Vote on production and labelling of GM foods in California

Safety and issues pertaining to GM food in California

Courtesy: The Sacremanto Bee

Susan Lang doesn’t know for certain if her son’s itchy skin and upset stomach were caused by eating food made from crops whose genes were altered in a lab.

But over the years, she believes she’s been able to soothe the 8-year-old’s eczema and digestive problems by eliminating genetically modified organisms from his diet.

“I know that when I feed this child better he does better, and feeding him better includes not feeding him GMOs,” Lang said.

The Fair Oaks woman concedes, however, that her evidence is not scientific, saying she has “more than a hunch, but I don’t have proof.”

Lang learned about genetic engineering – the process of splicing plant or animal genes to create new characteristics – as she began altering her family’s diet to help her son. In the process, she became concerned that consumers don’t know enough about the technology that goes into producing a huge part of the American food supply. Eventually she became a volunteer for the Proposition 37 campaign.

The measure on Tuesday’s California ballot asks voters if food companies should be required to label genetically engineered food. At the core of the debate is a seemingly simple question: Is it safe to eat?

Proposition 37 supporters offer little scientific evidence that genetically modified food is dangerous to human health. A recent French study that found rats developed tumors after months of eating genetically modified corn was quickly panned by the scientific community.

Supporters instead point out perceived deficiencies in most studies that exist, raise questions about the procedures for approving the food and argue that the biotechnology industry has undue influence on government regulators.

“Experts are still debating if foods modified with DNA from other plants, animals, bacteria and even viruses are safe,” says a radio ad urging a “yes” vote on Proposition 37. “But while the debate goes on, we all have the right to make an informed choice.”

Opponents are making the case that labeling the food implies health dangers that haven’t been proved.

“As a doctor, it concerns me when families are given misleading health information,” Dr. Sherry Franklin of San Diego says in a No on 37 ad.

The ad also points out that the American Medical Association has said there is “no scientific justification” for labeling genetically engineered food.

That is true – but incomplete. The association that represents the nation’s doctors also calls for greater “availability of unbiased information and research activities on bioengineered foods.” And it says there should be a different system for testing genetically engineered food before it hits store shelves. Right now, the testing process is voluntary; the medical association says it should be mandatory.

The voluntary testing system is a concern to Proposition 37 supporters. They say it puts too much control in the hands of companies that stand to profit from their biotech inventions.

Altered crops in many foods

Most corn, soybeans, canola and sugar beets grown in the United States are engineered to kill pests or withstand being sprayed with weed killers such as Round-Up. Those genetically engineered crops wind up in thousands of non-organic grocery products in the form of corn syrup, sugar,canola oil or soy-based emulsifiers. Some non-organic papaya, crook neck squash and corn on the cob is also genetically modified.

“There is no evidence that there is any health issue with any of the products on the market. And there is nothing particular to the technology itself that makes it dangerous,” said Kent Bradford, director of the Seed Biotechnology Center at UC Davis, which uses genetic engineering to develop agricultural seeds.

He dismisses the idea that there is not enough testing of genetically engineered food, saying the voluntary testing by companies that modify crops has created a pile of credible evidence.

But such tests are biased by commercial interest and too short to show the long-term impacts of eating engineered food, says anti-GMO activist Jeffrey Smith, who has written two books and made a film criticizing the technology.

Smith lives in Iowa but has been touring California promoting his work and Proposition 37. His film, “Genetic Roulette,” features about a dozen doctors describing health problems – including allergies, diabetes, gastrointestinal distress and autism – they associate with eating GMOs.

“I decided strategically – because I think it’s a greater motivation – to focus on the health dangers,” said Smith, whose background is in marketing not science.

One solution, he said, is labeling engineered food so people know what they’re eating.

Proposition 37 is more about ideology than science, said Bob Goldberg, a UCLA biologist who teaches a class on genetic engineering.

“I’m against this proposition because I’m a scientist and I’m a person who has done genetic engineering my entire career,” Goldberg said. “In many respects, I don’t view this as a political campaign, I view this as an anti-science campaign.”

Goldberg, a member of the prestigious National Academy of Sciences, said the organization believes it’s wrong to lump all genetically engineered foods into the same category because they use the same laboratory technique. Instead, he said, the safety of crops and food products – whether the result of genetic engineering or other scientific processes – should be judged on a case-by-case basis.

A National Academy of Sciences spokeswoman said the group has not evaluated whether it’s safe to eat genetically engineered food.

Goldberg points to a statement this month by the American Association for the Advancement of Science that says, “The science is quite clear: crop improvement by the modern molecular techniques of biotechnology is safe.”

Doctor suggests diet change

Dr. Kelly Sutton isn’t convinced. She is a board-certified internist in Fair Oaks who describes her approach to medicine as “holistic,” incorporating both science and spirituality.

“I’ve practiced for 40 years so I’ve come through a long stretch of seeing changes in health,” Sutton said, including huge increases in allergies, skin problems and cancer.

“We are living longer but living sicker,” she said.

When people come to her with such problems, Sutton said one of the first things she suggests is a change of diet, including a move toward organic and non-GMO foods. She said her patients’ health usually improves.

“I am only speculating from experience,” Sutton said. “There is no serious study that says genetically modified food does this but not that.”

Lang, the Fair Oaks mother, said the anecdotal evidence she’s seen in her son is enough for her to keep GMOs out of her kitchen by eating organic and avoiding most packaged foods.

A day after organizing a Proposition 37 rally with organic farmers last week, Lang made her family a soup of carrots, Swiss chard, broccoli and homemade chicken stock. Potatoes baked in the oven while she whipped up her own dressing for a salad and chopped mango to top fish cakes.

“Since the answers aren’t there,” Lang said, “I choose to proceed on a precautionary principle.”


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Viruses and Cell Programming

Changing pathways and using viruses for generating reprogrraming

A new research published in Cell, suggests that triggering a pathway designed to sense viral infection can help boost generation of induced pluripotent stem cells (iPSCs), suggesting that the viruses used by many reprogramming methods influence the fate of the cell. Thus, by targeting the pathway without using viruses could avoid the risk that the viruses’ genetic material will integrate into the genome and cause the cell to become cancerous—a common concern for iPSC therapies.

Shinya Yamanaka, 6 years ago, was able to  identify four key transcription factors, that, when transduced into cells using a viral vector, caused cells to de-differentiate into a stem-cell-like state. These cells had the potential to generate a multiplicity of human tissues. He shared this year’s Nobel Prize in Medicine for the achievement, which has already made significant contributions to biomedical research. However, there was a major hurdle on the path to clinical use: the strategy relies on a retrovirus that can integrate into host genomes, sometimes activating an oncogene that could render the cell cancerous. Injecting such cells as therapies thus raised concerns about the risk of patients developing tumors.

Hoping to devise a non-integrative carrier for Yamanka’s reprogramming factors, John Cooke, who studies vascular regeneration at Stanford University and colleagues created cell-permeant peptides (CPPs)—the transcription factors attached to an 11-amino–acid-long protein tag that allows them to pass through the cell membrane. But using CPPs to reprogram fibroblasts turned out to be a hundred times less efficient than using retroviral vectors. Compared to virally-transduced cells, CPP-programmed cells also expressed critical pluripotency target genes several days later and at much lower levels.

It occurred to Cooke’s postdocs Jieun Lee and Nazish Sayed that the viral vectors themselves might be sending an important signal to the fibroblasts the researchers were trying to reprogram. So they added a GFP-expressing viral particle during their CPP reprogramming protocol—and found that the virus boosted efficiency, even though the CPPs carried the transcription factors.

Sayed and Lee hypothesized that the viral particles were actually stimulating innate immune pathways in the fibroblasts. A key player in the activation of these pathways is the toll-like receptor 3 (TLR3), which is known to be activated by the double-stranded viral RNA (dsRNA) carried by the viruses. Sure enough, knocking down TLR3 reduced the efficiency of a retroviral reprogramming. Furthermore, adding a synthetic mimic of dsRNA during CPP reprogramming had the reverse effect, boosting the number of human fibroblasts that completed the transition to iPSCs.

The researchers were even able to nail down the mechanism. It turns out that TLR3 stimulation leads to epigenetic changes that allow easier transcription factor binding to their target genes.

“In fibroblasts, much of the genome is in a closed conformation, so transcription factors have trouble accessing promoters,” explained Cooke. “But activation of innate immunity [by TLR3] puts chromatin in an open configuration so transcription proteins work.” It may also be possible to target the chromatin directly, he noted.

It’s not the first time epigenetic marks have been fingered as key players in cellular reprogramming, and it’s probably not the last. “It will be interesting to use genome-wide epigenetic studies to elucidate the epigenetic similarity between embryonic stem cells (the gold standard of pluripotency) and reprogrammed cells in the presence and absence of active TLR3 stimulation,” Kitai Kim, a cancer and stem cell biologist at Memorial Sloan-Kettering Cancer Center, wrote in an email.

Additionally, the work may have implications for the origin of cancer. “iPSC reprogramming and tumorigenicity share noticeable levels of the similarity,” said Kim, who did not participate in the research. Cooke and his colleagues agree and are planning to study how inflammation may help create an open chromatin state that enables new differentiation pathways. “The state of chronic inflammation is often associated with cancer,” Cooke noted, speculating that inflammation may push chromatin toward a plastic state that enables malignant transformation.

Jieun Lee et al., “Activation of innate immunity is required for efficient nuclear reprogramming,”Cell, 151:574-558, 2012.


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Performance Ranking of Scientific Papers: University of Agriculture among top 300

UAF among top 300 universities

The University of Agriculture, Faisalabad, has made it to top 300 universities of the world on the basis of Performance Ranking of Scientific Papers for World Universities conducted by the National Taiwan University Ranking.

The world top 300 universities’ ranking published by Higher Education Evaluation and Accreditation Council of Taiwan (HEEACT) has rated UAF at 158th position with 14.96 quality points in the category of Agriculture and Environmental Sciences. Whereas well known universities of the world, including University of Oxford, got 14.88 points, Ataturk University (14.79), Columbia University (14.73), University of Michigan – Ann Arbor (14.72), University of Cambridge (14.57), University of California –Riverside (14.11), University of Zurich (14.09), Charles Sturt University (14.05), University of Colorado – Boulder (13.81), University of New England, Australia (13.44), Ankara University ( 13.42), University of Hong Kong (12.39), Technical University of Berlin (11.45), University of Amsterdam (10.22), The University of Manchester (10.07), and Punjab Agricultural University of India (9.97) points.

According to the NTU Ranking website, the quality points in ranking are based on research productivity (weighed 20 per cent) consisting of number of published articles of the last 11 years (10 per cent) and the number of research articles of the current year (10 per cent). The research impact (weighed 30 per cent) – number of citations of the last 11 years (10 per cent); the number of citations of the last two years (10 per cent) and the average number of citations of the last 11 years (10 per cent).

Similarly, research excellence weighed 50 per cent – the h-index of the last two years (20 per cent); the number of highly-cited papers (15 per cent) and the number of articles of the current year in high-impact journals (15 per cent).

In an email sent to UAF Vice-Chancellor Prof Dr Iqrar Ahmad Khan, the NTU Ranking research team stated that the UAF had been ranked excellently in the 2012 Performance Ranking of Scientific Papers for World Universities.

“The Performance Ranking of Scientific Papers for World Universities is a stable and reliable ranking for universities devoted to scientific research. It is entirely based on statistics of scientific papers which reflect three major performance criteria – research productivity, research impact, and research excellence,” the team stated.

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Biomedical research centre at King Edward Medical Univeristy

 Approval for biomedical research centre by KEMU syndicate

Important decisions were made at the 18th meeting of The King Edward Medical University Syndicate . This includes approval for establishment of Advanced Research Centre for Biomedical Sciences (ARCBS).

Chaired by KEMU Vice-Chancellor Prof Dr Asad Aslam Khan, the syndicate accorded approval to establishment of ARCBS with the aim of supervising and enhancing research for PhD and masters study programmes.

The approval for appointing eligible candidates against the newly created posts under the Tenure Track System was also accorded.

Health Special Secretary Babar Hayat Tarar, representatives of higher education and finance departments Zark Mirza and Shoaib Iqbal Syed, MPAs Dr Asad Ashraf, Saeed Akbar Khan, Prof (retired) Munirul Haq, HEC representative Prof Kamran Khalid Cheema, KEMU Registrar Prof Fareed Ahmad Khan, Professor of ENT Dr Azhar Hameed, Prof Atif Hasnain Kazmi, Prof S. M. Awais, and Mayo Hospital MS Dr Zahid Pervez, also attended the meeting besides other senior faculty members.

The objective of the ARCBS for which funding had been approved in KEMU Budget and Finance Meeting 2012-13 was to provide the requisite research infrastructure at KEMU to enhance, expand, and support institutional capacity to conduct state-of-the-art biomedical, clinical and bio-behavioural research for expanding research capacity and enhancing research productivity of ARCBS investigators and the King Edward Medical University as a whole.

“The project aims at augmenting the existing world-class research biotechnology and biomedical facilities at KEMU and enhancing the capacity to conduct health disparities at ARCBS through recruitment of a critical mass of investigators and technical personnel,” Asad Aslam told the meeting.

He said the centre would setup appropriate research facility to accommodate research projects being conducted by faculty and students and provide relevant administrative support to researchers allowing them to focus their efforts on teaching and research.

The syndicate also accorded approval to commencement of MD Nephrology at KEMU and constitution of a ‘vigilance committee’ comprising KEMU vice chancellor, chairman of hospital committee, dean of respective faculty, and two retired professors of KEMU — Prof Dr Muhammad Nawaz Chughtai and Prof Dr Ahmad Wasim Yousuf. The syndicate also approved appointments made in Advanced Diagnostic Lab and promotion of employees from BS-1 to BS-16.


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Endogenous Retroviruses

Old Viruses turn deadly upon revival

An interesting study has been published in Nature on Oct 24. Fragments of ancient viruses buried in the genomes of mammals and other vertebrates typically lay dormant but can awaken in immune-compromised mice and may cause cancers. This initiates for the resurrection of such viruses, known as endogenous retroviruses (ERVs), could be other microbes, which are unfettered in such immune-compromised mice.

“This study provides a link between exposure to other microbes—commensals or even pathogens—and activation of endogenous retroviruses, which in mice leads to cancer,” said senior author George Kassiotis, an immunologist at The National Institute of Medical Research in the United Kingdom. But other researchers are skeptical of the connection.

What are ERVs?

ERVs are the broken remains of ancient retroviral infections, in which fragments of viral RNA are reverse-transcribed into DNA and become part of the host genome, where they collect mutations that prevent them from forming new viruses.  In healthy mice, such viral DNA is not typically transcribed, but Kassiotis and his team of researchers found that mice genetically incapable of producing antibodies had increased expression of genes from certain ERVs in macrophages—enough to actually recombine and start assembling viruses. Those new viruses carried a mix of genes from two ERVs, each of which was incapable of replicating on its own, but together formed a replicating, infectious virus.

Experimental evidence

Though researchers had suspected that ERVs could reactivate and recombine, the study provides direct evidence of such an event, says immunologist David Markovitz of the University of Michigan, who was not involved with the study. “It’s extremely interesting that the mice activate or reactive their expression of ERVs in the absence of antibodies,” he said, “and that [the researchers] saw corrections in mutated genes that actually leads to replication of virus.”

Modern retroviruses have long been associated with the development of cancers, and Kassiotis’s team thought the ancient viruses could be similarly dangerous. Indeed, mice with infectious, recombined retroviruses developed significantly more tumors in their spleens and thymus, where levels of retroviral expression were high.

But, despite this link between ancient viruses and active cancer, some retroviral experts are more intrigued by what the authors think is the cause of viral reactivation.  “The interesting wrinkle on this study is the apparent importance of the immunodeficiency,” sad virologist John Coffin, of Tufts University, who was not involved in the study.

Previous data have indicated that signals from bacteria in the mouse gut could lead to increased EVR expression, but that antibodies usually block those microbial signals. Thus, Kassiotis’s team hypothesized that in the absence of such antibodies in their immunodeficient mice, invading microbes could activate ERV expression.

Indeed, when placed in germ-free environments, or fed acidic water that would limit their gut microbes, the immune-deficient mice experienced less viral reactivation.

Markovitz agreed. Many factors influence and are influenced by the microflora of the gut, so it’s unclear whether changes in the microflora is the cause of viral reactivation or if it’s merely a coincidence, he said. “Thinking [the trigger is] the microbiome is attractive, but there’s no evidence for that.”

Still, the study provides a starting point to explore the interplay between gut microbes and retroviruses that lead to cancers in mice and other organisms. If true, Kassiotis speculated, the implications could be far-reaching. “You could imagine a link between persistent infection or inflammation or even diet with the propensity to develop certain leukemias,” he said.

But the link to human health is even further way, cautions geneticist Dixie Mager of the University of British Columbia, Canada, who was not involved in the study. There are specific features of the mouse model that make it possible for these viruses to recombine in mice that aren’t present in humans, she explains. “It is therefore extremely unlikely that ‘active’ human ERVs could be generated by similar mechanisms in immune compromised individuals.”


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Possible usage of siRNA for HCV

siRNA mediated silencing of IRES domain III by Qudsia Mairaj


Hepatitis C is a liver disease caused by hepatitis C virus (HCV). It can develop as a milder infection of a few weeks duration or it may lead towards a serious, persistent chronic infection [1]. HCV is leading cause of end stage chirrohsis and hepatocellular carcinoma [2]. According to WHO (world health organization) data, about 160 million people globally are chronically infected with HCV and it makes 2/3% of the world population [7].In Pakistan, about 6% of population is infected by HCV [4].

HCV is a single stranded RNA virus of positive polarity and it is an enveloped virus[4]. HCV belongs to Hpacivirus genus, which is a related to family Flaviviridae[5].Its genome is 9.6 kb in size [6]. At the 5’ and 3’ are UTR (untranslated regions) are not translated, but are crucial for translation and replication of virus. 5’ UTR has ribosome binding entry site (IRES). This IRES is responsible for recruiting translational machinery to carry out the process of translation [16]. It translates a long polypeptide chain of 3000 amino acids. Structural proteins coded by HCV genes are core proteins, E1 and E2, and nonstructural proteins are NS2, NS3, NS4,NS4A, NS4B,NS5,NS5A and NS5B coded by regulatory genes.

HCV life cycle:

Liver is the primarily target organ of HCV and it affects liver cells [7]. Its life cycle involves certain steps which are attachment, entry and penetration into liver cells through cell-mediated endocytosis [9], replication and translation, assembly and maturation and release of infectious virions. It uses certain cell receptor for its entry that are CD81 [18, 19], low density lipoprotein (LDL) receptor [17], highly sulfated heparin sulfate, scavenger receptor Class B type 1 (SR-B1) [19] and DC-SIGN (dendritic cell-specific interacellular adhesion molecules 3 grabbing non integrin) L-SIGN (DC-SIGNr’ liver and lymph node specific) [8]. Most recently another receptor for HCV entry has been identified that is Claudin-1 [8]. E1 and E2 are two important viral proteins that interact with variety of cell receptor during entry. Fusion of virus is then mediated by viral proteins RdRp (NS5) and NS3 [9]. Translation is carried out in membranous webs formed on the surface of ER (endoplasmic reticulum). Resulted long polypeptide will be subjected to proteolytic cleavage by certain host and viral proteases to form functional proteins. Then the assembly of new viruses takes place, maturation occurs and virions are released to infect new host cells.

Current treatment for HCV infection:

We know that HCV genome is a +ve strand or in other words it is a mRNA. Hence when it enters the host step, after locating its specific site (ER) it starts translation. So it, instead of making copies of genome, makes proteins. Hence it starts an immediate pathogenic response to body and leads towards infection within less period of time.

Different approaches are in practice for the treatment of HCV. Most commonly used antiviral drugs include Ribavirin and pegylated interferon alpha (pegIFN alpha). But these are not specific aniviral drugs [20]. Not only they prove ineffective in some cases, but pegIFN alpha and RBV are difficult to tolerate. Viruses can develop resistant against these drugs. In case of HCV, its replication is carried out by RNA dependant RNA-polymerase (RdRp), which does not have a proof reading activity and has very high error rate. It results in the mutation of HCV genome leading towards the formation of quasi species. These mutant viruses may develop resistant against a particular antiviral drug. Apart from that antiviral drugs have many side effects including toxic effects, allergic effects etc.

IRES as a target for HCV therapy through siRNA:

IRES (internal ribosomal entry site) of HCV is best studied among other viral IRES [15]. HCV IRES is present in folded form forming many stem loops known as domains (I, II, III, IV), a pseudoknot and a helical structure. These all elements take part in forming a tertiary structure for efficient binding of 40S ribosome subunit and eIF3 (eukaryotic initiation factor 3).

Of all four domains most important domains for siRNA targeting is domain III. Study in mice showed that domain III is the only domain that interacts efficiently with all other III domains, suggesting that it holds all other domains of IRES [16]. It further interacts with eIF3 and recruits ribosome for translation [17].

Apart from this most important function of IRES domain III, IRES is highly conserved region which makes it an attractive target for siRNA therapy. Within the IRES, domain III has an internal loop (loop IIIb) and an adjacent mismatched helix which is nessary for IRES-dependant initiation of translation and it is highly conserved [22] and hence a wonderful target for siRNA mediated silencing of HCV translation. As IRES is necessary for viral translation, it won’t be able to carry out translation after degradation by siRNA and no replication will take place. Hence viral infection can be overcome at early stage of viral life cycle right after entry of virus into cell.

siRNA as a promising future antiviral therapy for HCV:

Among possible therapeutic therapies, RNA interference (RNAi) is an emerging new technique and it’s believed to be proved successful for the treatment of Hepaptitis C [10]. RNAi is a regulatory mechanism of most eukaryotic cells. It involves the active RISC (RNA induced silencing complex) which carries out post-transcriptional gene silencing. siRNA is a double stranded short stretch of nucleotide ranging between 21-22 nucleotides with a characteristic 3′ overhang. After its processing, it becomes single stranded “guide strand” and binds to its target mRNA and degrades it [11]. It can be prepared synthetically in vitro.

HIV-1 was the first primate virus shown to be inhibited by siRNA [12]. Problem with the siRNA is the difficulty with its delivery into cells. Once it is gotten into its target place it can do its job very well but first there is need to deliver it into target location. A new technique is developed to use aptamer for siRNA delivery into cells. These are oligonucleotides present naturally or can be synthesized. Their property is that they have high affinity and specificity for the target molecule to which they bind [24]. They have their own specific and stable three-dimensional structure which provides them with high specificity with respect to their target molecule.

Different types of aptamer have been applied for the affective drug delivery of drugs into specific cells. The molecules that are needed to be delivered into cells, are attached to aptamer through direct conjugation or by means of some functional groups [13].

Most well established aptamers for siRNA delivery are the prostate-specific-membrane antigen (PSMA) aptamers that bind with high affinity to PSMA [14]. It proved a successful method for delivery of siRNA into cells. If siRNA conjugated with a specific aptamer is used as an antiviral therapy for HCV it would be very successful. For efficient delivery of these siRNA-aptamer chimeras, nanoparticle vectors can be used which displays large surface area for siRNA-aptamer binding and exposing aptamer for binding to cell receptor [23]. Following this strategy, if we make a construct of siRNA-aptamer chimeras against domain III of IRES, especially the sub-domain/internal loop IIIb, it would prove a very efficient method to inhibit the HCV infection in early stages of viral life cycle.

This siRNA-aptamer has many outcomes. Relatively low concentration of siRNA molecules would be required as only specific cell would be targeted, target will be more specific and response will be fast. As IRES is conserved region, maximum viral infection will be inhibited. Aptamer is safe to use and it is less toxic and less immunogenic.



2)      Mühlberger, N., R. Schwarzer, B. Lettmeier, G. Sroczynski, S. Zeuzem and U. Siebert (2009) HCV-related burden of disease in Europe: a systematic assessment of incidence, prevalence, morbidity, and mortality. BMC Public Health 9:34

3)      Khaliq, S., S. Jahan, A. Pervaiz, U.A. Ashfaq and S. Khaliq (2011) Down-regulation of IRES containing 5’UTR of HCV genotype 3a using siRNAs. Virology Journal 8:221

4)      Blight, K.J., A.A. Kolykhalov,K.E. Reed,E. V. Agapov, C.M. Rice (1998) Molecular virology of hepatitis C virus: an update with respect to potential antiviral targets. Antiviral Therapy 3:71-81

5)      Raney, D.K., S.D. Sharma, I.M. Moustafa and C.E. Cameron (2010) Hepatitis C Virus Non-structural Protein 3 (HCV NS3): A Multifunctional Antiviral Target. The journal Of Biological Chemistery 285:22723-22725


7)      Hahn, V.T. (2011) Arrest All Accessories — Inhibition of Hepatitis C Virus by Compounds that Target Host Factors

8)       Zeisel.B.M., H. Barth, C. Schuster and T.F. Baumert (2009) Hepatitis C Virus Entry: Molecular Mechanisms and Targets for Antiviral Therapy. Frontiers in bioscience 14:3274-85

9)       Jazwinski.B.A., M.D and A.J. Muir (2011) Direct-Acting Antiviral Medications for Chronic Hepatitis C Virus Infection. Gastroenterol Hepatol 7:154-162

10)   Chevalier1,C., A. Saulnier, Y. Benureau, D. Fléchet, D. Delgrange, F. Colbère-Garapin, C. Wychowski and A. Martin (2007) Inhibition of Hepatitis C Virus Infection in Cell Culture by Small Interfering RNAs. Molecular Therapy 15:1452-1462

11)   Kim,H.D. and J.J. Rossi (2008) RNAi mechanisms and applications. Biotechniques 44:613-616

12)   Rossi,J.J. (2006) RNAi as a treatment for HIV-1 infection. BioTechniques 40:S25-S29

13)   Zhoul,J. and J.J. Rossi (2010)  Aptamer-targeted cell-specific RNA interference. Silence 1:4

14)   McNamara, O.J., E. R. Andrechek, Y. Wang, K.D. Viles1, R.E. Rempel, E. Gilboa,  B.A. Sullenger and  P.H. Giangrande (2006) Cell type–specific delivery of siRNAs with aptamersiRNA chimeras. Nature Biotechnology 24:1005-1015

15)   Jang, S.K. (2006) IRES elements of picornaviruses and hepatitis c virus. Virus Research 119:2-15

16)   Buratti,E., S. Tisminetzky, M. Zotti, and F.E. Baralle (1998)  Functional analysis of the

interaction between HCV 50UTR and putative subunits of eukaryotic translation  nitiation factor eIF3. Nucleic Acids Research 26:3179-3187

17)   Joyce, A.M. and D. Lorne J. Tyrrell (2010) The cell biology of hepatitis C virus. Microbes and Infection

18)    Meuleman,P., J. Hesselgesser, M. Paulson, T. Vanwolleghem, I. Desombere, H. Reiser, G.L. Roels (2008) Hepatology 48:1761-1768

19)   Scarselli,E., H. Ansuini, R. Cerino, R.M. Roccasecca, S. Acali, G. Filocamo, C. Traboni, A. Nicosia, R. Cortese and A. Vitelli (2002) The human  scavenger receptor class B type I is a novel candidate receptor for the hepatitis C virus. Embo Journal 21:5017-5025


21)   Nulf,J.C. and D. Corey (2004) Intracellular inhibition of hepatitis C virus (HCV) internal ribosomal entry site (IRES)-dependent translation by peptide nucleic acids (PNAs) and locked nucleic acids (LNAs). Nucleic Acids Research 32:3792-3798

22)   Collier,J.A., J. Gallego, R. Klinck, P.T. Cole, S. J. Harris, G.P. Harrison, F. Aboul-ela, G. Varani, and S. Walker

23)   Bagalkot,V. and X. Gao (2011) siRNA-Aptamer Chimeras on Nanoparticles: Preserving Targeting Functionality for Effective Gene Silencing. ACS Nano 5:8131-8139

24) Que-Gewirth,N.S. and B. A. Sullenger (2007) Gene therapy progress and prospects: RNA aptamers. Gene Therapy 14:283-291


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Novel DNA Methylation in Protozoa

Epigenetics Mechanism in Protozoa reported by Maria Atia

As per the previous knowledge it is known that methylation of the DNA means that it will undergo gene expression process. But exceptions are always there. In this case the exception is being made by a fresh- water protozoan named Oxytricha trifallax. On 17th October, 2012, a study was published in the journal Genome Biology in which it has been reported that DNA methylation in Oxytricha trifallax means that the marked DNA is junk. This new finding is in contradiction with an old report that Oxytricha, having four nuclei, does not have any kind of methylation on it.

John Bracht, chief author of this study and a postdoctoral researcher at Princeton University, commenting on this report said that this finding is a very surprising one as a lot of studies had been done in 80s and 90s to identify the DNA methylation in this protozoan but all showed negative results. He further said that this modification which occurs in the DNA is quite similar to that which happens in humans except that the functions are reversed in humans.

An evolutionary geneticist, Laura Landweber, Princeton, has described the life cycle of Oxytricha which is different from others. In this protozoan a total of four nuclei of two types are present. One type is of the micronucleus and the other type is of the macronucleus. The micronucleus arises from germ-line and remains transcriptionally silent throughout its life span. 95% of the genome is present in this nucleus. The rest 5% is present in the macronucleus. Transcription successfully occurs of this 5% DNA.

Landweber further detailed the mating process of Oxytricha. Asexual reproduction of cells through budding occur when the cells are getting proper and enough nutrition. When the available food starts to finish out and the cells fail to get enough nutrition it switches to another method for mating. The micronuclei pair undergoes meiosis to form 8 haploid cells. Two of these cells are exchanged with another Oxytricha.

One native and one foreign haploid cell fuse to form a diploid micronucleus. All the nuclei except the new diploid micronucleus get destroyed. Mitosis occurs and the diploid micronucleus divides to give a new micro and macro- nucleus. After the original number of nuclei has been restored in the cell, the macronucleus gets rid of the 95% DNA. Why it does that is still a mystery.

Although Bracht knew all about negative results on DNA methylation for this protozoan but was not satisfied with the findings. He had a feeling that the methylation may be involved with the DNA disposal and proper timing and equipment is required to catch it. So he tried his theory with sensitive instruments. He worked through the mating cycle and pause the cell cycle at every step in order to identify the DNA methylation. He used glowing methylation-specific tags for the identification.

Positive results were obtained from both types of nuclei. Using mass spectrometry he also located the position of the methyl tags which was the junk DNA, thrown away later by the cell. From this it can be concluded that only the DNA destined to be discarded is marked with methyl groups.

Wei-Jen Chang of Hamilton College seemed less amazed and was in fact happy that somebody has identified the methylation. He has thinks of it as a landmark in the field.

The presence of the methyl tags has been confirmed but how the DNA ends up methylated still remains to be found out. Scientists are also trying to figure out that how the methylation of DNA leads to the deletion of the DNA. Methyl tags are a result of the action of enzymes called methyltransferases. No counterparts of this enzyme have been located on the Oxytricha genome so far.

With all these new findings the scientists are ready to catch whatever the protozoan has to throw next in terms of the DNA methylation process, says Landweber. She also said that we have not succeeded in identifying the methylation method but chances are that it is there. Chang however says that the protozoan might have another alternative way of DNA methylation which in turn would be interesting to know about.

Until the alternative method could be identified, intelligent guesses are all that can be made about it and how they will help us to understand epigenetics more.


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