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HIV and AIDS
Published in Rae-Ellen W. Kavey, Allison B. Kavey, Viral Pandemics, 2020
Rae-Ellen W. Kavey, Allison B. Kavey
Like all lentiviruses, HIV populations have enormous genetic variation revealed by molecular phylogenetic studies. HIV is reported to have the highest recorded biological mutation rate currently known to science. Point mutations due to base substitutions occur very frequently, primarily because – as in all RNA viruses – the absence of proofreading makes the process of RNA synthesis error-prone. This results in a baseline spontaneous mutation rate of at least 1% per year. Within a single infected individual, the virus evolves extremely frequently and rapidly, resulting in multiple mutant versions of the virus.54 As with the influenza virus, there is a second important mechanism for genetic variation: recombination – the exchange of entire gene sequences at unselected positions – occurs when a target cell is infected with different HIV subtypes. Recombination of HIV-1 subtypes is considered a driving force for its diversity worldwide, responsible for frequent and important genetic variation in the virus; approximately 1 in 400 newly produced HIV virus particles is a recombinant virus containing combined genetic material. Such a recombinant is called a unique recombinant form (URF). If an inter-subtype recombinant virus succeeds in being transmitted to many people, it becomes one of the circulating strains in the HIV epidemic and is classified as a “circulating recombinant form (CRF)”; at least 89 different CRFs have been identified.55
The Jackson Laboratory Mouse Mutant Resource
Published in John P. Sundberg, Handbook of Mouse Mutations with Skin and Hair Abnormalities, 2020
Despite advances in molecular technologies that increase our ability to create mouse models of inherited human conditions and clone the mutated genes, spontaneous mutations have and will continue to contribute to our understanding of basic mammalian biology. Most important, spontaneous mutations provide potential models for human disorders for which the mutated gene has not yet been cloned. In addition, the genetic defects in most spontaneous mutations of human beings and other mammals are usually confined to a single gene, i.e., small insertions or deletions or single base pair changes.1 The most successful approach to date for cloning mutated genes that provide model systems has been the candidate locus approach. A cloned gene mapped to the same chromosomal site as a spontaneous mutation is considered a candidate for the mutation and analyzed accordingly. Finally, when targeted and transgenic mutations mutate genes already identified by existing spontaneous mutations, the spontaneous mutations have greatly increased the speed and ease of analyzing the induced mutations.
Maximum Permissible Dose
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
Exposure to manmade radiation below the level of background radiation will produce additional effects that are less in quantity and no different in kind from those which man has experienced and has been able to tolerate throughout history. Continuous exposure of the population to the background radiation of 3 rem/30-year generation increases the rate of mutation by 1–6% of spontaneous mutation.
History of radiation genetics: light and darkness
Published in International Journal of Radiation Biology, 2019
The refractory nature of germ cells to undergoing radiation-induced mutagenesis may be attributed to the lack of induction or to a strong negative selection against mutation-carrying zygotes or fetuses. As mentioned earlier, the probability of the negative selection hypothesis seems to be low. The question can then be modified to asking why the mutation yields were so high at specific loci when compared with that at other many genes. Imagine that when the SLT experiments were planned in the 1950s, any gene could have been the candidate as long as the mutant phenotype was clearly recognizable. One important requirement, however, was that the mutant mice be alive and fertile under the homozygous conditions used for the tester strain. Mutant mice in those days originated from pet mice and have a long history [e.g. mutant piebald-like mice appeared in Japanese Ukiyo-e prints in the Edo period (1603–1868)]. It seems likely that these genes were prone to undergoing spontaneous mutations since maintaining some degree of variation in coat colors, for example, should be evolutionarily advantageous in order to adapt to sudden environmental changes. In addition, for as yet unknown reasons, genes with higher spontaneous mutation rates tend to be more responsive to radiation (both in fruit flies and mice: Shukla et al. 1979). While the 6 or 7 selected specific genes used for the SLT experiments had long been thought to be representative of many genes in the genome, this is probably not the case.
Dengue vaccine: a key for prevention
Published in Expert Review of Vaccines, 2020
Usa Thisyakorn, Terapong Tantawichien
The DNA approach also carries unique risks. The first is the theoretical risk of nucleic acid integration into the host’s chromosomal DNA to potentially inactivate tumor suppressor genes or activate oncogenes. This risk appears to be well below the spontaneous mutation frequency for mammalian cells. However, if a mutation due to DNA integration is a part of a multiple hit phenomenon leading to carcinogenesis, it could take many years for this problem to become evident. Another concern is that foreign DNA may induce anti-DNA antibodies leading to autoimmune diseases such as systemic lupus erythematosus. However, to date, studies on lupus-prone mice, normal mice, rabbits, and people have not validated this concern [13,37].
Study of mutation from DNA to biological evolution
Published in International Journal of Radiation Biology, 2019
Masako Bando, Tetsuhiro Kinugawa, Yuichiro Manabe, Miwako Masugi, Hiroo Nakajima, Kazuyo Suzuki, Yuichi Tsunoyama, Takahiro Wada, Hiroshi Toki
In this way, we are now faced with the questions, ‘What makes such an amount of the spontaneous mutation frequency?’ and ‘What kind of mechanism provides the spontaneous mutation frequency quantitatively?’ These questions will be discussed in the following sections.