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Konten disediakan oleh Hiram College Podcasting and Brad Goodner. Semua konten podcast termasuk episode, grafik, dan deskripsi podcast diunggah dan disediakan langsung oleh Hiram College Podcasting and Brad Goodner atau mitra platform podcast mereka. Jika Anda yakin seseorang menggunakan karya berhak cipta Anda tanpa izin, Anda dapat mengikuti proses yang diuraikan di sini https://id.player.fm/legal.

On the Bus with Troy Vollhoffer

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From Backroom Bars to Broadway with Dustin Lynch 36:27

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Not many artists actually hail from Tennessee, but the scenic valleys and rolling hills of The Volunteer State are part of Dustin Lynch’s DNA. In this episode of On the Bus, Country Thunder CEO Troy Vollhoffer sits down with Dustin to discuss his journey from playing fraternity parties and weddings across the southeast to being the first country artist with a club residency at the Wynn in Las Vegas. Plus, stick around for our new segment, Thunder Strike, where Troy features upcoming festival performer Riley Green’s hit song “Damn Good Day to Leave” to give you a taste of what’s to come at Country Thunder in 2025.…

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Podcast associated with Hiram College Genetics course. Focus is on the history of genomics and how a genomic view of life has impacted basic science as well as applied fields such as medicine and agriculture.

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#Science #Podcasting Education #Natural Sciences #Hiram College #Brad Goodner #Genomics #Dna Sequencing

Genomics Revolution

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#Science #Podcasting Education #Natural Sciences #Hiram College #Brad Goodner #Genomics #Dna Sequencing

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Genomics Revolution

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MERS - A Recent, Ongoing But Overshadowed Coronavirus Epidemic 4:29

5 years yang lalu4:29

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Genomics Revolution Guest Hosts: Matthew Hecker & Miranda Mordue Episode 54: MERS Coronavirus- Middle East Respiratory Syndrome-related coronavirus Hello, and welcome to Genomics Revolution. This is Matthew Hecker, and this is Miranda Mordue, bringing you in from the Hiram College Genetics course of 2020. As we stand in April 2020, the world is currently in a state of flux with COVID-19, a novel coronavirus that is taking the world by storm, and not in a good way. In light of COVID-19, our topic for today is another variety of novel coronavirus, MERS-Coronavirus. This stands for Middle East Respiratory syndrome coronavirus, but we’ll be calling it MERS from here on out. MERS was first reported in 2012 in Saudi Arabia in the respiratory tract of a businessman who had died from viral pneumonia. It was the first highly pathogenic coronavirus since the SARS coronavirus in 2003. This virus had a very high mortality rate of greater than 35%. The MERS genome is single stranded RNA and is made up of about 30,000 bases. Though sometimes it is difficult to think about the scale of genetics, this is a relatively small genome size that contains only 10 Open Reading Frames, or ORFs. Each of these ORFS is a section in which transcription can occur. One of these ORFs encodes for a “polyprotein.” This is a large encoded structure that can be cleaved in order to serve different purposes, basically a conglomeration of different proteins that can be broken up and used as necessary. In the case of MERS, this polyprotein encodes viral replicase and the methods of interaction with ribosomes. Basically, this polyprotein is what allows for the infection and takeover of host cells to replicate itself, while the rest of the ORFs translate to structural and functional proteins. These other proteins are responsible for getting the polyprotein into host cells. Knowing this, what else can genetics tell us about MERS? Based on genomic comparison, it is very likely that the strain of MERS that eventually came to affect humans began development in the dromedary camel. With MERS, the evidence of human to human transmission is differing based on location the virus was found. In Riyadh, there were cases of human transmission, but in other places, it was not observed. This means that some of the infections of humans beyond the initial case are a result of contact with livestock. Because of this discreet infection from various sources, it was actually discover that that are many different strains of MERS. In a study from 2013, 21 samples of MERS were examined from different patients, and 10 different genomes were produced for the virus. This means that MERS infections are not limited to human contact and this will obviously affect the manner in which the virus must be addressed. MERS has also shown some resistance to the innate immune response of the body. The codon selectivity in MERS is variable in three genetic clusters, which have developed a codon bias to survive inside the host. By using different codon sequences, the immune system is not able to recognize the virus as effectively. In different strains, this leads to adaptation to resist the human immune system, making MERS a more dangerous virus. As of now, there is no specific “cure” for MERS, but levels of infection remain relatively low due to low human to human transmission in strains, as well as potentially lethal symptoms from the onset which cause quarantining very quickly. I’d hate to end on too negative a note, so let me just say this: Scientists all over the world are very capable at what they do, and they will be able to figure out a way to defeat MERS, as well as the current COVID-19. Just remember to continue listening and learning! Thank you all for listening! This has been Genomics Revolution. Sources: 1) Cotten et al., 2013. The Lancet Vol 382, pp 1993-2002. Transmission and evolution of the Middle East Respiratory syndrome coronavirus in Saudi Arabia: A descriptive Genomics Study. 2) Alnazawi et al., 2017. Biol. Pharm. Bull. Vol 40 pp 1289-1298. Comparative Genomic Analysis MERS CoV Isolated from Humans and Camels with Special Reference to Virus Encoded Helicase. 3) Shapiro et al., 2016. Disaster and Military Medicine 2:9. Middle EAst Respiratory Syndrome Coronavirus: A Review of the Current Situation in the World. 4) Chafekar, A., & Fielding, B. C., 2018. Viruses vol. 10,2 93. MERS-CoV: Understanding the Latest Human Coronavirus Threat.…

Genomics Revolution

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SARS - The First Coronavirus Near-Pandemic 5:06

5 years yang lalu5:06

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Genomics Revolution Guest Hosts: Denise Hart & Madyson Morris Episode 53: SARS Coronavirus Welcome to Genomics Revolution. This is Denise Hart and Madyson Morris from the 2020 Hiram College Genetics course hosting this episode on the SARS coronavirus. The acronym SARS stands for Severe Acute Respiratory System.1 To distinguish between the virus and the disease it causes, we will call the virus the SARS coronavirus and the disease SARS from here on out. Today, we will discuss the SARS coronavirus genome, as well as the outbreak that occurred across the globe from 2002 to 2003. Did you know that SARS coronavirus was once the largest RNA virus genome? This genome is also single-stranded and it has 29,751 RNA molecules. The genome has 14 genes and 29 mature proteins. The largest gene found within the SARS coronavirus genome encodes a polyprotein. This polyprotein gets cut into 16 mature proteins. In addition to these mature proteins, the genome also shows that hypothetical proteins, unique to SARS-coronavirus, exist. Researchers used BLAST, along with other function prediction programs, to determine the function of these proteins.3Their research concluded that the genome has carbon-oxygen lyase, oxidoreductases that act on CH-OH groups, an ATP-binding cassette transporter, structural proteins, and a voltage-gated ion channel.3 So, why should we care about SARS coronavirus and the disease it causes? The outbreak started almost 20 years ago!2 We should care about understanding this virus because it causes most patients to develop pneumonia, hence the “Severe Acute Respiratory System” title. Pneumonia can be a very deadly disease if not treated right away. We should also care about educating ourselves on SARS coronavirus because during the outbreak, 8,098 people suffered from SARS as well as pneumonia or respiratory distress syndrome. 774 of those people died.1,2 If contracted, SARS coronavirus can have detrimental side effects, and having a good understanding of this virus could potentially prevent future outbreaks and pandemics caused by it. SARS coronavirus originally started out in bat species, but is able to be contracted by humans. The symptoms of SARS coronavirus in humans include fever, dry cough, headache, muscle aches, and difficulty breathing. These symptoms are very typical of Coronavirus- and true for most of the 36 types of coronaviruses.6 While it is good to be aware of these symptoms, 1 symptom really sets SARS coronavirus apart from other strains: urinary abnormalities. For the first patients with SARS, they were diagnosed with other ailments due to these unique symptoms. It wasn’t until the genome was sequenced that researchers learned that SARS not only turns cells along the respiratory tract into host cells, but also cells in the intestines, liver, heart, vascular endothelium, testis, and the kidneys!6 Not only did some of the patients with SARS get treated for other ailments due to having urinary abnormalities, some of the patients with SARS received treatment but nothing happened!6,8 These were patients with the common symptoms. They received treatment but they did not get better. This was because the SARS coronavirus had mutated 14 times.6,7 Some patients had the original strain and others had one of the mutated strains. The treatment of the original strain did not help patients with a mutant strain. Researchers used high density sequencing arrays to find the places in the SARS coronavirus genome that had mutated.5,6 The scientists found that in mutant strains, 5-6 nucleotides were inserted or deleted. 5,6 This small change caused the virus to be harder to treat because of the variations between each mutation. As these mutations were being discovered, the need to understand this virus was vital because of the global outbreak. Although there were not enough cases to consider it a pandemic, a virus causing a global outbreak still needs to be understood to prevent the outbreak from turning into a pandemic! In order for a disease to be considered a pandemic, it must affect several countries and a very large amount of people. The CDC does not define how many countries or people, but a pandemic does affect more people than an outbreak.4 It’s about time to wrap up. Today we learned about the SARS coronavirus and the global outbreak of SARS from 2002 to 2003. What we want you to take away from this episode of Genomics Revolution are four things: Number 1: SARS coronavirus was one of the largest RNA virus genomes at the time. The size of the genome increased the amount of time needed for geneticists to understand the virus to create presentation education and control measures for the public. Number 2: Whenever the SARS coronavirus genome experiences a mutation, the mutation is an insertion or deletion of 5 or 6 nucleotides. Number 3: While SARS is an acronym for Severe Acute Respiratory System, the virus targets not just the respiratory tract, but also other organs such as the kidney and heart. Number 4: Understanding viruses like this one is important to the future of science so that when a new strain of virus arises, we may be able to fight it quicker than the last one! Thanks for listening to Genomics Revolution. Bye guys! Bye! References: 1. SARS. Centers for Disease Control and Prevention. 2017 Dec 6 [accessed 2020 Apr 9]. https://www.cdc.gov/sars/about/fs-sars.html 2. SARS (Severe Acute Respiratory Syndrome). World Health Organization. 2012 Apr 26 [accessed 2020 Apr 9]. https://www.who.int/ith/diseases/sars/en/ 3. Cai CZ, Han LY, Chen X, Cao ZW, Chen YZ. Prediction of Functional Class of the SARS Coronavirus Proteins by a Statistical Learning Method. Journal of Proteome. 2005 Aug 10 [accessed 2020 Mar 28]. https://doi.org/10.1021/pr050110a 4. Caceres V. What's the Difference Between an Epidemic and Pandemic? U.S. News & World Report. [accessed 2020 Apr 9]. https://health.usnews.com/conditions/articles/whats-the-difference-between-an-epidemic-and-pandemic 5. Wong CW. Tracking the Evolution of the SARS Coronavirus Using High-Throughput, High-Density Resequencing Arrays. Genome Research. 2004;14(3):398–405. doi:10.1101/gr.2141004 6. Cheng VC, Lau SK, Woo PC, Yuen KY. Severe Acute Respiratory Syndrome Coronavirus as an Agent of Emerging and Reemerging Infection. American society for microbiology. 2007;20(4):660–694. 7. Graham RL, Sparks Jifr S, Eckerie LD, Sims AC, Denison MR. SARS Coronavirus replicas proteins in pathogenesis. Virus Res. 2008;133(1):88–100. 8. Hung LS. The SARS epidemic in Hong Kong: what lessons have we learned? Jrsm. 2003;96(8):374–378. doi:10.1258/jrsm.96.8.374…

Genomics Revolution

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Zika - The World Traveler Builds Up to a Scare 2:56

5 years yang lalu2:56

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Genomics Revolution Guest Hosts: Keegan Rankin and Torey Coward Episode 52: Zika Script: Keegan: Hello welcome to the podcast! I'm Keegan! Torey: And I’m Torey Coward! Keegan: And we are here today to talk to you about the Zika Virus. I’ll start us off with some general information. The Zika Virus belongs to a group of viruses known as flaviviruses. Flaviviruses are single-stranded RNA viruses encapsulated by a protein coat. Some of Zika Virus’ closest relatives include Yellow Fever Virus and West Nile Virus. They replicate in the cytoplasm of host cells. All zoonotic flaviviruses are rely on arthropods as vectors. In the case of Zika, its two primary vectors are Aedes aegypti (Yellow Fever Mosquito) and Aedes albopictus (Asian Tiger Mosquito). The reservoir of the virus are primates, including humans. This virus is usually spread to a host through the bite of a mosquito, but it can also be transmitted by coming into contact with infected blood and saliva. Common symptoms include fever, headache, rash, joint and muscle pain and conjunctivitis. Symptoms usually last for several days to a week. Torey: I’ll speak briefly about the genome of the Zika Virus. As Keegan stated before, the Zika Virus is a single-stranded RNA, and since it has been sequenced, we know today that it consists of nearly 10.8 thousand bases. There are 3424 amino acids that generate the polyprotein that the virus encodes for. The polyprotein is made up of 10 proteins, one capsid, a precursor membrane protein, an envelope protein, and 7 non-structural proteins. Keegan: The Zika Virus was first isolated from a Macaque in 1947 obtained from the forest of Uganda. Though 80% of those infected are asymptomatic and 20% of patients contract mild, non-lethal symptoms, the real danger arises when the infected patient is pregnant. Getting Zika Virus while pregnant puts the child at risk of lethal birth defects such as microcephaly. Microcephaly is a genetic defect that causes an infant’s brain and head to be smaller than normal, healthy infants. This can result in seizures, intellectual impairment, hearing loss, visual problems, and even infant mortality. Prevention of the spread and contraction of Zika Virus is imperative to prevent infant mortality. Studying Zika Virus and other flaviviruses on a genetic level has given use crucial revelations as to how Zika works and can spread. One such revelation is that many of its genes can be successfully targeted, which brings about the possibility of new treatments and vaccines. Another revelation is that certain mRNAs coding for viral replication have been isolated and can be targeted, yielding the possibility of developing treatments that suppress the virus further, stopping its growth. Another discovery in researching Zika virus is that it also can use other organisms as reservoirs. Research suggests that Zika Virus can possibly be transmitted by birds, horses, goats, cattle, and bats. Torey: Hopefully the information that we have provided for you today had been insightful and helped to foster a greater understanding of the Zika Virus. From the genus and sequence, to the pathway and effects of this intriguing virus. Keegan: And that concludes our talk for today! Thank you so much for listening to us and stay safe out there! Works Cited: Facts about Microcephaly. Centers for Disease Control and Prevention. 2020 Feb 18 [accessed 2020 Apr 9]. Flavivirus. Flavivirus - an overview | ScienceDirect Topics. [accessed 2020 Apr 9]. Malone RW, Homan J, Callahan MV, Glasspool-Malone J, Damodaran L, Schneider ADB, Zimler R, Talton J, Cobb RR, Ruzic I, et al. Zika Virus: Medical Countermeasure Development Challenges. PLoS neglected tropical diseases. 2016 Mar 2 [accessed 2020 Apr 9]. Zika Virus. Centers for Disease Control and Prevention. 2019 Nov 20 [accessed 2020 Apr 9]. Molecular cloning and characterization of the genes encoding the proteins of Zika virus. NCBI-PubMed. [Accessed 2020 April 9]…

Genomics Revolution

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Out of the Woods: Ebola as a Zoonotic Viral Disease 5:51

5 years yang lalu5:51

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Genomic Revolution Guest Hosts: Alexus Acton & Rachna Prasad Episode 51: Ebola Script: Rachna: Welcome to Genomics Revolution. This is Alexus Acton and Rachna Prasad from the 2020 Hiram College Genetics course hosting this episode on the Zaire Ebolavirus. This virus causes the disease ebola that originated from human animal contact, most likely from a bat (1). The Ebola Virus Disease, or EVD for short, was first discovered in 1976 with 2 consecutive outbreaks of fatal hemorrhagic fever in Central Africa. The first outbreak was in the Democratic Republic of Congo, which was formerly called Zaire, in à village near the Ebola river, which accounted for nearly 2700 deaths. The second outbreak was in South Sudan. Originally scientists believed it was spread by à single infected person travelling between the two areas, but it was later discovered they were two genetically distinct viruses - the Zaire ebolavirus and the Sudan ebolavirus.(4) The most recent, and familiar Ebola outbreak occurred in 2014-2016, originating in Southeastern Guinea. It rapidly spread to urban populations within weeks, and soon turned into à global epidemic. (4) Lexi: With this virus going many months without detection we should care about knowing about this virus because the human-human transmission chain was growing exponentially. Before the World health Organization declared it an outbreak, it had already spread over country borders infecting thousands of people (1). Ebola virus is a negative- sense single strand RNA ((-)ssRNA) that has a 19 kilobase genome (1). There are several encoded proteins from EVD which are nucleoprotein (NP), viral proteins (VP) as well as RNA polymerase (L), and Glycoprotein (GP) (2). VP24 is a membrane associated protein, VP30 and VP35 are polymerase matrix proteins, and VP40 is a matrix protein (2). VP40 is the primary EVD matrix protein and regulated assembly and progress of infectious particles (2). It assembles on the inner leaflet of the plasma membrane in human cells to regulate viral budding. Each of these genes encodes for a single protein product with the exception of GP. Gp encodes three proteins of different sizes with a full length of 676 residues. Glycoprotein 1 and 2, mediates viral-host cell attachment and fusion (2). Like other RNA viruses ebola quickly generates mutations through error prone replication. The various glycoproteins are produced from frameshift as a result of mRNA editing (1). Rachna: Ebolavirus belongs to à group of viruses called filoviruses. A phylogenetic analysis revealed that the Sudan Ebola virus diverged early from the other strains, showing that the Bundibugyo and Tai Forest were closely related to Zaire Ebola Virus (2). EBOV is à single stranded RNA virus. This gives it a higher likelihood of acquiring meaningful genetic adaptations and evolving into different strains, when compared to other DNA viruses. (5) À 2017 study, by Tao Li et al., conducted on 514 different EBOV genome sequences from patients with confirmed EVD cases showed that 11 different lineages of EBOV arose from one outbreak in Sierra Leone alone. It also showed that different lineages of EBOV had different fatality rates and certain strains with specific SNPs correlated with higher fatality rates. Variation in nucleotide sequences can help target each Ebolavirus strain from one another, ultimately leading to better diagnosis and therapeutics. This is important to note as the divergence of diseases from other common viruses could potentially be headway in targeting vaccines and treatments to those infected. Lexi: Evidence demonstrates cooperative dimeric binding of double stranded RNA by ebolavirus VP35. The C-terminal domain of viral protein 35 dimerizes upon binding to double stranded RNA, showing coppertivity (3). Reston ebolavirus is named to show where it was derived from, which has previously been shown to be critical for RNA binding, but is also important for VP35 dimeric interface binding (3). These researches mutated R312/301 which likely abolished dsRNA binding which disrupted the formation of the viral protein dimer leaving it in unstable formation (3). This is important as the binding mechanism permits the ebola virus from avoiding the innate immune response and enhancing harmfulness to human cells. (3). This alone can help researchers target the structure based conformational states or protein targeting drugs for drug development and biodefense mechanisms. Rachna: One study showed that multi sequence alignment generated several conserved sequences from each protein mentioned above. Using an Ebola strain from 1976 and a recent strain of 2014, the two sequences were 100% identical (6). The conservation allowed for detection of B and T cell epitopes which covered between 25.37 and 61.51% of the population (6). B cell epitope is the portion of the antigen which interacts with B lymphocytes to trigger immune responses (6). The importance of this is to understand the efficacy in eliciting immunity through humoral and cell-mediated immune responses. T cell immune response usually promises long lasting immunity, and here the prediction of T and B cell epitopes provides two alternative but effective immune response mechanisms. Lexi: Thank you for tuning in on this podcast of Genomics Revolution. We hope you enjoyed your time and learned something new about Ebola. References: 1. Holmes, Edward C., et al. “The Evolution of Ebola Virus: Insights from the 2013–2016 Epidemic.” Nature, vol. 538, no. 7624, 13 Oct. 2016, pp. 193–200., doi:10.1038/nature19790. 2. Jun, Se-Ran et al. “Ebolavirus comparative genomics.” FEMS microbiology reviews vol. 39,5 (2015): 764-78. doi:10.1093/femsre/fuv031 3. Kimberlin, C. R., et al. “Ebolavirus VP35 Uses a Bimodal Strategy to Bind DsRNA for Innate Immune Suppression.” Proceedings of the National Academy of Sciences, vol. 107, no. 1, 14 Sept. 2009, pp. 314–319., doi:10.1073/pnas.0910547107. 4. Li T, Yao HW, Liu D, et al. Mapping the clinical outcomes and genetic evolution of Ebola virus in Sierra Leone. JCI Insight. 2017;2(15):e88333. Published 2017 Aug 3. doi:10.1172/jci.insight.88333 5. Regnery, RL., Johnson, KM., and Kiley, MP. Virion nucleic acid of Ebola virus. J. Virol. 1980; 36(2): 465-469. 6. Yasmin, T., and A. H. M. Nurun Nabi. “B And T Cell Epitope-Based Peptides Predicted from Evolutionarily Conserved and Whole Protein Sequences of Ebola Virus as Vaccine Targets.” Scandinavian Journal of Immunology, vol. 83, no. 5, 2016, pp. 321–337., doi:10.1111/sji.12425.…

Genomics Revolution

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Alexander the Great, Watch Out for the Dead Birds! 3:33

5 years yang lalu3:33

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Genomics Revolution Guest Hosts: Alysa Giudici & Rachel Jerkins Episode 50: West Nile Fever Script: Rachel: Hey everybody, and welcome to another episode of Genomics Revolution. This is Rachel Jerkins and Alysa Giudici (Guh-Dee-Cee), here to talk about the West Nile Virus. Rachel: The West Nile Virus comes from the flavivirus genus and the family flaviviridae. In 1937, the virus was first discovered in the West Nile area of Uganda in Africa. It is a single-stranded RNA virus around 11kbp in size with stem loops on the 5’ and 3’ ends. The genome codes for 10 proteins— 3 for structure in the coding region, plus seven not in the new virus structure from the non-coding region. Rachel: The West Nile Virus causes a disease called West Nile fever (Richter et al. 2017). It is believed to spread when a mosquito bites an infected bird and then bites a person. It wasn’t until 1999 that the virus made its first appearance in the western hemisphere (White et al., 2001). It is crucial to study the disease because it can be a fatal neurological disease and has now spread across a majority of the globe.It is believed to be the main cause of viral encephalitis around the world (Chancey et al. 2015) Alysa: Thanks Rachel, Since the sequencing of the genome, there are many key findings that have emerged. The virus thrives utilizing a vector-virus relationship. The entry of the WNV is through receptor mediated endocytosis once the virus attaches to the cell surface (Colpitts et al.) Interestingly, the virus was able to be tracked through an enzootic cycle involving Culicidae mosquitoes and birds. The birds act as a form of host reservoirs allowing the virus is amplified through the bird – mosquito – bird cycle, until the fall when female mosquitoes begin to “bite” humans. Although many external factors can contribute to the amplification cycle, the disease does exist in multiple habitats (Peterson, 2002). This form of transmission causes the virus to transmit quickly and effectively. Alysa: The apparent symptoms appear to be anorexia, nausea, vomiting, eye pain, headache, etc. that last roughly 3-6 days (Peterson, 2002). These symptoms eventually, if untreated became neurological and possibly deadly. After research, it was determined that there are, however, two lineages of the West Nile Virus. The 1st lineage is the one that is known to affect humans. Not only is the West Nile Virus detrimental to humans, but it is also a leading neurologic disease in many animals such as the equine population. Further sequencing of this genome and Reverse transcription-PCR has further educated the veterinary world as well. Recent evidence acquired by Venter et al. in horses suggests that the lineage 2 strains are highly neuroinvasive in humans and mice. A disease that we continue to fight in humans is also a disease we will continue to fight in animals as well. Who would have guessed that? Thanks for listening. Works Cited: Richter, J., C. Tryfonos, A. Tourvas, D. Floridou, N. Paphitou, and C. Christidoulou (2017). Complete genome sequence of West Nile virus (WNV) from the first human case of neuroinvasive WNV infection in Cyprus. Amer. Soc. for Microbio. 5(43) 1-2. Doi: 10.1128/genomeA.01110-17 Chancey, C., A. Grinev, E. Volkova, and M. Rios. (2015). The global ecology and epidemiology of West Nile virus. BioMed Res. Int. 376230. Doi: 10.1155/2015/376230 White, D. J., Kramer, L. D., Backenson, P. B., Lukacik, G., Johnson, G., Oliver, J., … Campbell, S. (2001). Mosquito Surveillance and Polymerase Chain Reaction Detection of West Nile Virus, New York State. Emerging Infectious Diseases, 7(4), 643–649. doi: 10.3201/eid0704.017407 Petersen, L. R., & Marfin, A. A. (2002). West Nile Virus: A Primer for the Clinician. Annals of Internal Medicine, 137(3), 173. doi: 10.7326/0003-4819-137-3-200208060-00009 Colpitts, T. M., Conway, M. J., Montgomery, R. R., & Fikrig, E. (2012). West Nile Virus: Biology, Transmission, and Human Infection. Clinical Microbiology Reviews, 25(4), 635–648. doi: 10.1128/cmr.00045-12 Venter, M., Human, S., Zaayman, D., Gerdes, G. H., Williams, J., Steyl, J., Leman, P. A., Paweska, J. T., Setzkorn, H., Rous, G., Murray, S., Parker, R., Donnellan, C., & Swanepoel, R. (2009). Lineage 2 west nile virus as cause of fatal neurologic disease in horses, South Africa. Emerging infectious diseases, 15(6), 877–884. https://doi.org/10.3201/eid1506.081515…

Genomics Revolution

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The Insane Zoonotic Trip That is Rabies 4:52

5 years yang lalu4:52

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Genomics Revolution Guest Hosts: Giselle Bahena & Diamond Johnson Episode 49 – Rabies Lyssavirus Script: Welcome to Genomics Revolution. This is Giselle Bahena and Diamond Johnson from the 2020 Hiram College Genetics course hosting this episode covering the Rabies lyssavirus. As the scientific name of this virus implies, the disease that results from such infection is commonly known as Rabies. This disease has been around since antiquity and the earliest writings about it was found in 300BC in Mesopotamia.2 It was discovered through the infectious bite from one animal to the other. The biggest red flag that indicated a rabid animal was excessive salivation which then required preventative actions to take place in order to protect against the virus being transmitted elsewhere. It is important to understand the virus as transmission does not only occur between one animal and the other, rather humans are also at risk from such infectious bites as well. Thousands of people in third would countries continue to die of Rabies and if one is not educated nor treated for the disease, its impact on the central nervous system will take place and result in death. The Rabies virus genome is a single stranded, antisense, non-segmented, negative stranded RNA of approximately 12kb.1. There is a 50 nucleotide leader sequence that is followed by the the five genes in the genome. The proteins encoded by these five genes are nucleoprotein(N), phosphoprotein(P), matrix protein(M), glycoprotein(G) and polymerase(L), all of which make up the structure of the bullet-shaped virion.1 Fusion of the rabies virus envelope to the host cell membrane initiates the infection process and from this point the bullet-shaped virion, with 10nm spike-like glycoprotein peplomers covering its surface, penetrates and enters the host cell cytoplasm via pinocytosis.1 Next, the viral RNA is uncoated and the transcription process of producing messengers RNAs(mRNAs) begins. Since the lyssavirus is a negative single stranded RNA genome, these mRNAs must be transcribed as they are needed to permit virus replication later on in its cycle of infection and replication.1 Now, the synthesized mRNAs are translated into the genomes structural proteins. As G protein glycosylation is processing, the first step in viral replication occurs by synthesizing full length positively stranded copies of the genome that serve as templates for the final synthesis of the negatively stranded genome.1 When this switch to replication occurs, RNA transcription then becomes non-stop as stop codons are ignored. Finally, the assembly process of the bullet-shaped virion takes place and proceeds to its budding formation. There has been an unrecognized member of the lyssavirus genus found in bats that is similar to the one found in dogs, both of which have been seen to be transmitted in humans.3 This is important because with the genome sequence of the lyssavirus, another member in the family was able to be identified along with other animals who would not be typically associated with caring the such virus. On a similar note, sixty nine rabies virus isolates from various parts of the world were partially sequenced and compared to thirteen representative isolates of the six lyssavirus genotypes in order to analyze their genetic diversity.4 The analysis was performed on each of their complete nucleoprotein coding gene and it was discovered that all of the rabies virus isolated belonged to genotype 1, most likely diverging by the accumulation of synonymous mutations.4 With this being said, having the knowledge that the nucleoprotein is highly conserved among all the isolates is important as it can be used as a potential target for preventing the viral Rabies infection. For example, a complementary RNA can can be created to hybridize with the nucleoprotein mRNA and prevent its translation by targeting it for degradation. This would ultimately prevent one of the key structural proteins of the bullet-shaped virion to be made and prevent the virus from being transmitted. It has also been discovered that the human monoclonal antibody (HuMAbs) may serve as an alternative treatment against less affordable treatments. HuMAbs was found to be the best monoclonal antibody as it neutralized all the rabies viruses it was tested against, it recognized both minor site A and antigenic site III and was able to protect hamsters from the most lethal dose of the virus.5 This is another important finding as even if an individual is infected, HuMAbs can be applied for post-exposure protection against the viral genome. Thank you for listening to this episode of Genomics Revolution, we hope you enjoyed your time and were able to learn something new from this talk. References: 1. What is Rabies? Centers for Disease Control and Prevention. 2019 Jun 11 https://www.cdc.gov/rabies/about.html 2. A brief history of rabies: Microbiology. 2017 Apr 12 https://www.labroots.com/trending/microbiology/5761/brief-history-rabies 3. A brief history of rabies: Microbiology. 2017 Apr 12 https://www.labroots.com/trending/microbiology/5761/brief-history-rabies 4. Kissi B, Tordo N, Bourhy H. Genetic Polymorphism in the Rabies Virus Nucleoprotein Gene. Virology. 1995;209(2):526–537. 5. Sloan SE, Hanlon C, Weldon W, Niezgoda M, Blanton J, Self J, Rowley KJ, Mandell RB, Babcock GJ, Thomas WD, et al. Identification and characterization of a human monoclonal antibody that potently neutralizes a broad panel of rabies virus isolates. Vaccine. 2007;25(15):2800–2810.…

Genomics Revolution

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Update on Current HIV Treatments 4:15

5 years yang lalu4:15

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Some More Information on How HIV Causes AIDS & on New Drugs: https://m.youtube.com/watch?v=BADDj82oces (Battle between HIV & Immune System video from Nature Reviews) https://www.npr.org/sections/health-shots/2019/05/30/727731380/old-fight-new-front-aids-activists-want-lower-drug-prices-now (National Public Radio (NPR) segment “AIDS Activists Take Aim at Gilead to Lower Price of HIV Drug PrEP” https://www.npr.org/sections/health-shots/2019/06/11/731350223/expert-panel-recommends-wider-use-of-daily-pill-to-prevent-hiv (NPR segment “Expert Panel Recommends Wider Use of Daily Pill to Prevent HIV” https://www.npr.org/sections/health-shots/2019/12/04/784733337/hiv-prevention-drugs-are-available-for-free-how-do-you-get-them (NPR segment “HIV Prevention Drugs are Available for Free: How Do You Get Them”…

Genomics Revolution

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Trailer: Zoonotic Viral Diseases 0:45

5 years yang lalu0:45

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Brad sets the table for the last set of 2020 Hiram College Genetics course guest podcasts.

Genomics Revolution

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HIV & AIDS - The Killer That Robs Us of Our Immune Defenses 4:55

5 years yang lalu4:55

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Genomics Revolution Guest Hosts: Emily Harris & Tim Murton Episode 48: HIV & AIDS Script: Welcome to Genomics Revolution! This is Emily Harris and this is Tim Murton. We are from the 2020 Hiram College Genetics course, and we are hosting this episode on the genome of Human Immunodeficiency Virus, or HIV. HIV targets a host’s immune system and causes it to fail. This complication is referred to as HIV infection, and can eventually develop into acquired immunodeficiency syndrome, or AIDS, which is the most advanced stage of HIV infection (1). This virus is in the genus lentivirus, the family of Retrovirdae, and the subfamily Orthoretrovirinae (1). HIV is typically divided into two types, HIV-1 and HIV-2, and each type can be subdivided into several smaller groups based on differences in viral antigens, and from where each strain evolved (3). HIV was recognized on a wide scale during an outbreak in the 1980s, but was actually first discovered in humans between 1920 and 1940 (1). After years of studying the virus, it was discovered that it is spread through contact with infected bodily fluids like blood, semen, breast milk, or several others. It was also discovered that the virus was very similar, genetically, to simian immunodeficiency-deficiency virus, or SIV, which is a non-human primate immunodeficiency virus (1). HIV-1 appears to have evolved from SIV strains in chimpanzees in Central Africa, and HIV-2 likely evolved from a strain in West African mangabeys (1). So it is believed that the virus was transmitted to humans when these primates were hunted for meat and their infected blood was ingested. The virus then mutated and evolved in humans into HIV (3). Now let’s talk about the HIV genome. The genome of this virus consists of two single stranded RNA molecules and is roughly 9,200 bases in size (2). After sequencing the genome, it was found that it contains 9 genes and encodes 15 viral proteins, which is relatively small when we consider how powerful of a virus it is (3). HIV is also classified as an enveloped retrovirus (1). This means the virus uses a special enzyme called reverse transcriptase, which turns its RNA into DNA, then uses that DNA to infect a host (1). They literally insert a copy of their own genome into a host’s genome! So this virus works in a very intelligent way making treatment for infection extremely difficult, especially before the virus was understood. This is why it was so important to sequence the HIV genome. By learning more about the genetic makeup of HIV, it became easier to understand how the virus operates, how it evolves and what it evolved from, how to prevent possible outbreaks, and what types of treatment may work. Sequencing the genome even opened the door to possible gene therapy that can be used to treat or hopefully even cure the disease someday! Sequencing the HIV genome told us a lot about the virus, so let’s highlight a few of the key findings. Sequencing the genome is how we found out that HIV is closely related to SIV (5). This information was crucial because then we were able to use our understanding of SIV to help come up with a better treatment for HIV. Another finding was that there are subtypes of HIV-1 such as the CG-0018a-01 HIV-1 genome (7). This subtype-L was found in the Democratic Republic of the Congo. The research showed that this subtype-L was found to be transmitting in the DRC and that there could be more strains circulating (7). Knowing this was extremely important because it shows the dangers of mutations, and how easily the virus can evolve and create new strains. This let scientists know to look out for new strains of HIV that could be more easily transmitted and harder to combat than the original strain. Sequencing the HIV genome also showed us that HIV-1 genetic material is damaged by hypermutation (6). G-to-A hypermutation, for example, damages the virus by producing abnormal amounts of transitions from guanine to adenine. These mutations are thought to be caused by HIV’s reverse transcriptase enzyme, which has the ability to hypermutate in the presence of unbalanced nucleotide pools during the cell cycle (6). This is important because it shows that the virus has a weakness that is possibly being caused by a host mechanism that can decrease virus replication. This finding implies that if we can promote hypermutation states in HIV, we may be able to induce non-reversible mutagenesis of the viral DNA. This strategy may pave the way to discovering a cure for HIV! Thanks for listening! References: [1] Arbeitskreis Blut, Untergruppe ‘Bewertung Blut- assoziierter Krankheitserreger’: Human immuno- deficiency virus (HIV). Transfus Med Hemother 2004;31:102–114. [2] Feinberg Mark B, Greene Warner C (1992). "Molecular Insights into human immunodeficiency virus type1 pathogenesis". Current Opinion in Immunology. 4 (4): 466–474. doi:10.1016/s0952-7915(06)80041-5. PMID 1356348. [3] Li G, Piampongsant S, Faria NR, Voet A, Pineda-Peña AC, Khouri R, Lemey P, Vandamme AM, Theys K (February 2015). "An integrated map of HIV genome-wide variation from a population perspective". Retrovirology. 12 (1): 18. doi:10.1186/s12977-015-0148-6. PMC 4358901. PMID 25808207. [4] German Advisory Committee Blood (Arbeitskreis Blut), Subgroup ‘Assessment of Pathogens Transmissible by Blood’ (2016). Human Immunodeficiency Virus (HIV). Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie, 43(3), 203–222. [5] Janini, M., Rogers, M., Birx, D. R., & McCutchan, F. E. (2001). Human immunodeficiency virus type 1 DNA sequences genetically damaged by hypermutation are often abundant in patient peripheral blood mononuclear cells and may be generated during near-simultaneous infection and activation of CD4(+) T cells. Journal of virology, 75(17), 7973–7986. [6] Williams, K. C., & Burdo, T. H. (2009). HIV and SIV infection: the role of cellular restriction and immune responses in viral replication and pathogenesis. APMIS : acta pathologica, microbiologica, et immunologica Scandinavica, 117(5-6), 400–412. [7] Yamaguchi, Julie BS; Vallari, Ana MS; McArthur, Carole MD, PhD; Sthreshley, Larry PhD; Cloherty, Gavin A. PhD; Berg, Michael G. PhD; Rodgers, Mary A. PhD. (2020) Complete Genome Sequence of CG-0018a-01 Establishes HIV-1 Subtype L. JAIDS Journal of Acquired Immune Deficiency Syndromes: Volume 83 - Issue 3 - p 319-322…

Genomics Revolution

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HPV - The Trigger Behind Several Cancers 4:55

5 years yang lalu4:55

4:55

Genomics Revolution Guest Hosts: Sheree Nobles & Joshua Gregory Episode 47: Human Papillomavirus (HPV) Script: Josh- Hello everyone, and welcome to this episode of Genomics Revolution! We’re your guests hosts today, Sheree Nobles and Joshua Gregory. Today we’ll be talking about Human Papillomavirus, or HPV as it’s commonly known. This is a sexually transmitted infection, and to keep on topic with this year’s theme, it’s a virus. Sheree- There isn’t a scientific name for it, so much as a bunch of scientific names, as there are over 100 different human papillomaviruses. These viruses can cause not only genital warts, but warts elsewhere, and have even been linked to cervical cancers. Josh- Five types of HPV were found prior to 1983, but most of those HPVs were present in animals, not humans. HPV 6 was found by German virologist Harold zur Hausen shortly before HPV 11 was found by the same man in 1983. Shortly after that, he found HPVs 16 and 18, which together are present in roughly 70% of cervical cancers. Sheree- zur Hausen was originally studying cervical cancer, and the only reason he thought to look for viruses was because the cancer seemed to be “infectious” despite cancer not behaving the way the should . It was when his friend, a U.S. researcher named Richard Shope, told him about a virus in rabbits that would cause warts and cervical cancer did he think about the possibility of a virus causing the disease. Josh- It’s important to note that most HPVs don’t cause cancer, or any symptoms at all. More often enough, HPV is present in a human, but does not cause any symptoms before the immune system removes it. It’s only a few types of the virus that can stay around long enough to induce cancer, like HPV 16 or 18. This is because the virus affects a cell’s growth cycle while trying to reproduce, causing the cells to grow rapidly and for warts to form, and sometimes causing tumors as well. Sheree- This is why it’s important to understand the virus. Cervical cancer only has a 66% survival rate, so if it can be avoided, it should be. Because HPV is so closely related to the cancer, it makes sense that we should try to understand it completely to try and stay safe from deadly diseases. It’s also important to realize that someone can be carrying the virus without showing any symptoms, and could possibly transfer it to another person, spreading the virus and its dangerous symptoms. Josh- Not only should we understand the virus, but everyone should also get tested regularly to make sure whether or not they’re carrying HPV. Now the virus itself isn’t too complicated. Its genome is made of double-stranded DNA in a circular formation, with a singular DNA molecule. It is roughly 7916 base pairs in length with 8 ORFs, though this data is subject to slight change between different types of HPV. Sheree- There were three findings that we thought were really important. One, HPVs are separated into two unofficial classifications: low and high risk. Most human papillomaviruses never cause any symptoms, let alone serious diseases, but even still, they can be transferred between people. If someone has a compromised immune system, an HPV that doesn’t hurt one person could hurt them. Two, certain HPVs are much more likely to cause cervical cancer. Josh- HPVs 16 and 18 are some of the more dangerous types of the virus you can get. Together they are present in approximately 70% of all cervical cancer cases. This is due to their ability to target retinoblastoma (Rb) protein families and p53 in our cells. This can induce telomerase production, causing the cell to be unable to repair damaged DNA, a crucial task for cancer cells to continue to survive. And last but not least, HPV is total is present in around 99.7% of cervical cancer samples, as found in 1999 by a group of scientists including U.K. Researcher Professor Julian Peto. Sheree- These findings are important for several reasons. They tell us that anyone could be carrying HPV at any time and not know it. This is a common trend among some viruses, much like the corona virus that is currently causing an uproar. They also tell us that cervical cancer, which only has a 66% survival rate, is so closely linked to HPV that we should take every care to avoid contracting HPV. Lastly, knowing the mechanism of HPV causing cancer brings us a step closer towards finding an actual cure for existing HPV infection, not just prevention, a vaccine, or surgery. Josh- This has been an episode of Genomics Revolution, and we thank you all for listening to us ramble about a virus. Sheree- We’ve had some fun recording this for you, and we hope you’ll take away from this the importance of understanding viruses and the diseases they can cause. Josh- This has been Josh, Sheree- and Sheree, Josh- and we hope you have a great day, take care! References: IARC Working Group on the Evaluation of Carcinogenic Risk to Humans. “Human Papillomavirus (HPV) Infection.” Human Papillomaviruses., U.S. National Library of Medicine, 1 Jan. 1970, www.ncbi.nlm.nih.gov/books/NBK321770/ . “HPV: the Whole Story, Warts and All.” Cancer Research UK - Science Blog, scienceblog.cancerresearchuk.org/2014/09/16/hpv-the-whole-story-warts-and-all/. Burk, Robert D., et al. “Human Papillomavirus Genome Variants.” Virology, Academic Press, 31 Aug. 2013, www.sciencedirect.com/science/article/pii/S0042682213004388 . Liu, Ying, et al. “Whole-Genome Analysis of Human Papillomavirus Types 16, 18, and 58 Isolated from Cervical Precancer and Cancer Samples in Chinese Women.” Scientific Reports, Nature Publishing Group UK, 21 Mar. 2017, www.ncbi.nlm.nih.gov/pmc/articles/PMC5428204/#!po=25.0000.…

Genomics Revolution

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Hepatitis C - Until Now, the Silent Hepatitis Epidemic 5:51

5 years yang lalu5:51

5:51

Genomics Revolution Guest Hosts: Abbey Anderson & Samantha Mansfield Episode 46: Hepacivirus (Hepatitis C) Script: Hello! This is Sammie and Abbey coming at you live from a safe social distance! Today we are here to talk to you about Hepacivirus which is commonly known as Hepatitis C virus. We are going to spend some time talking about when and how the virus was discovered, the reasons that we should care about this virus, the genome of Hepatitis C, and key findings about HepC virus. Sammie: Every story starts somewhere and the uniqueness of this virus is how it was discovered. This virus was first named in 1989. Doctors knew that this might have had something to do with blood transfusions, but it was called non-A, non-B hepatitis because they could not pinpoint the exact virus down. Later it became known that there were several different genotypes of the hepatitis C virus. This virus is widespread and curable now a days if caught early enough. The spread of this virus occurs by sexual intercourse, blood to blood contact, or improperly sterilized equipment (2). While we now understand how to take precautions against HepC, many people today are still infected by the virus through needle sharing. With the present opioid epidemic, especially in our great state of Ohio, we must understand the vast impacts that drug sharing can cause. This leads into why we should care about the virus that turns into a serious disease. Abbey: According to the CDC, there are 2.4 million people in the United States alone living with hepatitis C. Worldwide, HepC affects more than 170 million people. This virus is often ignored until it is too late. There are two phases of hepatitis C which occurs when the person is infected but shows no symptoms. Even if there are symptoms, most people never realize until they are diagnosed with liver disease. According to the San Francisco Department of Health, in 15-40% of the persons with acute hepatitis C, the immune system will fight off the infection and there will be no presence of the virus within 6 months and the liver heals completely. In most other people, the immune system cannot clear the virus and after 6 month time window this is then classified as chronic hepatitis C. This disease will cause the liver to become more and more inflamed and scarred over several years. According an article written by the University of Texas Hepatitis C is the leading cause of liver cancer (5). Sammie: According to a microbiology textbook edited by Dr. Tan Seng-Lair, The hepatitis C virus belongs to the family Flaviviridae. This family genome consists of a positive strand RNA molecule that ranges in size from 9.6 to 12.3 thousand nucleotides.The Hepatitis C virus open reading frame is known to contain 9,024-9,111 nucleotides, depending on the genotype. It is a double stranded RNA molecule. Hepatitis C virus encodes a single polyprotein, and this is processed to generate 10 polypeptides (1). The number of predicted coding proteins is 11. Abbey: Now it is time to talk about why sequencing this viral genome helped our understanding of Hepatitis C. Remember those genotypes mentioned earlier? Yep, they really come into play here. From sequencing the HepC virus, scientists have discovered that this virus exists in 8 different genotypes, all with different geographical distributions according to a study that was looking at where the highest burden of HepC occurs in Southeast Asia (3). The analysis of Hepatitis C Virus nucleotide sequences has worked as an epidemiological marker, allowing scientists to trace the source of HepC infection within a given population (6). Until 2019, it was believed that HepC only existed in 6 genotypes with more than 50 subtypes. The best part is, not all of these 8 genotypes have been sequenced! In case you are interested in classifying the next Hepatitis C type, the complete genome sequence must differ from other sequences by 30% in genotype or by 15% in subtype (4). From sequencing these genomes, researchers have also been able to determine which genotypes and subtypes are more prevalent in specific regions around the world. They often follow patterns of human migration. For example, subtypes 1a, 1b, 2a, 2b, 2c, and 3a are found worldwide and make up the largest portion of HepC infections (4). Other subtypes, recall that there are over 50, are extremely rare and are found in restricted geographical locations such as West Africa, Central Africa, India, and even Canada. Sammie: Finally, we should mention the most important use of sequencing the HepC genome...HepC treatments. According to the National Institute of Health, by having a sequenced genome, scientists began to target different genes in order to develop drugs that would combat Hepatitis C. Some drugs target the gene responsible for the activity of HepC polymerase, the enzyme that aids in replication of the virus. Other drugs target genes that encode the virus’s structural proteins. Abbey: While it may seem that we know a lot about Hepatitis C virus today, we are still a long ways away from a vaccine. Because this virus mutates so rapidly and exists in so many genotypes, making a vaccine is more complicated than it seems. We hope you enjoyed learning a little bit more about Hepatitis C, and remember, make sure you avoid needle sticks! See you next time on Genomics Revolution. References: 1) Dubuisson, J. (2007). Hepatitis C virus proteins. World Journal of Gastroenterology , 13(17), 2406. doi: 10.3748/wjg.v13.i17.2406 2) Hepatitis C. (n.d.). Retrieved April 5, 2020, from https://www.sfcdcp.org/infectious-diseases-a-to-z/hepatitis-c/ 3) Ngoc, C. L., Thanh, T. T. T., Lan, P. T. T., Mai, T. N., Hoa, T. N., My, N. N., … Vizions. (2019, March 19). Differential prevalence and geographic distribution of hepatitis C virus genotypes in acute and chronic hepatitis C patients in Vietnam. Retrieved April 5, 2020, from https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0212734#sec005 4) Spitz, N., Barros, J., doO, K., Brandao-Mello, C., & Araujo, N. (2019). The First Complete Genome Sequences of Hepatitis C Virus Subtype 2b from Latin America: Molecular Characterization and Phylogeographic Analysis . Viruses , 11(11). doi: 10.3390/v11111000 5) Underferth, D., & MD Anderson Cancer Center. (2019, May 8). Hepatitis C and liver cancer: What to know. Retrieved April 5, 2020, from https://www.mdanderson.org/publications/focused-on-health/HepatitisC-liver-cancer-What-you-need-to-know.h16Z1591413.html 6) Zein, N. N. (2000). Clinical Significance of Hepatitis C Virus Genotypes. American Society for Microbiology . doi: https://dx.doi.org/10.1128/cmr.13.2.223-235.2000…

Genomics Revolution

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Trailer - Sexually Transmitted & Blood-borne Viruses 0:49

5 years yang lalu0:49

0:49

Brad jumps in with a trailer for 4 episodes dealing with viruses that are transmitted by sex and transfer of bodily fluids.

Genomics Revolution

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Hepatitis B - B for Blood and Other Bodily Fluids 3:02

5 years yang lalu3:02

3:02

Genomics Revolution Guest Hosts: Ciara Love & Cara Katzendorn Episode 45: Hepatitis B Virus Script: Hi, my name is Ciara and today we’re going to talk about a virus called Hepatitis B. This virus is a type of species in the orthohepadnavirus genus as well as a member of the hepadnaviridae family. This virus causes a world-wide known disease called Hepatitis B or HBV. HBV causes liver cancer and the vaccine that was invented for Hepatitis B was one of the first anti-cancer vaccine. The virus was discovered in 1965 by Dr. Baruch Blumberg, which he had won a Nobel Prize for. He worked with a microbiologist named Irvine Millman, to help develop a blood test for the virus that blood centers were using in 1971. The first vaccine was originally the virus treated by heat, and then later in 1986 genetically engineered Hepatitis B vaccines were created. We should care about understanding this virus because it affects everyone and some people carry this virus their whole lives. This virus is a partial double dna stranded molecule that usually replicates by reverse transcription and has between 3182-3248 base pairs depending on the genotypes. The hepatitis B genome includes four open reading frames for viral proteins. These four groups are surface antigens, core protein, polymerase, and protein X whose function is unclear but may be connected to this virus’s influence on the development of liver cancer. Therapies and vaccines continue to advance in the hopes of finding cure for this disease. In 2015, a study published in the Journal of Clinical microbiology demonstrated researchers improving techniques of identifying this virus throughout all 10 different genotypes found in patients. They designed a mix of primers based on sequencing from over 5000 Hbv patients that would help in creating a more analytically sensitive PCR amplification for detection of this virus. This may be used as a universal detection method for all genotypes of this disease. In 2012 researchers set out to identify the functional effects of HBV viral integration into the human genome, in hopes of indicating how this virus connects with liver cancer. They found that the virus had many possible effects by insertional mutagenesis, viral promoter-driven transcriptional up-regulation, and genomic instability. This study opens possibilities for future studies that will hopefully be able investigate medicines to prevent the development of liver cancer in HBV patients. Research continues to develop our understanding of this virus and the diseases associated with infection, and a cure for patients in on the horizon. Resources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5313610/ https://www.ncbi.nlm.nih.gov/pubmed/12480564 https://www.hepb.org/prevention-and-diagnosis/vaccination/history-of-hepatitis-b-vaccine https://hbvdb.lyon.inserm.fr/HBVdb/HBVdbGenome http://garfield.library.upenn.edu/classics1979/A1979HW50100001.pdf https://www.ncbi.nlm.nih.gov/pubmed/26112647 https://jcm.asm.org/content/53/6/1831 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3317142/?report=reader#!po=46.4286…

Genomics Revolution

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Soon We Can Say Goodbye to Polio 0:57

5 years yang lalu0:57

0:57

Genomics Revolution Kiyana Caver & Brittany Weaver Genetics Podcast Transcript Episode 44: Poliovirus Script: Hello, I am Kiyana & I am Brittany and we will discuss the virus poliovirus which causes polio. Polio can also be known as poliomyelitis. It stems from the Greek meaning of an inflammation of the gray matter. In the early 20thcentury there weren’t many diseases that had parents worried about the health and wellbeing for their children. However, poliomyelitis is something that parents were fearful of their children getting. Poliomyelitis was a disease that was more common to catch during the summer as that is when polio was more likely to come about, in warmer weather. This disease is very contagious and it is caused by a virus that attacks the nervous system, it also can lead to spinal cord and or brain stem paralysis if it is not treated soon. The people that are mostly affected by it are younger children, usually children become affected with the disease before they turn 5 years old (7 & 6). Polio was most likely spread through contact between people by nasal and oral secretions and by coming into contact with contaminated feces. Polio enters through the mouth, multiplies through the digestive tract where it continues to multiply. Polio was discovered in 1908 by Karl Landsteiner and Erwin Popper. Poliovirus was discovered as scientists were proving that it was not a bacterium that had been causing paralysis, but instead it was a virus (5). Despite it being discovered it the early 1900’s, poliovirus did not peak in the United States until around 1952 when almost 60,00 cases had sparked throughout the United States. Poliovirus is a RNA genome with a protein capsid made up of one single RNA positive sense stand, that is about 7500 nucleotides long. There is one primary RNA molecule in the genome, which has been shown to have 8 unused start codon sites that are in front of the active AUG start codon. The molecule also has 23 RNA hairpin secondary structures (3). Poliovirus has one main cleavage of a precursor polypeptide called NCVP 1 which encodes for proteins VP 1, 2, 3, and 4 (1). Poliovirus originated from a single precursor molecule called NCVPOO [noncapsid viral protein (NCVP] (2). Poliovirus is a well known and studied virus because between the period of the 1940’s-1950’s the virus was at its most epidemic (8). Polio had crippled around 35,000 people every year in the US alone. A study was preformed in 1994-1995 that showed over 1 million people had survived poliovirus but, over 443,000 people reported having been paralyzed, as it affects a persons nervous system. During the epidemic when it was at its highest affect there were reports of about 27,000 people reporting paralyzation and about 6,000 deaths. When poliovirus was sequenced it led to many discoveries that affected the treatment and prevention of polio in the world. Research found that there were 3 serotypes of poliovirus that caused paralysis in diffferent ratios, type 1 was the most paralytic and accounted for about 80% of paralyzation, type 2 had 8% and type 3 had 13%. This finding was important because it allowed for more focus to be pulled onto why one type was more paralytic than others. Another key finding was that of inactivated poliovirus also known as IPV being introduced for polio in 1955 and oral poliovirus also known as OPV in 1961. These were both used to protect immunized patients and it was found that OPV could spread from the vaccinated to close companions when in contact, increasing the immunity in the US, which was seen when the number of annual inciddences fell drastically. Knowing that OPV was a good way of immunization it was studied along with the wild poliovirus sequence to see how many doses of OPV was approximately needed to eradicate wild poliovirus. The US and other countries tested the possibility of eradicating the wild poliovirus and was first succesful in Cuba through the eradication of wild poliovirus. It was found that if a child by the age of 12 months had 3 doses of OPV that percentage of cases of wild poliovirus decreases. The eradication of all indigenous wild poliovirus occurred in 1991 (4). This is Brad Goodner and I need to step in with an add-on to Brittany’s last sentence. After success in Cuba, the eradication of wild poliovirus in 1991 was from the entire Western Hemisphere through an organized immunization effort using the oral poliovirus vaccine. Since then, efforts have continued worldwide and we are so close to complete eradication of polio that immunization programs have switched from the oral vaccine to the inactivated vaccine to prevent OPV-derived shedding of live virus that might cause rare infections on non-immunized individuals. Hopefully, we are only a few years away from saying goodbye to this small but devasting virus. This has been our genomic podcast on poliovirus, thank you for listening and we hope you now know more about poliovirus. References: 1. Rekosh, David. “Gene Order of the Poliovirus Capsid Proteins.” Journal of Virology , vol. 9, no. 3, Mar. 1972, pp. 479–487., doi:10.1128/jvi.9.3.479-487.1972. 2. Nomoto, A., et al. “Complete Nucleotide Sequence of the Attenuated Poliovirus Sabin 1 Strain Genome.” Proceedings of the National Academy of Sciences , vol. 79, no. 19, Jan. 1982, pp. 5793–5797., doi:10.1073/pnas.79.19.5793. 3. Simoes, E A, and P Sarnow. “An RNA Hairpin at the Extreme 5 End of the Poliovirus RNA Genome Modulates Viral Translation in Human Cells.” Journal of Virology , vol. 65, no. 2, Feb. 1991, pp. 913–921., doi:10.1128/jvi.65.2.913-921.1991. 4. Nathanson, N., and O. M. Kew. “From Emergence to Eradication: The Epidemiology of Poliomyelitis Deconstructed.” American Journal of Epidemiology , vol. 172, no. 11, 26 Oct. 2010, pp. 1213–1229., doi:10.1093/aje/kwq320. 5. “NMAH: Polio: The Polio Genome.” NMAH | Polio: The Polio Genome, 1 Feb. 2005, https://amhistory.si.edu/polio/virusvaccine/livingchem.htm 6. “Polio.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 9 Dec. 2017, www.mayoclinic.org/diseases-conditions/polio/symptoms-causes/syc-20376512 . 7. “Poliomyelitis.” World Health Organization, World Health Organization, www.who.int/news-room/fact-sheets/detail/poliomyelitis . 8. “Post-Polio Syndrome Fact Sheet.” National Institute of Neurological Disorders and Stroke, U.S. Department of Health and Human Services, www.ninds.nih.gov/disorders/patient-caregiver-education/fact-sheets/post-polio-syndrome-fact-sheet .…

Genomics Revolution

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Viral Pathogen No More - See Ya Smallpox 6:40

5 years yang lalu6:40

6:40

Genomics Revolution Mit Patel and Andrew Pemberton Episode 43: Variola Virus (Cause of smallpox) Script: Welcome to the Genomic Revolution Podcast! This is Mit Patel and Andrew Pemberton from the 2020 Hiram College Genetics course hosting this episode on an orthopoxvirus known as the Variola virus. This virus causes the disease that many of our parents or grandparents may have gotten when they were younger but rather for us millennials we are vaccinated for it. The variola virus or VARV causes the disease smallpox. However, there are some mysteries as to how it originated. According to Igor Babkin, an author of The Origin of the Variola, the descriptions of smallpox can be seen in ancient literature books from India which were written in 6th or even 15th century BC. Historical evidence shows that smallpox has been seen in many countries including India, china, egypt, and even parts of europe. The variola virus has been proven to be only transmitted between sensitive people but it does not show any signs of affecting an animal. Therefore as a result, the majority of the sensitive people will have two outcomes: be immune or die which will cause the virus to fade. Many researchers have come to conclude that animal domestication, land farming, and large human settlements about 6000 to 10000 years ago truly caused the emergence of smallpox (Babkin, 2015). Now you listeners may be wondering why I should care about a disease that we already have a vaccination for? But, truly understanding the history and information on how the resolution was found, gives the idea of how important this virus is. When smallpox was around, it was certainly a devastating disease. On average, out of 10 people about 3 of them would die. And due to this, control efforts started to be implemented. One of the first methods was the use of variolation. Variolation, named after the variola virus, was first used in Asia where a small dried smallpox scab was blown into the nose of an individual. This individual would then contract the disease but a milder form. At the end, the individual would be immune to smallpox. Due to this, only about 1%-2% percent died rather than 30%. By 1700, variolation had spread to India, Africa, and the Ottoman empire. Europeans and Americans tended to variolate by puncturing the skin (CDC, 2016). On the other hand comes the factual information. So the variola virus is a double stranded DNA with a length of approximately 190 kbp, specifically 186,102 base pairs. A 102 kbp is compromised for a central conserved domain, which encodes for multiple different proteins. The virus encodes for about 200 proteins altogether all having different functions. About 80 of those encoded proteins are located in the terminal regions of the genome, where proteins related to host immune invasion are encoded. The variola virus belongs to the genus of Orthopoxvirus a nd is in the family of Poxvirus (Babkin and Babkina). Research done by Mackett and Archard performed DNA sequencing of several organisms from the genus of Orthopoxvirus (Mackett and Archard). Using restriction endonuclease, they analyzed the genome structure of several viruses and discovered that there is a central conserved region in Orthopoxvirus organisms (Mackett and Archard). It was determined that these highly conserved regions are important to vital function of the virus, including DNA replication and repair, transcription and such (Mackett and Archard). The sequenced DNA also showed variation of the terminus end. This variation is how the Orthopoxvirus viruses vary and is how monkeypox virus infects monkeys and why variola virus is specific to humans (Mackett and Archard). Genome sequencing of the variola virus and closely related virus has revealed which regions of the DNA determine function of the Orthopoxvirus including the variola virus. Another area where the genome sequence of Variola Virus has been used is to create a phylogenetic tree, or a tree that shows evolutionary relationships among different organisms and in our case viruses. In a paper published by Smithson and other authors, their core group members used one of the first sequenced ancient variola virus genomes. With this, they removed sequencing tags and conducted manual gap-spanning reads. This new assembly was used along with other orthopoxvirus genomes like camelpox and taterapox to determine the last common ancestor of the VARV virus. Their analysis of these different genomes including variola virus lead them to conclude that single nucleotide polymorphisms and amino acid changes in the vaccinia virus ortholog associated to the VARV host specificity and virulence. Furthermore, it was found that these traits were introduced prior to the rise of recent pox viruses. An interesting fact from this paper is that when comparing the ancient and modern VARV genome sequences there is measurable drift in Adenine and thymine richness (Smithson, 2017). A large worry of many is the reemergence of the smallpox virus. In a paper by Theves and others, they exhumed bodies from an elite burial dating back to 1730s to 1740s, due to the burial time being in the winter and lack of trauma, the authors hypothesized that they died because of a pathogen. At first they thought it might have been a bacterial pathogen, but when they could not find any evidence they searched for a virus (Thèves et al.). After some searching they were able to identify some DNA fragments that were from the poxvirus family, since they were humans, it was smallpox (Thèves et al.). The worry of reemergence prompts researchers to sequence all variations of the variola virus, even ancient variations, in order to have the best possible chance to combat the variola virus if it were to mutate and evolve to infect people again. We would like to thank you all for listening and we would also like to thank Professor Goodner for allowing us to join Genomics Revolution! We hope that you got a great understanding about the variola virus. References: Babkin, Igor, and Irina Babkina. "The Origin Of The Variola Virus". Viruses, vol 7, no.3, 2015, pp. 1100-1112. MDPI AG, doi:10.3390/v7031100. Accessed 9 Apr 2020. “History of Smallpox.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 30 Aug. 2016, www.cdc.gov/smallpox/history/history.html. Mackett, M, and L.C. Archard. "Conservation And Variation In Orthopoxvirus Genome Structure". General Virology, vol 45, no. 3, 1979, pp. 683-701., Accessed 4 Apr 2020. Smithson, Chad et al. “Re-Assembly and Analysis of an Ancient Variola Virus Genome.” Viruses vol. 9,9 253. 8 Sep. 2017, doi:10.3390/v9090253 Thèves, C. et al. "The Rediscovery Of Smallpox". Clinical Microbiology And Infection, vol 20, no. 3, 2014, pp. 210-218. Elsevier BV, doi:10.1111/1469-0691.12536.…

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