Статті в журналах: "Viral genetics"

1

Wimmer, Eckard, and Rob Goldbach. "Viral genetics." Current Opinion in Genetics & Development 2, no. 1 (February 1992): 59–60. http://dx.doi.org/10.1016/s0959-437x(05)80322-3.

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2

Gao, Hong, and Marcus W. Feldman. "Complementation and Epistasis in Viral Coinfection Dynamics." Genetics 182, no. 1 (March 6, 2009): 251–63. http://dx.doi.org/10.1534/genetics.108.099796.

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3

Lieberman, Paul M. "Epigenetics and Genetics of Viral Latency." Cell Host & Microbe 19, no. 5 (May 2016): 619–28. http://dx.doi.org/10.1016/j.chom.2016.04.008.

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4

Fleuriet, Annie. "Evolution of the Proportions of Two Sigma Viral Types in Experimental Populations of Drosophila melanogaster in the Absence of the Allele That Is Restrictive of Viral Multiplication." Genetics 153, no. 4 (December 1, 1999): 1799–808. http://dx.doi.org/10.1093/genetics/153.4.1799.

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Abstract A minority of flies in natural populations of Drosophila melanogaster are endemically infected by a rhabdovirus, sigma. The virus is vertically transmitted through male and female gametes. Two alleles of a fly locus, the ref(2)P locus, are present as a polymorphism in all populations: O permissive, and P restrictive for viral multiplication and transmission. Two viral types are known, Type I, which is very sensitive to the P allele, and Type II, which is more resistant. Previous observations have shown that, in presence of the P allele, viral Type II is selected for, in both natural and experimental populations. The aim of the present study was to determine whether, in the absence of P, Type I is selected for, or whether the two types are equivalent. For this purpose, experimental populations deprived of the P allele and differing in the initial proportions of the two viral types were established. After several generations, and despite a possible bias toward Type I, the frequencies of Type I and Type II clones differed in the various populations, depending on their initial values. These findings do not rule out selective advantage of viral Type I in the absence of P, but suggest that, if any, this advantage is in no way comparable to that displayed by viral Type II in the presence of P.

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5

Smith. "Genomics of Avian Viral Infections." Genes 10, no. 10 (October 15, 2019): 814. http://dx.doi.org/10.3390/genes10100814.

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The poultry industry currently accounts for the production of around 118 million metric tons of meat and around 74 million metric tons of eggs annually. As the global population continues to increase, so does our reliance on poultry as a food source. It is therefore of vital importance that we safeguard this valuable resource and make the industry as economically competitive as possible. Avian viral infections, however, continue to cost the poultry industry billions of dollars annually. This can be in terms of vaccination costs, loss of birds and decreased production. With a view to improving the health and welfare of commercial birds and to minimizing associated economic losses, it is therefore of great importance that we try to understand the genetic mechanisms underlying host susceptibility and resilience to some of the major viral pathogens that threaten the poultry species. Some avian viruses, through their zoonotic potential, also pose a risk to human health. This Special Issue will present papers that describe our current knowledge on host responses to various viral pathogens, the genetics underlying those responses and how genomics can begin to provide a solution for resolving the threat posed by these infections.

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6

Crill, W. D., H. A. Wichman, and J. J. Bull. "Evolutionary Reversals During Viral Adaptation to Alternating Hosts." Genetics 154, no. 1 (January 1, 2000): 27–37. http://dx.doi.org/10.1093/genetics/154.1.27.

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Abstract Experimental adaptation of the bacteriophage ϕX174 to a Salmonella host depressed its ability to grow on the traditional Escherichia host, whereas adaptation to Escherichia did not appreciably affect growth on Salmonella. Continued host switching consistently exhibited this pattern. Growth inhibition on Escherichia resulted from two to three substitutions in the major capsid gene. When these phages were forced to grow again on Escherichia, fitness recovery occurred predominantly by reversions at these same sites, rather than by second-site compensatory changes, the more frequently observed mechanism in most microbial systems. The affected residues lie on the virion surface and they alter attachment efficiency, yet they occur in a region distinct from a putative binding region previously identified from X-ray crystallography. These residues not only experienced high rates of evolution in our experiments, but also exhibited high levels of radical amino acid variation among ϕX174 and its known relatives, consistent with a history of adaptation involving these sites.

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7

Gratia, Jean-Pierre. "André Gratia: A Forerunner in Microbial and Viral Genetics." Genetics 156, no. 2 (October 1, 2000): 471–76. http://dx.doi.org/10.1093/genetics/156.2.471.

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8

Adamson, Amy L., Kultaran Chohan, Jennifer Swenson, and Dennis LaJeunesse. "ADrosophilaModel for Genetic Analysis of Influenza Viral/Host Interactions." Genetics 189, no. 2 (July 20, 2011): 495–506. http://dx.doi.org/10.1534/genetics.111.132290.

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9

Stedman, Kenneth M., Christa Schleper, Evelyn Rumpf, and Wolfram Zillig. "Genetic Requirements for the Function of the Archaeal Virus SSV1 in Sulfolobus solfataricus: Construction and Testing of Viral Shuttle Vectors." Genetics 152, no. 4 (August 1, 1999): 1397–405. http://dx.doi.org/10.1093/genetics/152.4.1397.

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Abstract Directed open reading frame (ORF) disruption and a serial selection technique in Escherichia coli and the extremely thermophilic archaeon Sulfolobus solfataricus allowed the identification of otherwise cryptic crucial and noncrucial viral open reading frames in the genome of the archaeal virus SSV1. It showed that the 15.5-kbp viral genome can incorporate a 2.96-kbp insertion without loss of viral function and package this DNA properly into infectious virus particles. The selection technique, based on the preferential binding of ethidium bromide to relaxed DNA and the resulting inhibition of endonuclease cleavage to generate a pool of mostly singly cut molecules, should be generally applicable. A fully functional viral shuttle vector for S. solfataricus and E. coli was made. This vector spreads efficiently through infected cultures of S. solfataricus, its replication is induced by UV irradiation, it forms infectious virus particles, and it is stable at high copy number in both S. solfataricus and E. coli. The classification of otherwise unidentifiable ORFs in SSV1 facilitates genetic analysis of this virus, and the shuttle vector should be useful for the development of genetic systems for Crenarchaeota.

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10

Ekechukwu, M. C., D. J. Oberste, and B. A. Fane. "Host and phi X 174 mutations affecting the morphogenesis or stabilization of the 50S complex, a single-stranded DNA synthesizing intermediate." Genetics 140, no. 4 (August 1, 1995): 1167–74. http://dx.doi.org/10.1093/genetics/140.4.1167.

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Abstract The morphogenetic pathway of bacteriophage phi X 174 was investigated in rep mutant hosts that specifically block stage III single-stranded DNA synthesis. The defects conferred by the mutant rep protein most likely affect the formation or stabilization of the 50S complex, a single-stranded DNA synthesizing intermediate, which consists of a viral prohead and a DNA replicating intermediate (preinitiation complex). phi X 174 mutants, ogr (rep), which restore the ability to propagate in the mutant rep hosts, were isolated. The org (rep) mutations confer amino acid substitutions in the viral coat protein, a constituent of the prohead, and the viral A protein, a constituent of the preinitiation complex. Four of the six coat protein substitutions are localized on or near the twofold axis of symmetry in the atomic structure of the mature virion.

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11

Franchini, Genoveffa, Richard F. Ambinder, and Michèle Barry. "Viral Disease in Hematology." Hematology 2000, no. 1 (January 1, 2000): 409–23. http://dx.doi.org/10.1182/asheducation.v2000.1.409.20000409.

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As part of the international outreach of the American Society of Hematology, this review addresses some aspects of the genetics, biology, epidemiology, and clinical relevance of viruses that cause a variety of hematopoietic disorders in human populations. The viruses described here have a different pattern of geographical distribution, and the disease manifestations may vary according to environmental and/or genetic characteristics of the host. Epstein-Barr virus, a linear double-stranded DNA virus (herpesvirus), and the human T-cell leukemia virus, a retrovirus with a single-stranded diploid RNA genome, are associated among other diseases with lymphoma and leukemia/lymphoma, respectively. Both viruses cause a lifelong infection, but only a small percentage of infected individuals develop hematopoietic neoplasms. Epidemiological data suggest that the time of infection may be important in determining disease outcome in both HTLV-I and EBV infection. The pathogenic mechanisms used by these viruses are of most interest since they may recapitulate growth dysregulation steps also occurring in other hematopoietic malignancies.In Section I Dr. Franchini reviews the biology, genetics and diseases associated with HTLV-I and HTLV-II. In Section II, Dr. Ambinder reviews the biology of EBV infection and its relationship to the pathogenesis of Hodgkin's disease and other malignancies.In Section III, Dr. Barry reviews the viral hemorrhagic fevers caused by RNA viruses such as Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae, which can lead to acute syndromes that can be fatal. However, prompt diagnosis is key for patient management as well as for limiting their spread to others. These syndromes have become the focus of public concern and represent not only a clinical challenge, since in most cases no specific antiviral treatment is available, but also a challenge for future basic research on their biology and pathogenesis since little is known at present.

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12

Franchini, Genoveffa, Richard F. Ambinder, and Michèle Barry. "Viral Disease in Hematology." Hematology 2000, no. 1 (January 1, 2000): 409–23. http://dx.doi.org/10.1182/asheducation.v2000.1.409.409.

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Abstract As part of the international outreach of the American Society of Hematology, this review addresses some aspects of the genetics, biology, epidemiology, and clinical relevance of viruses that cause a variety of hematopoietic disorders in human populations. The viruses described here have a different pattern of geographical distribution, and the disease manifestations may vary according to environmental and/or genetic characteristics of the host. Epstein-Barr virus, a linear double-stranded DNA virus (herpesvirus), and the human T-cell leukemia virus, a retrovirus with a single-stranded diploid RNA genome, are associated among other diseases with lymphoma and leukemia/lymphoma, respectively. Both viruses cause a lifelong infection, but only a small percentage of infected individuals develop hematopoietic neoplasms. Epidemiological data suggest that the time of infection may be important in determining disease outcome in both HTLV-I and EBV infection. The pathogenic mechanisms used by these viruses are of most interest since they may recapitulate growth dysregulation steps also occurring in other hematopoietic malignancies. In Section I Dr. Franchini reviews the biology, genetics and diseases associated with HTLV-I and HTLV-II. In Section II, Dr. Ambinder reviews the biology of EBV infection and its relationship to the pathogenesis of Hodgkin's disease and other malignancies. In Section III, Dr. Barry reviews the viral hemorrhagic fevers caused by RNA viruses such as Arenaviridae, Bunyaviridae, Filoviridae, and Flaviviridae, which can lead to acute syndromes that can be fatal. However, prompt diagnosis is key for patient management as well as for limiting their spread to others. These syndromes have become the focus of public concern and represent not only a clinical challenge, since in most cases no specific antiviral treatment is available, but also a challenge for future basic research on their biology and pathogenesis since little is known at present.

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13

Kannan, Maathavi, Zamri Zainal, Ismanizan Ismail, Syarul Nataqain Baharum, and Hamidun Bunawan. "Application of Reverse Genetics in Functional Genomics of Potyvirus." Viruses 12, no. 8 (July 26, 2020): 803. http://dx.doi.org/10.3390/v12080803.

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Numerous potyvirus studies, including virus biology, transmission, viral protein function, as well as virus–host interaction, have greatly benefited from the utilization of reverse genetic techniques. Reverse genetics of RNA viruses refers to the manipulation of viral genomes, transfection of the modified cDNAs into cells, and the production of live infectious progenies, either wild-type or mutated. Reverse genetic technology provides an opportunity of developing potyviruses into vectors for improving agronomic traits in plants, as a reporter system for tracking virus infection in hosts or a production system for target proteins. Therefore, this review provides an overview on the breakthroughs achieved in potyvirus research through the implementation of reverse genetic systems.

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14

Warren, Cody J., and Sara L. Sawyer. "How host genetics dictates successful viral zoonosis." PLOS Biology 17, no. 4 (April 19, 2019): e3000217. http://dx.doi.org/10.1371/journal.pbio.3000217.

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15

Flint, Jane, and Thomas Shenk. "VIRAL TRANSACTIVATING PROTEINS." Annual Review of Genetics 31, no. 1 (December 1997): 177–212. http://dx.doi.org/10.1146/annurev.genet.31.1.177.

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16

McGee, Lindsey W., Andrew M. Sackman, Anneliese J. Morrison, Jessica Pierce, Jeremy Anisman, and Darin R. Rokyta. "Synergistic Pleiotropy Overrides the Costs of Complexity in Viral Adaptation." Genetics 202, no. 1 (November 12, 2015): 285–95. http://dx.doi.org/10.1534/genetics.115.181628.

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17

Wilke, Claus O. "Probability of Fixation of an Advantageous Mutant in a Viral Quasispecies." Genetics 163, no. 2 (February 1, 2003): 467–74. http://dx.doi.org/10.1093/genetics/163.2.467.

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Abstract The probability that an advantageous mutant rises to fixation in a viral quasispecies is investigated in the framework of multitype branching processes. Whether fixation is possible depends on the overall growth rate of the quasispecies that will form if invasion is successful rather than on the individual fitness of the invading mutant. The exact fixation probability can be calculated only if the fitnesses of all potential members of the invading quasispecies are known. Quasispecies fixation has two important characteristics: First, a sequence with negative selection coefficient has a positive fixation probability as long as it has the potential to grow into a quasispecies with an overall growth rate that exceeds that of the established quasispecies. Second, the fixation probabilities of sequences with identical fitnesses can nevertheless vary over many orders of magnitudes. Two approximations for the probability of fixation are introduced. Both approximations require only partial knowledge about the potential members of the invading quasispecies. The performance of these two approximations is compared to the exact fixation probability on a network of RNA sequences with identical secondary structure.

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18

Tallóczy, Zsolt, Rebecca Mazar, Denise E. Georgopoulos, Fausto Ramos, and Michael J. Leibowitz. "The [KIL-d] Element Specifically Regulates Viral Gene Expression in Yeast." Genetics 155, no. 2 (June 1, 2000): 601–9. http://dx.doi.org/10.1093/genetics/155.2.601.

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Abstract The cytoplasmically inherited [KIL-d] element epigenetically regulates killer virus gene expression in Saccharomyces cerevisiae. [KIL-d] results in variegated defects in expression of the M double-stranded RNA viral segment in haploid cells that are “healed” in diploids. We report that the [KIL-d] element is spontaneously lost with a frequency of 10−4–10−5 and reappears with variegated phenotypic expression with a frequency of ≥10−3. This high rate of loss and higher rate of reappearance is unlike any known nucleic acid replicon but resembles the behavior of yeast prions. However, [KIL-d] is distinct from the known yeast prions in its relative guanidinium hydrochloride incurability and independence of Hsp104 protein for its maintenance. Despite its transmissibility by successive cytoplasmic transfers, multiple cytoplasmic nucleic acids have been proven not to carry the [KIL-d] trait. [KIL-d] epigenetically regulates the expression of the M double-stranded RNA satellite virus genome, but fails to alter the expression of M cDNA. This specificity remained even after a cycle of mating and meiosis. Due to its unique genetic properties and viral RNA specificity, [KIL-d] represents a new type of genetic element that interacts with a viral RNA genome.

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19

Miller, Craig R., Paul Joyce, and Holly A. Wichman. "Mutational Effects and Population Dynamics During Viral Adaptation Challenge Current Models." Genetics 187, no. 1 (November 1, 2010): 185–202. http://dx.doi.org/10.1534/genetics.110.121400.

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20

Ketkar, Harshada, Daniella Herman, and Penghua Wang. "Genetic Determinants of the Re-Emergence of Arboviral Diseases." Viruses 11, no. 2 (February 12, 2019): 150. http://dx.doi.org/10.3390/v11020150.

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Mosquito-borne diseases constitute a large portion of infectious diseases, causing more than 700,000 deaths annually. Mosquito-transmitted viruses, such as yellow fever, dengue, West Nile, chikungunya, and Zika viruses, have re-emerged recently and remain a public health threat worldwide. Global climate change, rapid urbanization, burgeoning international travel, expansion of mosquito populations, vector competence, and host and viral genetics may all together contribute to the re-emergence of arboviruses. In this brief review, we summarize the host and viral genetic determinants that may enhance infectivity in the host, viral fitness in mosquitoes and viral transmission by mosquitoes.

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21

Traina-Dorge, Vicki L., Jean K. Carr, Joan E. Bailey-Wilson, Robert C. Elston, Benjamin A. Taylor, and J. Craig Cohen. "CELLULAR GENES IN THE MOUSE REGULATE IN TRANS THE EXPRESSION OF ENDOGENOUS MOUSE MAMMARY TUMOR VIRUSES." Genetics 111, no. 3 (November 1, 1985): 597–615. http://dx.doi.org/10.1093/genetics/111.3.597.

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ABSTRACT The transcriptional activities of the eleven mouse mammary tumor virus (MMTV) proviruses endogenous to two sets of recombinant inbred (RI) mouse strains, BXD and BXH, were characterized. Comparison of the levels of virus-specific RNA quantitated in each strain showed no direct relationship between the presence of a particular endogenous provirus or with increasing numbers of proviruses. Association of specific genetic markers with the level of MMTV-specific RNA was examined by using multiple regression analysis. Several cellular loci as well as proviral loci were identified that were significantly associated with viral expression. Importantly, these cellular loci associated with MMTV expression segregated independently of viral sequences.

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22

DALEY, MARK, and IAN MCQUILLAN. "FORMAL MODELLING OF VIRAL GENE COMPRESSION." International Journal of Foundations of Computer Science 16, no. 03 (June 2005): 453–69. http://dx.doi.org/10.1142/s0129054105003091.

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The study of viruses in molecular genetics, as biological entities with extremely small genomes, and in medicine, as pathogens, represents an important area of inquiry with significant potential for improving scientific knowledge in both domains. One of the most fascinating genetic adaptations of viruses is the ability to compress their own genomes. We exposit here a formal model of gene compression in viruses and study its properties from a formal-language-theoretic standpoint. In addition to enumerating abstract properties of gene compression for infinite languages, we pay particular attention to the case of finite languages and algorithms for identifying, classifying and quantifying gene compression in real viruses. Information of this sort has applications to automated classification of new viruses and the prediction of potential proto-oncogenes in the human genome.

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23

Hunter, Philip. "Viral taxonomy." EMBO reports 18, no. 10 (September 6, 2017): 1693–96. http://dx.doi.org/10.15252/embr.201744982.

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24

Hunter, Philip. "Viral vigilance." EMBO reports 9, no. 10 (September 5, 2008): 948–50. http://dx.doi.org/10.1038/embor.2008.181.

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25

RENARD, ANDRE, CHRISTIAN GUIOT, DOMINIQUE SCHMETZ, LISE DAGENAIS, PIERRE-PAUL PASTORET, DINO DINA, and JOSEPH A. MARTIAL. "Molecular Cloning of Bovine Viral Diarrhea Viral Sequences." DNA 4, no. 6 (December 1985): 429–38. http://dx.doi.org/10.1089/dna.1985.4.429.

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26

Rose, Noel R., David A. Neumann, and Ahvie Herskowitz. "Genetics of Susceptibility to Viral Myocarditis in Mice." Pathology and Immunopathology Research 7, no. 4 (1988): 266–78. http://dx.doi.org/10.1159/000157122.

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27

Shea, Patrick R., Kevin V. Shianna, Mary Carrington, and David B. Goldstein. "Host Genetics of HIV Acquisition and Viral Control." Annual Review of Medicine 64, no. 1 (January 14, 2013): 203–17. http://dx.doi.org/10.1146/annurev-med-052511-135400.

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28

Jouanguy, Emmanuelle. "Human genetic basis of fulminant viral hepatitis." Human Genetics 139, no. 6-7 (April 13, 2020): 877–84. http://dx.doi.org/10.1007/s00439-020-02166-y.

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29

Elena, Santiago F., Stéphanie Bedhomme, Purificación Carrasco, José M. Cuevas, Francisca de la Iglesia, Guillaume Lafforgue, Jasna Lalić, Àngels Pròsper, Nicolas Tromas, and Mark P. Zwart. "The Evolutionary Genetics of Emerging Plant RNA Viruses." Molecular Plant-Microbe Interactions® 24, no. 3 (March 2011): 287–93. http://dx.doi.org/10.1094/mpmi-09-10-0214.

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Over the years, agriculture across the world has been compromised by a succession of devastating epidemics caused by new viruses that spilled over from reservoir species or by new variants of classic viruses that acquired new virulence factors or changed their epidemiological patterns. Viral emergence is usually associated with ecological change or with agronomical practices bringing together reservoirs and crop species. The complete picture is, however, much more complex, and results from an evolutionary process in which the main players are ecological factors, viruses' genetic plasticity, and host factors required for virus replication, all mixed with a good measure of stochasticity. The present review puts emergence of plant RNA viruses into the framework of evolutionary genetics, stressing that viral emergence begins with a stochastic process that involves the transmission of a preexisting viral strain into a new host species, followed by adaptation to the new host.

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30

Tsai, W.-L., and R. T. Chung. "Viral hepatocarcinogenesis." Oncogene 29, no. 16 (March 15, 2010): 2309–24. http://dx.doi.org/10.1038/onc.2010.36.

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31

RAGNI, M. V., K. E. SHERMAN, and J. A. JORDAN. "Viral pathogens." Haemophilia 16 (June 22, 2010): 40–46. http://dx.doi.org/10.1111/j.1365-2516.2010.02292.x.

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32

Koch, Linda. "Marine genomics goes viral." Nature Reviews Genetics 17, no. 11 (October 3, 2016): 660. http://dx.doi.org/10.1038/nrg.2016.130.

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Domingo, Esteban, and Celia Perales. "Viral quasispecies." PLOS Genetics 15, no. 10 (October 17, 2019): e1008271. http://dx.doi.org/10.1371/journal.pgen.1008271.

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34

Edridge, Deijs, van Zeggeren, Kinsella, Jebbink, Bakker, van de Beek, Brouwer, and van der Hoek. "Viral Metagenomics on Cerebrospinal Fluid." Genes 10, no. 5 (April 30, 2019): 332. http://dx.doi.org/10.3390/genes10050332.

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Identifying the causative pathogen in central nervous system (CNS) infections is crucial for patient management and prognosis. Many viruses can cause CNS infections, yet screening for each individually is costly and time-consuming. Most metagenomic assays can theoretically detect all pathogens, but often fail to detect viruses because of their small genome and low viral load. Viral metagenomics overcomes this by enrichment of the viral genomic content in a sample. VIDISCA-NGS is one of the available workflows for viral metagenomics, which requires only a small input volume and allows multiplexing of multiple samples per run. The performance of VIDISCA-NGS was tested on 45 cerebrospinal fluid (CSF) samples from patients with suspected CNS infections in which a virus was identified and quantified by polymerase chain reaction. Eighteen were positive for an RNA virus, and 34 for a herpesvirus. VIDISCA-NGS detected all RNA viruses with a viral load >2 × 104 RNA copies/mL (n = 6) and 8 of 12 of the remaining low load samples. Only one herpesvirus was identified by VIDISCA-NGS, however, when withholding a DNase treatment, 11 of 18 samples with a herpesvirus load >104 DNA copies/mL were detected. Our results indicate that VIDISCA-NGS has the capacity to detect low load RNA viruses in CSF. Herpesvirus DNA in clinical samples is probably non-encapsidated and therefore difficult to detect by VIDISCA-NGS.

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35

Laman, Heike, David J. Mann, and Nic C. Jones. "Viral-encoded cyclins." Current Opinion in Genetics & Development 10, no. 1 (February 2000): 70–74. http://dx.doi.org/10.1016/s0959-437x(99)00045-3.

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36

Pybus, Oliver G., Andrew Rambaut, and Paul H. Harvey. "An Integrated Framework for the Inference of Viral Population History From Reconstructed Genealogies." Genetics 155, no. 3 (July 1, 2000): 1429–37. http://dx.doi.org/10.1093/genetics/155.3.1429.

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Abstract We describe a unified set of methods for the inference of demographic history using genealogies reconstructed from gene sequence data. We introduce the skyline plot, a graphical, nonparametric estimate of demographic history. We discuss both maximum-likelihood parameter estimation and demographic hypothesis testing. Simulations are carried out to investigate the statistical properties of maximum-likelihood estimates of demographic parameters. The simulations reveal that (i) the performance of exponential growth model estimates is determined by a simple function of the true parameter values and (ii) under some conditions, estimates from reconstructed trees perform as well as estimates from perfect trees. We apply our methods to HIV-1 sequence data and find strong evidence that subtypes A and B have different demographic histories. We also provide the first (albeit tentative) genetic evidence for a recent decrease in the growth rate of subtype B.

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37

Casanova, Jean-Laurent, and Laurent Abel. "Mechanisms of viral inflammation and disease in humans." Science 374, no. 6571 (November 26, 2021): 1080–86. http://dx.doi.org/10.1126/science.abj7965.

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Disease and accompanying inflammation are uncommon outcomes of viral infection in humans. Clinical inflammation occurs if steady-state cell-intrinsic and leukocytic immunity to viruses fails. Inflammation attests to the attempts of newly recruited and activated leukocytes to resolve infection in the blood or tissues. In the confusing battle between a myriad of viruses and cells, studies of human genetics can separate the root cause of inflammation and disease from its consequences. Single-gene inborn errors of cell-intrinsic or leukocytic immunity underlying diverse infections in the skin, brain, or lungs can help to clarify the human determinants of viral disease. The genetic elucidation of immunological deficits in a single patient with a specific vulnerability profile can reveal mechanisms of inflammation and disease that may be triggered by other causes, inherited or otherwise, in other patients. This human genetic dissection of viral infections is giving rise to a new biology and a new medicine.

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38

Lin, Sheng-Chieh, Geng-Hao Bai, Pei-Chun Lin, Chung-Yung Chen, Yi-Hsiang Hsu, Yuan-Chang Lee, and Shih-Yen Chen. "Molecular and Genetics-Based Systems for Tracing the Evolution and Exploring the Mechanisms of Human Norovirus Infections." International Journal of Molecular Sciences 24, no. 10 (May 22, 2023): 9093. http://dx.doi.org/10.3390/ijms24109093.

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Human noroviruses (HuNoV) are major causes of acute gastroenteritis around the world. The high mutation rate and recombination potential of noroviruses are significant challenges in studying the genetic diversity and evolution pattern of novel strains. In this review, we describe recent advances in the development of technologies for not only the detection but also the analysis of complete genome sequences of noroviruses and the future prospects of detection methods for tracing the evolution and genetic diversity of human noroviruses. The mechanisms of HuNoV infection and the development of antiviral drugs have been hampered by failure to develop the infectious virus in a cell model. However, recent studies have demonstrated the potential of reverse genetics for the recovery and generation of infectious viral particles, suggesting the utility of this genetics-based system as an alternative for studying the mechanisms of viral infection, such as cell entry and replication.

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39

Oldstone, Michael B. A. "Viral persistence." Cell 56, no. 4 (February 1989): 517–20. http://dx.doi.org/10.1016/0092-8674(89)90573-4.

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40

Andrade Júnior, Dahir Ramos de, and Dahir Ramos de Andrade. "The influence of the human genome on chronic viral hepatitis outcome." Revista do Instituto de Medicina Tropical de São Paulo 46, no. 3 (June 2004): 119–26. http://dx.doi.org/10.1590/s0036-46652004000300001.

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The mechanisms that determine viral clearance or viral persistence in chronic viral hepatitis have yet to be identified. Recent advances in molecular genetics have permitted the detection of variations in immune response, often associated with polymorphism in the human genome. Differences in host susceptibility to infectious disease and disease severity cannot be attributed solely to the virulence of microbial agents. Several recent advances concerning the influence of human genes in chronic viral hepatitis B and C are discussed in this article: a) the associations between human leukocyte antigen polymorphism and viral hepatic disease susceptibility or resistance; b) protective alleles influencing hepatitis B virus (HBV) and hepatitis C virus (HCV) evolution; c) prejudicial alleles influencing HBV and HCV; d) candidate genes associated with HBV and HCV evolution; d) other genetic factors that may contribute to chronic hepatitis C evolution (genes influencing hepatic stellate cells, TGF-beta1 and TNF-alpha production, hepatic iron deposits and angiotensin II production, among others). Recent discoveries regarding genetic associations with chronic viral hepatitis may provide clues to understanding the development of end-stage complications such as cirrhosis or hepatocellular carcinoma. In the near future, analysis of the human genome will allow the elucidation of both the natural course of viral hepatitis and its response to therapy.

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41

Aubry, Fabien, Antoine Nougairède, Lauriane de Fabritus, Gilles Querat, Ernest A. Gould, and Xavier de Lamballerie. "Single-stranded positive-sense RNA viruses generated in days using infectious subgenomic amplicons." Journal of General Virology 95, no. 11 (November 1, 2014): 2462–67. http://dx.doi.org/10.1099/vir.0.068023-0.

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Reverse genetics is a key methodology for producing genetically modified RNA viruses and deciphering cellular and viral biological properties, but methods based on the preparation of plasmid-based complete viral genomes are laborious and unpredictable. Here, both wild-type and genetically modified infectious RNA viruses were generated in days using the newly described ISA (infectious-subgenomic-amplicons) method. This new versatile and simple procedure may enhance our capacity to obtain infectious RNA viruses from PCR-amplified genetic material.

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42

Fleuriet, Annie. "Evolution of the Proportions of Two Sigma Viral Types in Experimental Populations ofDrosophila melanogaster." Genetics 157, no. 1 (January 1, 2001): 455–56. http://dx.doi.org/10.1093/genetics/157.1.455.

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43

Mallal, Simon. "Host genetics unplugged: removing the camouflage of viral adaptation." Current Opinion in HIV and AIDS 1, no. 3 (May 2006): 218–19. http://dx.doi.org/10.1097/01.coh.0000221595.34165.6f.

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44

Heim, Markus H., Pierre-Yves Bochud, and Jacob George. "Host – hepatitis C viral interactions: The role of genetics." Journal of Hepatology 65, no. 1 (October 2016): S22—S32. http://dx.doi.org/10.1016/j.jhep.2016.07.037.

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45

Griffin, Diane E. "Viral Encephalomyelitis." PLoS Pathogens 7, no. 3 (March 24, 2011): e1002004. http://dx.doi.org/10.1371/journal.ppat.1002004.

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46

Wawrzynczak, Edward. "A global marine viral metagenome." Nature Reviews Genetics 8, no. 1 (November 28, 2006): 3. http://dx.doi.org/10.1038/nrg2030.

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47

Wang, Mengyi, Jinyan Wu, Xiaoan Cao, Long Xu, Junhuang Wu, Haiyan Ding, and Youjun Shang. "Developments in Negative-Strand RNA Virus Reverse Genetics." Microorganisms 12, no. 3 (March 11, 2024): 559. http://dx.doi.org/10.3390/microorganisms12030559.

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Many epidemics are caused by negative-stranded RNA viruses, leading to serious disease outbreaks that threaten human life and health. These viruses also have a significant impact on animal husbandry, resulting in substantial economic losses and jeopardizing global food security and the sustainable livelihoods of farmers. However, the pathogenic and infection mechanism of most negative-stranded RNA viruses remain unclear. Reverse genetics systems are the most powerful tools for studying viral protein function, viral gene expression regulation, viral pathogenesis, and the generation of engineered vaccines. The reverse genetics of some negative-strand viruses have been successfully constructed, while others have not. In this review, we focus on representative viruses from the Orthomyxoviridae family (IAV), the Filoviridae family (EBOV), and the Paramyxoviridae family (PPRV) to compile and summarize the existing knowledge on reverse genetics techniques for negative-strand viruses. This will provide a theoretical foundation for developing reverse genetics techniques for some negative-strand viruses.

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48

Stanley, John. "Geminiviruses: plant viral vectors." Current Opinion in Genetics & Development 3, no. 1 (February 1993): 91–96. http://dx.doi.org/10.1016/s0959-437x(05)80347-8.

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49

Treco, Douglas A., and Richard F. Selden. "Non-viral gene therapy." Molecular Medicine Today 1, no. 7 (October 1995): 314–21. http://dx.doi.org/10.1016/s1357-4310(95)80030-1.

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50

Saelao, Perot, Ying Wang, Ganrea Chanthavixay, Rodrigo Gallardo, Anna Wolc, Jack Dekkers, Susan Lamont, Terra Kelly, and Huaijun Zhou. "Genetics and Genomic Regions Affecting Response to Newcastle Disease Virus Infection under Heat Stress in Layer Chickens." Genes 10, no. 1 (January 18, 2019): 61. http://dx.doi.org/10.3390/genes10010061.

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Newcastle disease virus (NDV) is a highly contagious avian pathogen that poses a tremendous threat to poultry producers in endemic zones due to its epidemic potential. To investigate host genetic resistance to NDV while under the effects of heat stress, a genome-wide association study (GWAS) was performed on Hy-Line Brown layer chickens that were challenged with NDV while under high ambient temperature to identify regions associated with host viral titer, circulating anti-NDV antibody titer, and body weight change. A single nucleotide polymorphism (SNP) on chromosome 1 was associated with viral titer at two days post-infection (dpi), while 30 SNPs spanning a quantitative trait loci (QTL) on chromosome 24 were associated with viral titer at 6 dpi. Immune related genes, such as CAMK1d and CCDC3 on chromosome 1, associated with viral titer at 2 dpi, and TIRAP, ETS1, and KIRREL3, associated with viral titer at 6 dpi, were located in two QTL regions for viral titer that were identified in this study. This study identified genomic regions and candidate genes that are associated with response to NDV during heat stress in Hy-Line Brown layer chickens. Regions identified for viral titer on chromosome 1 and 24, at 2 and 6 dpi, respectively, included several genes that have key roles in regulating the immune response.

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