasion and antimicrobial protection. It becomes deleterious when it responds to own DNA which is due to the defect of own nucleic acid metabolism. Some neurological, vascular, and skin symptoms which are typical for type I interferonopathies are reviewed in such multifactorial diseases as exanthematous lupus erythematosus, widespread vasculitis, and autoimmune multiple myositis [6, 7, 18] (\nTable 2\n).
\nI. Congenital interferonopathies | \nII. Acquired—secondary interferonopathies | \n
---|---|
\n1. IFN deficiency\n 1.1 Interferon α deficiency (IFNα) 1.2 Interferon β deficiency (IFNβ) 1.3 Interferon γ deficiency (IFNγ) \n2. Interferon overexpression\n 2.1 IFNα overexpression 2.1.1 Autoinflammatory syndromes and autoimmune diseases (systemic lupus erythematosus (SLE), systemic angiitis, dermatomyositis), Down syndrome 2.1.2 Type I interferonopathies: Aicardi-Goutières syndrome (AGS), familial chilblain lupus (FCL), spondyenchondromatosis, proteasome-associated autoinflammatory syndrome (PRAAS), Singleton-Merten syndrome (SMS) | \n1. IFN deficiency\n 1.1 IFNα deficiency 1.2 IFNβ deficiency 1.3 IFNγ deficiency \n2. Interferon system paralysis\n 2.1 Blockage IFNα adequate response 2.2 Blockage IFNβ adequate response 2.3 Blockage IFNγ adequate response \n3. IFN overexpression\n 3.1 Cytokine storm | \n
Classification of interferonopathies.
Syndrome | \nResponsible gene | \nPhenotypes | \n
---|---|---|
Aicardi-Goutières syndrome | \nTREX1, RNASEH2B, RNASEH2C, RNASEH2A, SANHD, ADAR, IFIH1 | \nEncephalopathy, muscular dystonia, microcephaly, calcification of the basal ganglia in the substance of the brain, cramps, fever, increased acute phase blood markers, cytopenia, increased levels of interferon in the cerebrospinal fluid | \n
Singleton-Merten syndrome | \nIFIH1 DDX58 RIG-I | \nCardiovascular diseases with aortic calcification, osteoporotic manifestations, dental and skeletal abnormalities, psoriatic skin lesions | \n
Proteasome-associated autoinflammatory syndromes Chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature (CANDLE) | \nPSMB4 PSMB3 PSMB8 PSMB9 POMP | \nErythematous skin lesions, panniculitis, lipodystrophy, arthritis with the development of joint contractures, myalgia, hepatomegaly, splenomegaly, calcification of the basal ganglia in the brain, fever, increased acute phase blood markers Recurrent fevers in the first months of life, along with characteristic skin lesions, lipodystrophy, violaceous swollen eyelids, arthralgias, extremity contractures, and delayed physical development as well as systemic inflammation markers have been identified as CANDLE-related clinical manifestations | \n
STING-associated vasculopathy with onset in infancy (SAVI) | \nTMEM173 | \nVasculopathy with the formation of distal gangrene; necrosis; erythematous rash on the face, tip of the nose, and auricles; interstitial lung disease, arthralgia, fever | \n
Spondyloenchondrodysplasia (SPENCD) | \nACP5 | \nSpondylometaphyseal dysplasia, stunting, calcification of the basal ganglia in the substance of the brain, arthropathy, thrombocytopenia, deficiency of cellular and humoral immunity | \n
ISG15 deficiency | \nISG15 | \nCalcification of the basal ganglia in the substance of the brain, convulsions, mycobacterial infections | \n
USP18 deficiency (pseudo-TORCH syndrome) | \nUSP18 | \nCerebral hemorrhage and calcification, hepatomegaly, thrombocytopenia | \n
Trichohepatoenteric syndrome 2 | \nSKIV2L | \nWatery diarrhea, brittle and tangled hair, liver damage, mental retardation | \n
Retinal vasculopathy with cerebral leukodystrophy (RVCL) | \nTREX1 | \nThe main characteristics of RVCL include the middle-age onset, the progressive visual loss due to retinal vasculopathy (telangiectasias, microaneurysms, and retinal capillary obliteration around the macula), and variable neurological manifestations such as dementia or migraine | \n
Familial chilblain lupus | \nTREX1 | \nRare monogenic form of cutaneous lupus erythematosus; partly ulcerating acral lesions or painful bluish-red papules located in the fingers, toes, nose, and ears; arthralgias, affecting mainly large joints, without evidence of true arthritis; photosensitivity; or mouth ulcers | \n
X-linked reticulate pigmentary disorder (XLPDR) | \nPOLA1 | \nGeneralized hyperpigmentation intermingled with small hypomelanotic macules during early childhood, a distinctive face characterized by an upswept frontal hairline and arched eyebrows, as well as severe photophobia, recurrent respiratory infections, and severe gastrointestinal disorders | \n
Genetic disorders associated with immune dysregulations and clinical characteristics of interferonopathies associated with type I IFN overexpression.
Data available on genetic defects of intracellular nucleic acid metabolism greatly facilitate understanding of the mechanisms of insufficient immune activation, which can help in the development of new therapeutic approaches to the treatment of autoinflammatory and autoimmune diseases [1, 2, 3]. The progress in understanding immunopathogenesis mechanism makes it possible to set the exact targets for new therapeutic strategy development [1, 2]. The immune dysregulation syndrome is characterized by a high level of IFNα, a deficiency of regulatory T-lymphocytes, impaired functioning of B cells, and low content of low-density neutrophils. These neutrophils easily form neutrophilic extracellular traps (NET), and the resulting DNA complexes provoke an increase in IFNα synthesis, and then pDC recognizes autoDNA and produces IFNα [10, 11, 19]. These disorders are observed primarily in systemic lupus erythematosus. New approaches in treatment of SLE and other type I interferonopathies have been developed. Monoclonal antibody therapy in type I interferonopathies treatment with SLE is sifalimumab, rontalizumab against IFNα, and anifrolumab against IFNα receptor (IFNAR). Baricitinib (JAK1/JAK2 inhibitor) is currently at clinical studies (phases 2 and 3) in small cohort of patients with interferonopathies [20, 21, 22]. It is also known that treatment with baricitinib decreased disease signs and symptoms and allowed a significant reduction of corticosteroid treatment in patients with CANDLE and SAVI [23] (\nFigure 2\n).
\nTarget therapies by biologics in the treatment of type I IFN overproduction. IFNAR, IFNα receptor; ISGs, interferon-stimulated genes; Tyk, tyrosine kinase; Jak, Janus kinase; pDC, plasmacytoid dendritic cell; STAT, signal transducer and activator of transcription.
There are genetic defects in the synthesis of IFNα/IFNβ and IFNγ and defects in the receptors for IFNα and IFNγ (IFNAR and IFNGR) including genetic disorders associated with low IFN production according to recent studies. Those genetic defects of IFNs are accompanied by clinical signs of severe recurrent viral and/or mycobacterial infection.
\nCongenital defects of type I IFN are associated with mutation of genes participating in synthesis of IFNα/IFNβ resulting to deficiency of various molecules (STAT1, UNC93B1, MCM4, TLR3, TRAF3, TRIF, TBK1) and decline level of IFNα/IFNβ. Deficiency of IFNγ, its receptor IFNGR (IFNγR1), and IL-12 plays an important role in IFNγ regulation [12, 24, 25]. Congenital defects of type I IFN have been globally systematized in 2015 by Bousfiha et al. [24]. It has been proven that it causes severe viral and bacterial intracellular infections which are the cause of deaths. Such patients are needed in replacement therapy with recombinant IFNα2b in complex with antioxidants. Congenital defects of IFNγR1 receptor are associated with severe intracellular mycobacterial infections. Combined genetic defects leading to deficiency of IFNα and IFNγ are associated with an autosomal recessive mutation in the STAT1 gene, which causes severe viral and mycobacterial infections [12, 24, 25] (\nTable 3\n).
\nPredominant susceptibility to viral infection | \n||
---|---|---|
Syndrome | \nResponsible gene | \nPhenotypes | \n
Herpes simplex encephalitis (HSE) | \nAR (autosomal recessive inheritance): UNC 9381 TLR3 TRIF AD (autosomal dominant inheritance): TLR3 TRIF TRAF3 TBK1 | \nDominant clinical phenotype is HSE during primary infection with HSV1, usually between 3 months and 6 years of age Specific tests examining the TLR3 pathway marked decrease on the ability of patient’s fibroblasts to produce IFNβ/IFNλ in response to TLR3 agonists and HSV1 infection | \n
Warts, hypogammaglobulinemia, infection, myelokathexis (WHIM) syndrome | \nAD: CCXR4 | \nWarts/human papilloma virus infection Neutropenia, reduced B cell numbers | \n
Epidermodysplasia verruciformis | \nEVER1/TMC6, EVER2/TMC8 | \nHuman papilloma virus (group B1) infection and skin cancer | \n
STAT1 deficiency STAT2 deficiency | \n\n | Viral infections | \n
CD16 deficiency | \n\n | Severe viral infections | \n
IRF7 deficiency | \n\n | Severe influenza disease | \n
\nSusceptibility to mycobacteria\n | \n||
Syndrome | \nResponsible gene | \nPhenotypes | \n
IRF8 deficiency | \nAR: IRF8 | \nSusceptibility to mycobacteria, Candida, myeloproliferation | \n
RORc deficiency | \nRORc | \nSusceptibility to mycobacteria, Candida\n | \n
MSMD IL-12-IFNγ axis deficiency | \nAD: IFNGR1 Complete AR IFNGR1 and AR IFNGR2 Partial STAT1 LOF (AD), partial IFNGR1, partial IFNGR2, complete IL-12R1, complete IL-12B, complete ISG15, XL CYBB, IRF8, Tyk2, XL NEMO | \nMycobacterial osteomyelitis Serious disseminated BCG and environmental mycobacteria infections (soft tissue, bone marrow, lungs, skin, bones, and lymph nodes), Salmonella spp., Listeria monocytogenes, and viruses Usually less severe | \n
Genetic disorders and clinical characteristics of interferonopathies associated with type I IFN deficiency.
There are secondary acquired disorders in the IFN system, which cause a weakening of antiviral resistance in adults and children [12]. Different viruses can damage synthesis and production of IFN at various interferonogenesis stages. These secondary defects of the type I IFN lead to the occurrence of severe viral infections (herpesviral encephalitis), recurrent acute respiratory viral infections (recARVI), chronic recurrent HSV1 infection, atypical chronic EBV infections, and other atypical cases of virus infection. It was shown that viruses can avoid the effects of IFN and inhibit the action and synthesis of IFN using various molecular mechanisms. Numerous studies demonstrated that a lot of viruses (all herpesviruses, majority of respiratory viruses, hepatitis B and C viruses, etc.) produce proteins capable of inhibiting synthesis and production of IFNα/IFNβ and IFNγ. Viruses can damage each stage of the expression of ISGs [9] (\nFigure 3\n).
\nBlockage of signaling pathways for the induction of interferon by viruses (red hexagons indicate the points of application of all herpesviruses, majority of respiratory viruses, chronic hepatitis B and C viruses, etc.). dsRNA, double-stranded RNA; IRF, IFN regulatory factor; IFNAR, IFNα receptor; ISGs, interferon-stimulated genes; Tyk, tyrosine kinase; Jak, Janus kinase; NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells; cGAS, cyclic GMP-AMP synthase; MAVS, mitochondrial antiviral-signaling protein; MDA5, melanoma differentiation-associated protein 5; STAT, signal transducer and activator of transcription; TRIF, TIR domain-containing adaptor inducing interferon-beta; Ku70, component of the nonhomologous end-joining pathway that repairs DNA double-stranded breaks.
Patients with recurrent acute respiratory viral infections and various chronic herpesvirus infections including recurrent herpes viral infections have secondary defects of IFN system. Immunocompromised children of various ages and adults may suffer from recARVI with the frequency of 10 to 16–24 and more times annually; almost in 100% of cases, it is associated with the presence of mono and mixed herpes viral infection. The frequency of recurrent chronic HSV1/HSV2 infection of facial and/or genital location in those patients may reach 16–24 times per year. Epstein-Barr virus may cause atypical virus infection associated with chronic fatigue syndrome [12].
\nThe problem of developing new approaches to the treatment of congenital and acquired defects of the IFN system is very acute [12, 26, 27, 28]. Acquired defects in the IFN system (93–96%) and impaired functioning of neutrophilic granulocytes (NG) are most often detected in patients with recurrent chronic herpes virus infections.
\nWe conducted experiment in vitro to study the effect of recombinant IFNα2b (rIFNα2b) on NG in viral (cells from patients with HSV1/HSV2 infection) and bacterial (model infection by fMLP) infections. The study showed positive regulation of the negatively charged IFNαβR1+IFNγR+TLR4+NG phenotype in patients with various chronic herpesvirus infections under the influence of rIFNα2b in vitro. It was noted that the number of NGs carrying IFNαβR1 and IFNγR and expression density of IFNαβR1 is increasing, wherein expression density of IFNγR and TLR4 is decreased [29]. rIFNα2b modulating effects on CD16+CD66b+CD33+CD11b+NG phenotype transformed by fMLP in experimental model of bacterial process in vitro, to promote remodeling of the pro-inflammatory NG phenotype into anti-inflammatory, have been shown [30]. Thus rIFNα2b has a protective effect on the NG phenotype according to experimental data.
\nIn clinical practice, the use of parenteral IFN to correct disorders in the IFN system is very difficult due to the presence of numerous side effects. One should also bear in mind the inefficiency of short courses of IFN therapy for restoration of the normal IFN system functioning in recARVI, recurrent chronic herpes viral infection of facial or genital location, and papilloma virus infection of the skin and mucosa characterized by recurrent episodes when the frequency of recARVI and/or recurrent attacks of HSV1/HSV2 infection may reach 14–24 and more per year. For over 20 years, we have been developing interferon therapy programs using drugs in Russian production—rectal suppositories and gel of recombinant human IFNα2b (rIFNα2b+aox) in combination with antioxidants (vitamins E and C) (Viferon) [12, 13, 14, 15, 26, 27]. During that period, we managed to demonstrate safety, antiviral, and immunomodulatory efficiency of this kind of IFN therapy, total absence of any side effects that are typical for parenteral IFN therapy, and total absence of antibodies against IFNα2b. Replacement therapy with rIFNα2b + aox is prescribed to patients with primary, genetically preconditioned, congenital or acquired IFN system disorders. In case of primary IFN system disorders, patients need a basic recovery therapy making it possible to eliminate viral antigens as much as possible; and then it is required to select dosage for permanent replacement therapy with rIFNα2b+aox. In case of acquired interferon deficiency, patients are prescribed with differentiated therapy with high, medium, and low doses of rIFNα2b+aox (\nFigure 4\n).
\nDynamics of changes in the system of IFN in immunocompromised children against the background of therapy with rIFNα2b+aox (Viferon).
At the same time, in case when we had treated the group of patients with combined immunodeficiency (defects of induced production of IFNα and IFNγ and dysfunctions of phagocytic and microbicidal activities of neutrophilic granulocytes) that was associated with recurrent acute respiratory viral infection and different chronic herpes viral coinfections, combined interferon and immunomodulatory therapy was used. The aim was to restore the levels of induced production of IFNα and IFNγ and to reconstruct dysfunctions of phagocytic and microbicidal activities of neutrophilic granulocytes and other deficient chains in antiviral immunity. One group of children, group 1, received an interferon therapy program (rIFNα2b+aox), and patients in group 2 received a program of combined interferon therapy (rIFNα2b+aox) and immunotherapy (glucosaminylmuramyldipeptide). The use of replacement and immunomodulatory mono-rIFNα2b+aox or in combination with immunotherapy (glucosaminylmuramyldipeptide) has helped us to receive very good clinical efficacies and has reached restoration of interferon status and normal functioning of neutrophilic granulocytes (p < 0.05) (\nFigure 5\n). At the same time, it is required to take into account both uneven viral infection syndrome manifestation and the rate of IFNα deficiency as well as peculiarities of immune system disorders in case of secondary immune deficiency [12, 13, 14, 15, 27].
\nThe state of the interferon system in immunocompromised children with recurrent respiratory infections on the background of differentiated programs interferon and immunotherapy. Note: group 1 received an interferon therapy program (rIFNα2b+aox); group 2 received a program of combined interferon therapy (rIFNα2b+aox) and immunotherapy (glucosaminylmuramyldipeptide); (*p < 0.05, reliability in relation to control).
Here is an example illustrating the change in clinical, immune, and interferon status in immunocompromised children with recurrent acute respiratory viral infections under the influence of interferonotherapy.
\nClinical case. Patient X, 3 years old. The child suffers from repeated acute respiratory viral infections 1–2 times per month (14–16 episodes per year); the duration of the acute period of respiratory viral infection is 7–10 days. The clinical symptoms of the disease were acute rhinitis, acute pharyngitis, acute laryngitis, acute tracheitis, febrile and subfebrile body temperature for 2–4 days, and severe symptoms of intoxication. The duration of the frequent incidence of acute respiratory viral infections is 2 years. The defects of the immune system are a decrease of CD3+CD4+ lymphocytes and CD3+CD8+ lymphocytes; a decrease of immunoregulatory index; neutropenia; a decrease of bacteria absorption and digestion processes by neutrophils; and a decrease of microbicidal activity of neutrophils. We tested spontaneous and Newcastle disease virus-induced IFN production during the incubation of peripheral blood (24 h, t 37°C in 5% CО2). The level of induced IFNα in the patient was 4 IU/ml versus 58 IU/ml in control. The patient was prescribed rIFNα2b+aox therapy with a total duration of 2.5 months.
\nTreatment program:
Local intranasal use of rIFNα2b+aox (Viferon gel, 36,000 IU/g), two to three times a day, 6 weeks.
Systemic rectal application of rIFNα2b+aox suppositories according to a “step-by-step” scheme:
300,000 IU per day, 10 days.
300,000 IU per day three times a week, 2 weeks.
300,000 IU per day two times a week, 2 weeks.
150,000 IU per day two times a week, 2 weeks.
150,000 IU per day once a week, 2 weeks.
Conducted local and systemic interferon therapy led to a reduction in the frequency of acute respiratory viral infections to three episodes per year lasting 5–7 days, proceeding in a milder form. Rehabilitation of immunity parameters occurred after 2.5 months of interferonotherapy, and the level of induced IFNα was normalized to 64 IU/ml.
\nSumming up the above information, we may conclude that new biological drugs based on mAb are effective and safe, and they are able to neutralize IFNα overexpression in type I interferonopathies, both in Mendelian’s diseases and in autoimmune disorders. At the same time, local and system use of rIFNα2b+aox (Viferon) in congenital and acquired IFN system defects associated with viral infection syndrome, where a differential dosage is selected individually taking into account the rate of deficiency and an adequate, extended course of therapy is optimal because it is associated with positive clinical and immunological effects without any negative and side effects. Our more than 20-year experience has shown that using recIFNα2b+aox in patients with congenital or acquired IFN system defects had demonstrated positive clinical effect and is safe [31]. IFN (rIFNα2b+aox) therapy can be used with very good clinical efficacy in cases of primary or secondary defects of induced production of IFNα and IFNγ. From the other side, it is very important that in patients with a genetic predisposition to the manifestation of autoimmune diseases, primarily vasculitis and systemic lupus erythematosus, we do not recommend to use IFN therapy.
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'IntechOpen’s Retraction and Correction Policy has been developed in accordance with the Committee on Publication Ethics (COPE) publication guidelines relating to scientific misconduct and research ethics:
\n\n1. RETRACTIONS
\n\nA Retraction of a Chapter will be issued by the Academic Editor, either following an Author’s request to do so or when there is a 3rd party report of scientific misconduct. Upon receipt of a report by a 3rd party, the Academic Editor will investigate any allegations of scientific misconduct, working in cooperation with the Author(s) and their institution(s).
\n\nA formal Retraction will be issued when there is clear and conclusive evidence of any of the following:
\n\nPublishing of a Retraction Notice will adhere to the following guidelines:
\n\n1.2. REMOVALS AND CANCELLATIONS
\n\n2. STATEMENTS OF CONCERN
\n\nA Statement of Concern detailing alleged misconduct will be issued by the Academic Editor or publisher following a 3rd party report of scientific misconduct when:
\n\nIntechOpen believes that the number of occasions on which a Statement of Concern is issued will be very few in number. In all cases when such a decision has been taken by the Academic Editor the decision will be reviewed by another editor to whom the author can make representations.
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\n\n3.1. ERRATUM
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