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NGS technologies for detection of SARS-CoV-2 strains and mutations
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Manisha Choudhury, Ayushi Verma, Ankit Halder, Arup Acharjee
Current testing procedures like RT-PCR testing can only detect the presence of the virus. No information on the virus’s genetic sequence, coinfection, or host immune response can be derived using RT-PCR. With the emerging mutations, it becomes imperative to use NGS technology to support the RT-PCR technique to ensure the accuracy of the test and derive valuable information. Because of this, there has been advancement in the NGS platforms, and, currently, two methods have been devised for SARS-CoV-2 sequencing. One work-flow is based on shotgun genomics and another on target enrichment. Several mutations such as amino acid deletion in nsp2 (Bal et al. 2020), truncated ORF (Batty et al. 2020), and nucleotide deletion in ORF (Holland et al. 2020) have been identified by SARS-CoV-2 genomic monitoring in the population. Early sequencing of the SARS-CoV-2 genome was carried out using viral metagenomic NGS (mNGS). However, this method lacks sensitivity in samples with low viral load, and a very high depth of sequencing is not possible (Bal et al. 2020). In such cases, targeted methods, including amplicon or capture-based enrichments, are used.
Cryptosporidiosis in Birds
Published in J. P. Dubey, C. A. Speer, R. Fayer, Cryptosporidiosis of Man and Animals, 2018
David S. Lindsay, Byron L. Blagburn
Most studies on experimentally induced crytosporidiosis in birds have been done with C. baileyi isolated from chickens. Oral inoculation of chickens194,306,463,468,469,478 or turkeys473 with C. baileyi oocysts generally does not produce clinical signs. Some birds may appear depressed and huddle, but otherwise are normal. Weight gains of infected birds may be reduced 1 to 2 weeks postinoculation.104,306,463 Parasite-induced lesions are generally confined to the BF and cloaca. These lesions consist of epithelial hyperplasia and hypertrophy with underlying inflammatory response. Bursal folical atrophy may also be observed. Coinfection of chickens with reovirus has little effect on oral C. baileyi infections, but shedding of both virus and oocysts appear to be enhanced by some unknown mechanism.306 Coinfection of chickens with infectious bursal disease virus and C. baileyi produces more severe bursal lesions, more infected birds, and a greater parasite density in infected birds.463
Chrysotile and mesothelioma
Published in Dorsett D. Smith, The Health Effects of Asbestos, 2015
Another important factor in the history of understanding asbestos fiber carcinogenesis, has been the fact that the incidence of mesothelioma in heavily exposed amphibole asbestos groups has ranged from 5% to 10%. Even though some individuals have been very heavily exposed to asbestos and have asbestosis, they never developed mesotheliomas. This suggests that there is a genetic factor that may increase susceptibility to the cancer-causing effects of the asbestos exposure, since one would expect that the incidence of mesothelioma would increase linearly with increasing asbestos exposure, but it does not. In fact, most of the mesotheliomas occur at low-to-moderate exposure levels, and continuous high-level exposures do not proportionately increase the risk of developing a mesothelioma. Michele Carbone and others had speculated that coinfection with the simian virus-40 may be an important factor in the causation of mesotheliomas. This monkey kidney virus contaminated the Salk poliovirus vaccine between 1955 and 1963. The authors have suggested that this virus increases the susceptibility to mesothelioma in individuals exposed to asbestos. (Qi F, Carbone M, Yang H, Gaudino G. Simian virus 40 transformation, malignant mesothelioma and brain tumors. Expert Rev Respir Med 2011;5(5):683–97.)
Dynamics of two pathogens in a single tick population
Published in Letters in Biomathematics, 2019
Alexis White, Elsa Schaefer, Chelsea Wright Thompson, Christopher M. Kribs, Holly Gaff
The equations describing host infections are given in Equations (3)–(5). Tick-to-host vector-borne transmission for pathogen i, , is modelled by The rate of transmission from tick-to-host is , which includes biting rate, probability of transmission, and proportion of hosts to ticks. This rate is multiplied by the proportion of the susceptible host population to the total population and by the number of vectors that carry pathogen i, which includes coinfected vectors. Similar dynamics are considered for hosts who become coinfected with both pathogens, with the exception that the proportion of susceptible hosts who can move to the coinfected class is simply for transmission of pathogen 2 and for transmission of pathogen 1. There is no evidence for cross immunity of these pathogens and thus susceptibility does not change after contracting a single pathogen. Host recovery, , from either pathogen is included within the model, allowing recovery from a single pathogen to the susceptible class. In the case of coinfection, is the rate of host recovery from coinfection into the pathogen 1 infected class, and similarly represents the rate of recovery from coinfection into the pathogen 2 infected class.