Wednesday, December 29, 2010

CSIR NET Life Science Old Papers

CSIR UGC NET life science previous papers are very useful to UGC NET aspirants.

CSIR UGC NET Previous papers for Download


CSIR UGC NET Life science Syllabus (Download)

S.No.
Year of Paper
Download link

1.

June 2004 Paper

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2

December 2004 Paper

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3

June 2005 Paper

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4

December 2005 paper

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5

June 2006 Paper

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6

December 2006 Paper

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7

June 2007   Paper
8
December 2007 Paper
9
June 2008 Paper
10
December 2008 Paper
11
June 2009 Paper
12
December 2009 Paper
13
June 2010 Paper
14
December 2010 Paper
 
Note: Do not forget to say Thanks for IFAS (Institute for Advanced Science) and kbiotech.
These are collection of pdf files from various sources. I think these are useful to success in the Net exam. THANK YOU
 
Reference site : Biochemistry Den

Thursday, December 23, 2010

Wednesday, December 1, 2010

The AGE of sensible cooking

If you thought your favourite char-grilled kebabs and diet sodas are a way to keep you fit and healthy, think again!

The AGE of sensible cooking

A combination of carbohydrates, protein and fat in food subjected to dry heat and high temperatures produce a toxic species of chemicals called Advanced glycation End products (AGEs).

The AGEs in our food can lead to several diseases and accelerate ageing. Diseases associated with their toxicity include obesity, metabolic syndrome, heart disease, diabetes, allergies, autoimmune diseases, digestive disorders, and several inflammatory conditions such as arthritis, asthma, ulcers, aches and pains.

Several studies also suggest that dietary AGEs are involved in insulin resistance (pre-diabetes), visceral obesity (abdominal fat) and plaque formation, leading to heart disease. Continuous intake of these compounds contributes to excessive accumulation into body tissues, which suppresses the immune system and resistance to diseases.

The AGE of sensible cooking

While these compounds are also formed by the body during normal metabolism, the highest contribution is through food. When these are digested and absorbed, they trigger oxidative damage to tissues due to generation of free radicals, which leads to serious health implications. Some of these can be as damaging as tobacco smoke.

Modern day diets are loaded with AGEs. They are commonly found in high protein and high fat foods, diet sodas and foods exposed to unusually high heat such as industrial ovens, deep frying, irradiation and broiling.

The amount of AGEs present in all food categories is also related to cooking temperature, length of cooking time, and presence of moisture. Excessive consumption of these compounds may partly be responsible for early incidence of adult diseases such as diabetes and heart disease, in the younger generations.

There is evidence to suggest that reducing the AGEs in our diets may improve our health and reduce risk of life-threatening disease.

The AGE of sensible cooking

While their complete avoidance is not possible, reduced exposure to these compounds can be achieved by:

- Using moist cooking methods like boiling, steaming, and stewing food, instead of frying and grilling.

- Shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients like lemon juice or vinegar.

  • When cooking, chop ingredients in small pieces to shorten cooking time.
  • Micro-wave the food in presence of sufficient liquid so it does not dry up. The formation of AGEs is delayed in presence of water.
  • Avoiding over-cooking and prolonged exposure to high temperatures.
  • Avoid heating oils to high temperatures while making tadkas and curries.
  • Avoid fast, highly processed and fried foods.

Increase consumption of antioxidants from fresh fruits, vegetables, whole grains, nuts and seeds. Cook with plenty of herbs and spices including turmeric, garlic, rosemary etc. Also, consuming protective foods like probiotics (lactobacillus strains) may be protective against the toxic effects of AGEs.

Source: Ishi Khosla/Indian Express

Tuesday, November 30, 2010

Multiple Choice Questions in Biochemistry by Vidya Sagar

"Mcqs in Biochemistry" by G. Vidya Sagar
Netlibrary Inc | Edition : 2008 | ISBN: 8122426271 | 300 pages | PDF | 1 MB

 

Description:

Competitive Examinations are the order of the day. All Colleges conducting professional courses at PG level are admitting students based on common entrance examination, which is of objective type. In Pharmacy, M.Pharm admissions are based on qualifying the GATE enterance examination conducted by Govt. of mcq in biochemistryIndia. In this book, The author has done good work in preparing several objective questions which help the students to face the subject in the examination with poise and confidence. The book is well balanced and consists of multiple choice questions from all the important topics like carbohydrate metabolism and other important Biochemical aspects. The typesetting and quality of printing is good. The author is also well experienced in taking up this type of work. I recommend this book to all the students preparing for GATE examination and also for Medical and Pharmacy College libraries.
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The CELL
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Practical Biochemistry & Molecular Biology
Wilson & Walker

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The Essential Molecules of Life
CARBOHYDRATES
Robert V Sock

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Introduction to Protein Structure by Branden and Tooze ebook
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Molecular Biology of the Cell, 5th Edition
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How to Study for Success
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Schaum’s Outlines of Immunology
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Fundamentals of Biochemistry J.L.Jain
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Ecology by Odum
   

Note: These are all Collection of referral links only

Wednesday, November 3, 2010

Schaum’s Outlines of Immunology analysis book

Based on material from 400-600 level Immunology courses, this concise and thorough review of modern concepts in molecular, cellular, and systemic immunology contains over two hundred detailed problems with step-by-step solutions. Taking a problem-solving approach, Schaum's Outline of imageImmunology is an excellent supplement to any systematic textbook of modern immunology, focusing on the basic tenets of immunology as applied to the dynamics of immune responses and their outcomes, and is perfect for pre-med students who need help in their required immunology courses, as well as for medical and veterinary students who want to update their knowledge

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Sunday, October 24, 2010

Malarial Mosquitoes Are Evolving Into New Species, Say Researchers

malarial mosquitoTwo strains of the type of mosquito responsible for the majority of malaria transmission in Africa have evolved such substantial genetic differences that they are becoming different species, according to researchers behind two new studies published in the journal Science.

Over 200 million people globally are infected with malaria, according to the World Health Organisation, and the majority of these people are in Africa. Malaria kills one child every 30 seconds.

The international research effort, co-led by scientists from Imperial College London, looks at two strains of the Anopheles gambiae mosquito, the type of mosquito primarily responsible for transmitting malaria in sub-Saharan Africa. These strains, known as M and S, are physically identical. However, the new research shows that their genetic differences are such that they appear to be becoming different species, so efforts to control mosquito populations may be effective against one strain of mosquito but not the other.

The scientists argue that when researchers are developing new ways of controlling malarial mosquitoes, for example by creating new insecticides or trying to interfere with their ability to reproduce, they need to make sure that they are effective in both strains.

The authors also suggest that mosquitoes are evolving more quickly than previously thought, meaning that researchers need to continue to monitor the genetic makeup of different strains of mosquitoes very closely, in order to watch for changes that might enable the mosquitoes to evade control measures in the future.

Professor George Christophides, one of the lead researchers behind the work from the Division of Cell and Molecular Biology at Imperial College London, said: "Malaria is a deadly disease that affects millions of people across the world and amongst children in Africa, it causes one in every five deaths. We know that the best way to reduce the number of people who contract malaria is to control the mosquitoes that carry the disease. Our studies help us to understand the makeup of the mosquitoes that transmit malaria, so that we can find new ways of preventing them from infecting people."

Dr Mara Lawniczak, another lead researcher from the Division of Cell and Molecular Biology at Imperial College London, added: "From our new studies, we can see that mosquitoes are evolving more quickly than we thought and that unfortunately, strategies that might work against one strain of mosquito might not be effective against another. It's important to identify and monitor these hidden genetic changes in mosquitoes if we are to succeed in bringing malaria under control by targeting mosquitoes."

The researchers reached their conclusions after carrying out the most detailed analysis so far of the genomes of the M and S strains of Anopheles gambiae mosquito, over two studies. The first study, which sequenced the genomes of both strains, revealed that M and S are genetically very different and that these genetic differences are scattered around the entire genome. Previous studies had only detected a few 'hot spots' of divergence between the genomes of the two strains. The work suggested that many of the genetic regions that differ between the M and S genomes are likely to affect mosquito development, feeding behaviour, and reproduction.

In the second study, the researchers looked at many individual mosquitoes from the M and S strains, as well as a strain called Bamako, and compared 400,000 different points in their genomes where genetic variations had been identified, to analyse how these mosquitoes are evolving. This showed that the strains appear to be evolving differently, probably in response to factors in their specific environments -- for example, different larval habitats or different pathogens and predators. This study was the first to carry out such detailed genetic analysis of an invertebrate, using a high density genotyping array.

As a next step in their research, the Imperial researchers are now carrying out genome-wide association studies of mosquitoes, using the specially designed genotyping chip that they designed for their second study, to explore which variations in mosquito genes affect their propensity to become infected with malaria and other pathogens.

Both of the studies just published were collaborations between researchers at Imperial and international colleagues, involving researchers from institutions including the University of Notre Dame, the J. C. Venter Institute, Washington University and the Broad Institute. Funding for the projects was provided by the National Human Genome Research Institute, the National Institutes of Health, the BBSRC, and the Burroughs Welcome Fund.

Saturday, October 23, 2010

Vaccines could help elephantiasis spread

PARASITIC worms can adjust their survival strategy based on their host's immune response. This means potential vaccines against elephantiasis might make the infection spread more easily through communities.

Elephantiasis infects 120 million people a year in Africa and Asia. Tiny filaria worms carried by mosquitoes block the lymph vessels that normally drain fluid from limbs or genitals, which then swell to grotesque proportions. The only prevention is a yearly dose of worming drugs, but fewer than half the people at risk receive them.

Work is under way on a vaccine, but Simon Babayan at the University of Edinburgh, UK, and colleagues, have discovered that some vaccines may make the worms worse. When filaria worms in mice sense that the mouse is mounting a strong immune reaction, they change their life cycle, producing more offspring in the blood earlier. This helps the worm ensure that it will be picked up and transmitted by another mosquito despite the immune attack (PLoS Biology, DOI: 10.1371/journal.pbio.1000525).

Unfortunately, experimental vaccines rely on the very immune reactions that warn the worms, Babayan says. People who get such a vaccine may defeat their own infection, but the worms' early response means they will pass on more infections.

Babayan says potential vaccines should be tested for whether their targets adapt to them in this way.

Synthetic DNA makers warned of bioterrorism threats

TO MAKE it harder for bioterrorists to build dangerous viruses from scratch, guidelines for firms who supply "custom DNA" are being introduced in the US.

The US and other countries restrict who can work with certain germs, but it might be possible to build some viruses from their genes. A number of firms supply DNA sequences to order. A 2005 investigation by New Scientist raised alarms when it found that only five out of 12 of these firms in North America and Europe always screened orders for sequences that might be used in bioweapons.

The US now wants firms to verify a customer's identity and make sure they are not on a list of banned buyers. It also wants them to screen orders for sequences that are unique to Select Agents, a list of microbes the US deems dangerous.

However, scientists commenting on the draft rules earlier this year fear that sequences from microbes other than Select Agents might also be dangerous. The US Department of Health says not enough is known about them to say which ones should arouse a firm's suspicions. Other potential weaknesses include the fact that the rules are voluntary, and that much custom DNA is made outside the US.

Cloning discovery may kill ethical objection

A key ethical objection to "therapeutic" cloning could be undermined if the results of experiments on abnormal cloned frog embryos are repeated in humans.

Therapeutic cloning involves the harvesting of embryonic stem cells from cloned embryos. Scientists hope the stem cells will provide powerful treatments for disease. But collecting them destroys the embryo - which is destroying a potential life, in some people's view.

However, this ethical problem would be avoided if healthy cells could be extracted from abnormal human embryos doomed to die anyway, and researchers have shown this is possible in frogs.

"If an embryo is certain to die, I can't see why anyone would object to someone taking cells and working with them," says John Gurdon, head of the team at the Welcome Cancer Research Institute in Cambridge, which experimented on the cloned frog embryos. "If it's destined to die within days, it's not a potential human," he says.

However, some pro-lifers disagree, saying they would only be satisfied that the procedure was ethical if the cells could be harvested without killing the defunct embryo. "It's a question of whether it curtails the life expectancy of the embryo," says Josephine Quintavalle of the UK's Pro-Life Alliance. She says that the principle of not killing an embryo is the same, whether its life expectancy is three days or three months.

Spare embryos

Couples undergoing treatment at fertility clinics almost invariably generate spare embryos that are visibly abnormal and doomed to die within two to three days. Now, through his work on frogs, Gurdon has shown that even if an abnormal embryo's fate is sealed, it contains cells which are completely normal and which develop normally into many tissue types.

To demonstrate this, Gurdon created genetically engineered frogs whose cells were equipped with a gene to make the green fluorescent protein (GFP) produced by some jellyfish.

Next, he took gut cells from the frogs and made them into cloned embryos by fusing them into normal frog eggs emptied of their own genetic material.

Half the embryos Gurdon created were complete duds, failing to divide at all. Another quarter developed into "partial embryos" which were clearly and visibly abnormal, with normal cells developing in only one half of the embryo, for example. These embryos all died a day later.

Growing up

But before they did, Gurdon extracted normal cells and grafted them into normal frog embryos. As the embryos developed, Gurdon could spot all tissues that came from the grafted cells, because they carried the GFP gene and so glowed green.

"The surprising result was that some of the cells from the cloned embryos did well and grew for months in the new host embryo," says Gurdon.

If the same was true of defunct human embryos, it might be possible to extract cells from them for crafting into tissues for patients. At the very least, says Gurdon, the cells could be used for research to find out how to fast-forward their development into any type of tissue

Alzheimer's protein may spread through infection

Neurologists have found that the brain plaques associated with Alzheimer's can form when the proteins responsible are injected into the bellies of mice, suggesting that the guilty proteins can get from the body's periphery to wreak havoc in the brain.

A protein called beta-amyloid makes up the brain plaques that accompany the disease. In 2006, Lary Walker at Emory University in Atlanta, Georgia, Mathias Jucker at the University of Tübingen in Germany and colleagues found that they could trigger Alzheimer's-like plaques by injecting samples of plaque-ridden brains into the brains of healthy mice. Now, Jucker and his colleagues at Tübingen have managed to create the same brain plaques by injecting the tissue elsewhere in the bodies of mice.

Mouse models

The group used mice genetically modified to produce large amounts of beta-amyloid, meaning they develop brain plaques similar to those seen in Alzheimer's disease in people. When the mice were around 2 years old, the team removed some of their beta-amyloid-laden brain tissue and injected it into the peritoneum – the lining of the abdomen – of young transgenic mice. Another group of transgenic mice received an injection of healthy brain tissue from normal mice of the same age that had not developed plaques.

Seven months later, before the mice had had a chance to develop plaques of their own accord, the team looked at their brains. The mice injected with healthy brain tissue had normal-looking brains, but those injected with beta-amyloid-heavy tissue had developed full-blown plaques similar to those seen in people with Alzheimer's.

If beta-amyloid in a mouse body's periphery can cause plaques in its brain, could Alzheimer's be transmitted by blood transfusions in humans? There's no evidence to suggest this might be the case, says Jucker. "We don't know if misfolded beta-amyloid can get out of the brain and into the bloodstream, for a start," he says.

Paul Salvaterra, a neurologist at the City of Hope hospital in Duarte, California, points out that Jucker's team only use an indirect measure of Alzheimer's because they focus only on plaques – just one aspect of the disease. "These authors are not studying Alzheimer's disease and certainly not studying infectious Alzheimer's disease," he says. "The type of [disease] they show is only suggestive of some aspects of Alzheimer's disease-related changes in the brain."

The early findings don't yet have implications for the general public, says Jucker, though he cautions that researchers should take care when handling amyloid proteins.

Friday, October 22, 2010

Universal cancer marker shows new treatment options

A single screening method that can force a wide range of cancers to reveal themselves has been discovered. The universal cancer marker could help doctors find and treat tumours, and provide surgeons with a "dotted line" to cut them out.


The key to the technique is the receptor for follicle-stimulating hormone (FSH). This receptor – typically involved in controlling women's reproductive cycles – appears in unusually large amounts in prostate tumours. So Aurelian Radu at Mount Sinai School of Medicine in New York and colleagues looked for it in 1336 human tumour samples, including prostate, breast, lung and liver cancers.


The group applied colour-labelled antibodies for the FSH receptor to the samples. They found that in every sample, the antibodies bound to blood vessels around the periphery of the tumour.


Radu doesn't yet know why tumour blood vessels express the receptor, though he thinks it might play a role in the formation of new vessels.

 

One-stop screening

 


The marker could be useful in pinpointing and treating tumours, says Radu. Currently, different imaging techniques are used to identify different types of tumour. "Using this marker, we can use one imaging technique for the whole body," says Radu. He hopes broader screening will enable earlier detection of secondary tumours.


Kairbaan Hodivala-Dilke at Barts and The London School of Medicine and Dentistry's Institute of Cancer agrees: "It's certainly a good marker, and could be especially useful in surgery, which is a bit hit-and-miss at the moment," she says. Using colour-labelled antibodies to highlight the edges of a tumour could enable surgeons to "cut along the dotted line".


Additionally, by attaching a cancer drug to an FSH receptor antibody, "we have the potential to target therapy exclusively to the tumour", says Radu.


Drugs that inhibit the FSH receptor are already in development as potential contraceptives, says Radu. He hopes that some might be trialled as anti-cancer drugs in the future.

Gene therapy proposed to treat depression

A NOVEL treatment for depression may soon get the go ahead: injecting genes directly into the brain. It would be the first attempt to treat a psychiatric illness with gene therapy.

A gene called p11 is vital for enabling neurons to respond to the neurotransmitter serotonin. A lack of p11 has been shown to lead to depression in humans.

To test whether gene therapy could help, Michael Kaplitt of the Weill Cornell Medical College in New York City and colleagues first demonstrated that mice lacking p11 showed symptoms of depression, failing to respond with the same vitality as healthy mice when exposed to challenges, such as showing decreased effort when having to swim to an island.

Next they injected viruses containing p11 directly into the nucleus accumbens of the mice lacking p11. This part of the brain is where a lack of p11 manifests itself as depression in humans. The team found this reversed the depression in the mice (Science Translational Medicine, DOI: 10.1126/scitranslmed.3001079).

Although the proposal to do the same in humans sounds drastic, Kaplitt points out that a similar procedure has already been used to deliver genes to the brain's of people with Parkinson's disease.

"We're already doing a primate study to support a potential human trial, so this is moving ahead very rapidly," says Kaplitt.
 
“Injecting a virus containing the missing gene into a mouse's brain reversed its depression”


Low levels of vitamin B12 linked to Alzheimer's

People with low levels of vitamin B12 may be at greater risk of developing Alzheimer's disease. The finding supports previous research showing large doses of B vitamins might halve the rate of brain shrinkage.


Babak Hooshmand and colleagues at the Karolinska Institute in Stockholm, Sweden, followed 271 healthy people aged 65 to 79 for seven years. The researchers measured the blood concentration of the amino acid homocysteine, high levels of which have been linked to negative effects on the brain, such as stroke. They also measured levels of active vitamin B12, which can decrease homocysteine levels.


By the end of the study, 17 people had developed Alzheimer's. A level of homocysteine moderately above average corresponded to a 16 per cent higher risk of developing Alzheimer's, while a level of active B12 slightly above average meant a 2 per cent lower risk.


"This is a very convincing study," says David Smith of the University of Oxford, who has investigated the effect of B-vitamin supplements on brain shrinkage. He says it is the first to show that low levels of active vitamin B12 are a risk factor for developing dementia several years later.


Although B12 deficiency is common among elderly people, more evidence is needed before recommending B12 supplements to stave off dementia, says Hooshmand.

Wednesday, October 20, 2010

Classification of Bacteriophages

Classification of Bacteriophages
On the basis of presence of single or double strands of genetic material, the bacteriophages are categorized as under:

1. The ssDNA Bacteriophages
(i) Icosahedral phages = φ ´ 174, St-1, φR, BR2, 6SR
U3 and G series e.g., G4, G6, G13, G16. All are like φ ´ 174.

(ii) Helical (filamentous)
(a) The Ft group: They are F specific phages and absorb to the tip of F type sex pilus, e.g., E.coli phages (fd, fl, N13).
(b) If group: They are absorbed to I-type sex pilus specified by R factors e.g., If1, If2, etc.
(c) The third group is specific to strains carrying RF1 sex factor.


2. The dsDNA Phages
Following are the examples of dsDNA phages:
(i) T-odd phage of E.coli e.g. T1, T3, T5, T7
(ii) T-even phage of E.coli e.g.T2, T4, T6
(iii) The other E.coli phages e.g., P1, P2, Mu, φ80.
(iv) The phages of Bacillus subtilis e.g., PBSI, PBSX, PBSI, SPOI, SPO2.
(v) The phage of Shigella a e.g., P2
(vi) The phage of Salmonella e.g., PI, P22.
(vii) The phage of Haemophilus e.g., HPl.
(viii) The phage of Pseudomonas e.g., PM2.


3. The ssRNA phages
Examples of the ssRNA bacteriophages are as below:
(i) Group I : E. coli. phages such as f2, MS2, M12, R17, fr, etc.
(ii) Group II : The QP phages.

4. The dsRNA phages
Example: The φ6 bacteriophage.

Replication of Prions

If prions lack their own nucleic acids and are merely proteins, a very important question requires an answer. How can a protein enter a host cell and direct the process of replication? To answer this question a large number of hypotheses have been put forward. An interesting hypothesis has been given by a group of scientists from the MRC Neuropathogenesis Unit at Edinburg. This hypothesis states that the existence of small piece of DNA gene (also called prp gene) is necessary to encode the amino acid sequence of prion protein at the time of its replication. This DNA gene is a component of the host genetic material (host DNA). The prion protein presumably serves as a promoter of DNA gene expression.

Recent studies indicate that prions represent a changed conformation of proteins normally found in cells. Once prions are produced, they somehow persuade the normal versions of the corresponding protein to assume the altered conformation and, thereby, become prions.

What is the Origin of Viruses?

Origin of Viruses
Three theories have been put forward to explain the origin of viruses. These theories are highly speculative and are as follows :

Survivors of Pre-Cellular First Living Inhabitants of the Earth
This theory intimately rests on the theory of origin of life on Earth. Life, according to this theory, originated from simple inorganic compounds by a slow biochemical evolution of “ordinary” chemical reactions spread over millions and millions of years.

It is speculated that during the course of origin of life on Earth somewhere at the stage when complex chemical molecules united to form still more complex molecules which could mate with still other metastable molecules till a relatively large molecule (like nucleoprotein) capable of growth and division, a simple virus or a protovirus may have originated (Haldane, 1954; Fraser, 1967). This theory, however, enjoys some insurmountable objections.

Present day viruses are all obligate parasites and it is difficult to conceive of their origin before the origin of their hosts (cells) which are at a far higher scale of evolution. Viruses use the same genetic code as cellular organisms and depend solely and entirely on ribosomes, transfer RNAs and enzymes of the host cell for protein biosynthesis. Moreover, viral nucleic acid has the same properties and the same mode of replication as the nucleic acid of cellular organisms.

Regression from More Highly Evolved Free-Living Microorganisms/Cells
Viruses are considered to have originated by retrogressive evolution from free-living cells, according to this theory. A parasite evolves retrogressively as it takes the ready made metabolites from its host instead of synthesizing them himself.
If the parasite continues to evolve retrogressively then, to save labour and energy, it would slowly loss some of its physiological, morphological and even genetical functions that become super-numerary in its new ecological niche and new mode of biological existence. A parasite would, therefore, get regressed to a much simpler organism. Obligate intracellular parasitism is the most specialized type of parasitism and such a parasite would ultimately possess only the bare minimum and this minimum is the possession of a nuclei acid (to ensure genetic continuity) enclosed within a protein shell (to ensure safety of the nucleic acid).

Shedding of all unnecessary morphological, physiological and genetical materials would necessarily reduce the size. A formerly free-living organism would thus be transformed into a virus. Green (1935), Laidlow (1938) and Burnet (1945) support the theory of retrogressive origin of viruses but the same is opposed by Luria and Darnell (1967) and Fenner (1968).

Derived from Normal Constituents of the Cell
An eukaryotic cell possesses organelles like chloroplasts and mitochondria which self-replicating semi-autonomous structures and reproduce their like. Chloroplasts and mitochondria increase in size and then divide while kinetosome is synthesized near a pre-existing one by assembly from the tubular materials. Besides they possess DNA which is functional and possesses its own mutational history, codes for the synthesis of mRNA and also presumably for protein.

Mitochondria mutate to non­functional forms in Neurospora and yeasts, while chloroplasts mutate to undeveloped, colourless proplastids in algae and higher plants. These mutations are based on genetic changes. Cells also contain certain organelles that exceptionally undergo autonomous unrestricted replications; examples are the centrioles in Marsilea and sperms and nuclear genes in the amphibian oocytes.

Viruses resemble above mentioned cellular organelles in chemical composition, possession of nucleic acid, genetic continuity of genome, independent mutational history, capacity to replicate independently under their own genetic control and also under the overall regulatory control of and within the premises of the host cell.

Many of the cellular organelles or factors possess some of the distinctive characters of viruses, or more specifically, of viral genetic determinant (reproductive independence, evolutionary independence, independent cell to cell transfer and infectivity and pathogenicity) while others could be conferred on them by a specific arrangement of nucleotides. Viruses could, therefore, be derived from any or several of these cellular components and it is possible that different viruses have originated differently. Some of the possibilities are given below:


1. Primordial self-replicating molecules may have mutated to regain the capacity to enter ('infect') the cell and then integrate with it. Such a molecule would be a 'virus'.

2. Some plasmids or even chromosomal segments may have evolved by merging of some primitive self-replicating molecules with the cellular genome. If this s true then it conceivable that some of the genes or groups of genes may revert to their ancestral habit and may have regained/evolved the genetic independence and independence and independent transfer of this genetic material. This would result in the ‘virus’.

3. Some genes of the cell could have escaped of the control mechanisms of the cell and may have acquired the capacity of autonomous replication independent of the division of the cell and capacity of independent transfer. Integration of these genes with the host genome would give us a prophage. Origin of bacteriophage from such prophage DNA has been outlined by Lindegren (1962). Luria and Darnell (1967) also suggest that bacteriophages containing DNA may have evolved from a number of genetic transfer elements (like F factor, bacteriocinogenic factor, etc.) occurring in the prokaryotic cells.

4. DNA viruses of eukaryotic cells may have originated from the functional DNA of cellular organelles (e.g., mitochondria and chloroplast) rather than for nuclear DNA (Matthews, 1970).

5. Origin of DNA plant viruses is somewhat more difficult to understand since there is no definite information with respect to the integration of plant viral nucleic acid into the genome of the plant cell. There is, however, some suggestive evidence in this connection. Some experimental evidence suggests that cut surfaces of barley seeds take up the DNA of the bacterium Micrococcus lysodeikticus and that it integrates into nuclear DNA of barley and replicates (Ledous and Huort, 1968).

In short, therefore, viruses may have originated from cell constituents which escape the control mechanisms of the cell, regained/developed the capacity of autonomous self-replication and ability to mediate their own independent cell to cell transfer and could enter or infect cells to which they did not belong.



What is the Structure, Chemical Nature, Replication of Prions (The Puzzling Proteins)?



C. Gajdusek (1957) came across a mysterious disease in New Guinea tribals which was later named as Kuru and prepared neuropathological specimens from a person who died of Kuru. William Hadlow (1957) who was working on scrapie disease of sheeps and goats examined Gajduseks neuropathological specimens and observed remarkable similarities between the abnormalities found in brains of Kuru victim and the sheeps and goats dying of scrapie.

Similar observations were made by British investigators T. Alpher, D. Haig and M. Clark during 1966. In 1970s S.B,. Prusiner, a bichemist at the University of California (USA), with his coworkers initiated the isolation and identification of the infectious agent of scrapie. After exhaustive research for a decade, he in 1982 discovered that the disease is caused by a proteinaceous infectious particle which he christened as prions. S.B. Prusiner has been awarded Nobel Prize in 1997 for the discovery of prions.
Prions represent the other extreme from viroids. They are considered to be devoid of their own genetic material (DNA or RNA) and consist of just a single or two or three protein molecules i.e., a prion is merely an infectious protein. The discovery of prion, an infectious protein, has threatened the universally accepted concept that only the genetic material (DNA, in some cases RNA) is infectious.

The prions, at present, are considered to be the causative agents of some of the diseases of animals and humans such as Scrapie disease of sheeps and goats, Bovine spongiform encephalopathy in cattle (BSE or Mad cow diseases);. Kuru, Creutifeldt Jacob disease (CJD), Gerstmann-Strausslar syndrome (GSS), Low Gehrig disease, Parkinsons disease, Serite domentia and Multiple sclerosis in humans. In 1996, information available from England indicates that the prion causing Bovine spongiform encephalopathy (BSE) in cattle might infect humans, resulting in a variant of Creutzfeldt Jacob disease (CJD), called variant CJD or vCJD.

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