Miscellaneous

Miscellaneous - An Interesting 'Virus'
While doing random websurfing today, I found this interesting picture of a 'virus'.
From the descriptions it says: This is the 'Flickr Virus', a microvirus that is affecting so many throughout the world. Little is known about its structure and how it transmitted, although recent work indicates that it is a small sphere of energy (possibly light) that travels via the internet. Infection usually occurs soon after a Flickr 'Pro Account' has been acquired.

Symptoms:
1. The patient has a craving for 'viewings' and 'comments' on his/her images and develops a compulsion to upload images to satisfy this need.
2. Obsessive checking for inclusion in 'Scout' and 'Explore'.
3. A compelling desire to add the tag 'interestingness'.

Treatment:
There is no real effective or permanent cure. Total abstinence from Flickr may work for short periods while the patient returns to a normal life style but this is usually only a temporary situation. Long term research, funding, and recognition as an illness is needed.Of course this might just be another one of my 'Refractographs' created out of light and only an image on your computer screen to be treated as a a bit of fun. On the other hand don't stare at it for too long or view large - it could be contagious! ;)

SARS!

Severe Acute Respiratory Syndrome (SARS)
Severe acute respiratory syndrome (SARS) is a respiratory illness caused by SARS coronavirus (SARS-CoV), which are positively stranded RNA enveloped viruses, with 8,096 known infected cases and 774 deaths (a case-fatality rate of 9.6%) worldwide between November 2002 and July 2003, listed in World Health Organisation(WHO) report in April 2004, originating from Guangdong China, where a farmer contracted symptoms and died soon after, without a definite diagnosis on his death. The disease soon spreads to other provinces of China like Shanxi and Tianjin. Several countries like Hong Kong, Toronto, San Fransisco, Taiwan and Singapore have local transmissions. Mortality by age group as of 8 May 2003 is below 1 percent for people aged 24 or younger, 6 percent for those 25 to 44, 15 percent in those 45 to 64 and more than 50 percent for those over 65. For comparison, the case fatality rate for influenza is usually around 0.6 percent (primarily among the elderly) but can rise as high as 33 percent in locally severe epidemics of new strains. The mortality rate of the primary viral pneumonia form is about 70 percent.
What is main source of virus? It was found by Chinese researchers from animals like palm civets (cat-like animal), that SARS coronavirus can spresd from the civets to humans. Other animals like raccoon dogs, ferret badgers, cats and Chinese Bats are also likely to have isolated the viruses, in which bats are aymptomatic to virus, but are possibly reservoirs for transmission of SARS-like coronavirus.

Viral replication
Replication takes place in cytoplasm in membrane-protected microenvironment and starts with the translation of the genome to produce the viral replicase. CoV transcription involves a discontinuous RNA synthesis (template switch) during the extension of a negative copy of the subgenomic mRNAs. The requirement for base pairing during transcription has been formally demonstrated in arteriviruses and CoVs. The CoV N protein is required for coronavirus RNA synthesis and has RNA chaperon activity that may be involved in template switch. Both viral and cellular proteins are required for replication and transcription. CoVs initiate translation by cap-dependent and cap-independent mechanisms. Cell macromolecular synthesis may be controlled after CoV infection by locating some virus proteins in the host cell nucleus. Infection by different coronaviruses cause in the host alteration in the transcription and translation patterns, in the cell cycle, the cytoskeleton, apoptosis and coagulation pathways, inflammation and immune and stress responses. The balance between genes up- and down-regulated could explain the pathogenesis caused by these viruses. Coronavirus expression systems based on single genome constructed by targeted recombination, or by using infectious cDNAs, have been developed. The possibility of expressing different genes under the control of transcription regulating sequences (TRSs) with programmable strength and engineering tissue and species tropism indicates that CoV vectors are flexible. CoV based vectors have emerged with high potential vaccine development and possibly for gene therapy.[19]

Symptoms of SARS are similar to influenza together with fever, muscle pain, lethargy, gastrointestinal symptoms, cough, sore throat, shortness of breath and other non-specific ones, in which the most common symptom is fever above 38 °C (100.4 °F). They usually appear between 2 days to at most 13 days following infection, usually within 2–3 days. About 10–20% of cases require mechanical ventilation.
Phlegm present in lungs can be an indication of SARS. This can be examined from Chest X-Ray.
There are also high white blood cell and platelet counts, some likely reasons are: tendency to relative neutrophilia and a relative lymphopenia, raised lactate dehydrogenase and creatine kinase and C-Reactive protein levels.
Some approved tests to identify SARS are: ELISA (Enzyme-Linked Immunosorbent Assay), Immunosorbent Assay and Polymerase Chain Reaction (PCR). However, there are some pros and cons to each test. For example, ELISA is reliable only 21 days after symptoms occur in patient, while immunosorbent assay takes only 10 days, but requires sophisticated equipment, like immunoflourescence microscope and PCR may not be sensitive, which means that patient may still suspect of infected from SARS even though tested negative.
The process of finding cause of virus was initially hypothesized that SARS was caused by paramyxovirus-like particles, from Hong Kong and German researchers, while Chinese researchers reported Chlamydia-like disease a likely cause. French and Hong Kong scientists soon found out that a newly discovered subtype of coronavirus was a likely cause of SARS, after cultivating virus in vitro and invent a test to identify virus. This was confirmed by Dutch scientists in 2003, by demonstrating that SARS coronavirus fulfilled Koch's postulates, using macaques as hosts, which developed same symptoms as SARS patients.
So far, antipyretic drugs with oxygen supplemental and ventilator support can treat SARS. Antiviral drugs like ribavirin and corticosteroids are the most common drugs to treat disease. Iminocyclitol 7 has also been found to have inhibited SARS-CoV by disrupting envelope assembly and inhibits production of human fucosidase. In vitro trials yielded promising results in treatment of SARS, but lacking of fucosidase can lead to fucosidosis which is a decrease in neurological function.
Acknowledgement
http://en.wikipedia.org/wiki/SARS

Here are links to World Health Organisation to guides of SARS surveillances and recommendations, plus risk assessment and preparedness framework to prevent a SARS pandemic:
http://www.who.int/csr/resources/publications/SARSNEWGUIDANCE/en/index.html
It may be dated to 2004, but is still quite useful to learn more about SARS.
Wilson reported.

Eradication of polio virus in the year 2014?

Did you know that in the year 2014 polio virus MIGHT get wiped out from the surface of mother earth?

The Bill & Melinda Gates Foundation, Rotary International and the British and German governments today pledged $630 million over the next five years to vaccine and other programs designed to wipe out polio.

"I am urging everyone to redouble their commitment and see the eradication effort to the end," Bill Gates said today during a teleconference with reporters. Gates said he's confident that polio will become the second viral disease that humankind eradicates (the first being smallpox in 1979), but he was loath to predict when that might happen.

The Gates Foundation, which has contributed $655 million toward polio eradication since 1999, today pledged an additional $255 million over the next five years. Rotary has promised $100 million, and the U.K. and Germany are forking over $150 million and $130 million, respectively. This money will go to a variety of resources and activities essential to the eradication effort, from purchasing vaccines to training programs for health workers.

A disease that attacks the nervous system, polio most commonly strikes children under age five, causing nothing more than flulike symptoms in most but permanent paralysis in others. One in every 200 cases results in paralysis, according to the World Health Organization (WHO). The virus is easily spread through dirty drinking water in areas with poor sanitation systems and continues to thrive in four countries—Nigeria, India, Afghanistan, and Pakistan, where it annually paralyzes about 2,000 children.

The disease came close to being wiped out in the U.S. in the 1960s, but there were sporadic outbreaks in pockets where the vaccine was shunned—such as among the Amish in Lancaster County, Pa., in 1979. The WHO finally declared the Americas polio-free in 1994.

Since 1988, the WHO, the U.S. and other governments as well as charitable orgs such as Gates and Rotary have contributed $6 billion to eradicating polio. The international effort has cut polio cases by over 99 percent, from some 350,000 in 1988 to about 1,600 last year.

The infusion of new funds will focus on overcoming specific hurdles in each of the four countries where the disease still exists. Afghanistan, for instance, is embroiled in a war, which makes it dangerous for vaccinators to distribute the medicines, and Nigeria has fallen behind in its eradication campaign, because local government officials in some of the country's northern states have failed to provide training for health workers or programs to educate parents on the import of vaccinating their children.

"We need new efforts from the leaders in these countries where polio is still endemic," Gates said. "There's no target date yet for eradication because nobody knows what it will take."

Source: http://www.sciam.com/blog/60-second-science/post.cfm?id=bill-gates-hands-over-millions-more-2009-01-21
By Amas goh

RABBIT?

Rabies virus (RV) rotating virion
Rabies viruses have a characteristic bullet shape. Their genomes are single stranded negative sense RNA. This RNA is combined with a nucleoprotein to create a nucleocapsid. The nucleocapsid is wound tightly as a helix (yellow in this graphic). The nucleocapsid helix is organised during morphogenesis and stabilised by matrix proteins. The matrix layer is surrounded by a viral envelope derived from the host cell during budding. The surface of the rabies virus is covered by spikes or knobs formed from glycoprotein. These are connected to the matrix by a transmembrane region.
Rabies viruses can infect mammals and are best known for causing rabies in dogs (rabid or mad dogs). It used to be called hydrophobia since the sight of water would cause terrible fear in those infected. Rabies is generally lethal unless treatment is given very quickly. Transmission to humans can occur from bats and other wild mammals in infected areas.

Bats might be a carrier?

Natural reservoir for emerging viruses may be bats. They are creatures of the night that are commonly held in fear. At first glance, those fears might seem to have some medical justification. Long known as vectors for rabies, bats may be the origin of some of the most deadly emerging viruses, including SARS, Ebola, Nipah, Hendra and Marburg. Instead of demonizing bats, however, research shows the real culprit behind these outbreaks could be human error.

The Nipah and Hendra viruses were the first emerging diseases linked to bats. Hendra claimed two of its three victims in its first and so far only known appearance in Australia. Meanwhile Nipah has in repeated Southeast Asian outbreaks killed nearly 200 people, and blood tests of wildlife have suggested that the viruses came from the largest bats, flying foxes.

The connection to SARS, or severe acute respiratory syndrome, was less direct. During the outbreak that began in China in 2002, investigators found that civets and two unrelated species harbored the SARS coronavirus, prompting mass culling of the mongooselike civets by the Chinese government.

Subsequent research, however, found no widespread SARS infection among wild or farmed civets, indicating that the disease arose in another species and might remain in wait there.
Want to know more? Visit this website
http://www.sciam.com/article.cfm?id=going-to-bat

By Amas Goh

Harmless little deer mouse...or not? (Remerging viruses)

Do you think that this deer mouse is cute? Do not let it’s cute look mislead you…
Hantavirus pulmonary syndrome (HPS) is a deadly disease from rodents. Humans can contract the disease when they come into contact with infected rodents or their urine and droppings.

HPS was first recognized in 1993 and has since been identified throughout the United States. Although rare, HPS is potentially deadly. Rodent control in and around the home remains the primary strategy for preventing Hantavirus infection. These incidents are used to remember that these re-merging viruses could appear once again…

The deadliest United States outbreak was on May 14, 1993 in the Four Corners area. Incubation is similar to Yellow Fever. Symptoms include mild onset with flu-like symptoms that rapidly progresses into kidney failure with intestinal bleeding (which is the hallmark of the disease).

The most common symptom in the United States is hypertension with chronic kidney failure. In the Four Corners outbreak, the disease had a very mild onset with flu-like symptoms, developing into lung hemorrhaging causing the infected person to suffocate in his or her own blood.

The mortality rate varies with the strain; the most deadly strain had a 62.5% mortality rate.
Transmission is from animal to human. Over 63 bird and rodent vectors have been identified for the 70 known strains of the virus. Scientists have concluded that the outbreak in the Four Corners area was due to a ten-fold increase in the population of the deer mouse and not to a virus mutation.
By Amas goh

Emerging Virus!

NEW AND EMERGING VIRUS
An emerging virus is defined as a disease of infectious origins with an incidence that has increased within the last 2 decades or threatens to increase in the near future by Centres for Disease Control (CDC).
Attention has been given to viruses which cause incurable, fatal disease such as haemorrhagic fever or AIDS. The term ‘emerging disease’ is used for diseases which have historically been rarely seen. The emergence of infections is not new. It has been happening throughout history and it covers the whole range of infections.

Where does emerging virus come from?
There are many ways in which virus can emerge from. A zoonosis is the transfer of infectious agent from an animal to human. Other sources can be mutation of genes, recombination like influenza antigenic shift, geographical contact like smallpox (now eradicated), rabbit haemorrhagic disease and reappearance (shingles). A true zoonosis is poorly transmissible between humans since human borne disease transmission come to dominate spread of the virus. One example is HIV (human immunodeficiency virus) which is zoonotic (transferred from African monkey to human. But even though HIV is a zoonotic origin, it can also be transmitted from human to human. Many viruses have the ability to adapt to co-existing normal host and cause relatively mild disease. Thus a virus may circulate around the animal and be unnoticed. If this virus were to be able to infect human it would be a severe disease. Environmental changes can cause humans to come in contact with animals more.
Dengue Haemorrahgic Fever (DHF) which is under flaviviridae is an arthropod-borne viral zoonosis. It’s endemic to tropical areas which have high rain fall and hot climate throughout the year. The host for DHF is monkey by aedes mosquitoes which is the vector of DHF.

Mutation
While all viruses must have been arisen by mutations at base, the effects of this process in the limited time available to study viruses are necessarily limited. Recently there has been more evidence in virus rising like AIDS. Serological methods prove that this disease is not seen in humans before the second half of 20th century. The appearance of rabbit Haemorrahgic disease or rabbit calicivirus (RCV) also represents an apparent new disease followed by massive and rapid spread of it. Antigenic drift in influenza virus are not easily resolved from parental strains and are not considered as new or emerging viruses. A more relevant example would be appearance of drugs- resistant variants of all viruses that are treated with antiviral drugs. Drug resistance arises from mutations this does not have to occur after the drug is used. It is seen that mutation during normal replication results in viruses which differ in genetic material and physical properties.

T-4 Phage virus replication cycle model used to study how viruses replicates

Did you know how did the scientist find out about the general virus replication cycle? They first studied the life cycle of the T4 Phage Virus Lytic Cycle. The virus infects bacteria cells and the process will be explained in the video below… marvelous smart lechers aren’t they?


By Amas goh

Replication cycle

Virus Replication Cycle

The virus replication system can be classified into eight stages which includes 1) Attachment 2) Penetration 3) Uncoating 4) Gene expression 5) Genome Replication 6) Assembly 7) Maturation 8) Release

Attachment: This is the crucial stage for the initiation of virus life cycle within a living cell. As a virion comes across a specific host cell, it first binds to the host cell.
Viruses have specific proteins on their surface to attach to a host cellular surface molecule. The cellular molecules that allow the virus to attach on the cell surface are called virus receptors and the virion proteins that mediate the attachment are called as attachment proteins.
The attachment proteins and their positioning vary for different type of viruses. This protein is needed by the virus to attach to its target (host) cell before it can enter that cell.
Penetration: Penetration occurs almost instantaneously after attachment and is a next step for gaining entry into the cytoplasm by crossing the plasma membrane. The penetration process differs for different viruses.
Penetration by the process of endocytosis is common to both enveloped and non-enveloped viruses. While some virus species can directly penetrate the plasma membrane and inject their genetic material into the cytoplasm, the majority of viruses enter cells via endocytosis. Direct penetration is observed only in non-enveloped viruses, membrane fusion is observed only in enveloped viruses. Some of the non-enveloped viruses like picornaviruses and phages are capable of directly injecting their genome into the host cell.
Uncoating: Uncoating occurs simultaneously with or rapidly after penetration. Hence, this stage is difficult to be studied and remains a relatively poorly understood stage of the replication cycle.
Uncoating in general refers to the events that expose the viral genome to the host cellular machinery and sets the stage for the viral genome to express its functions required for the replication.
This stage occurs simultaneously with or rapidly after penetration. In order to express the viral genome to the cell organelles, it is necessary that the virion coat be removed partially or completely. Therefore, once virions are in the cytoplasm, they are generally uncoated to some extent by a variety of processes, including simple dissociation and/or enzyme-mediated partial degradation of the particles, to release the viral genome as a naked nucleic acid or as a nucleoprotein complex.
Synthesis: The viral synthesis stage begins immediately after the process of uncoating- the process that exposes the viral nucleoprotein complex to the cellular environment. The synthesis stage leads to the massive production of viral components.
The viral genome synthesis involves two stage Genome expression and Genome replication. Genome replication is the production of viral genomes; Genome expression is the production of viral proteins. Genome expression is a multi-step process that includes transcription and translation.
Assembly follows the viral synthesis phase. With synthesis, the host cell is full of viral genomes and proteins but the viral components are produced separately at different locations.
Therefore, after synthesis, the next task for the viral components is to assemble so that progeny viruses are formed.
The assembly stage involves the forming of a stable protein coat and packing of viral genome into the protein coat. For the successful assembly, the virus must make suitable quantities of viral genome that approximately match the number of capsids being assembled.
Maturation follows assembly. However, this is true only for non-enveloped viruses. Maturation process in general, is the stage in which the assembled premature virions become infectious viral particles. The immature virions undergo structural modifications that lead to maturation. These structural changes cause the assembled virion particles to become stable and infectious.
In the case of non-enveloped viruses Maturation is an immediate effect of assembly and are mostly inseparable whereas for some viruses like enveloped, maturation occurs with the release process or after the release process.
Release is the last stage of virus replication cycle. In this stage, thousands of newly formed virus progeny leave the host cell in search of a new host cell, thus establishing an infection in the body.
For non-enveloped viruses, the maturation process is followed by release mechanism while in enveloped viruses; the release mechanism involves assembly and maturation of the viruses.The non-enveloped viruses attain full infectivity or mature fully inside the cell and are mostly released by rupturing the cell. This process is called as cell lysis while the enveloped viruses assemble and are simultaneously released by the process of budding. Some enveloped viruses like HIV can infect the neighbouring cells and spread infection through the process of cell-cell fusion.

PCR?

Polymerase Chain Reaction (PCR) - DNA amplification

Definition: PCR is a method for amplifying segments of DNA, by generating multiple copies using DNA polymerase enzymes under controlled conditions. As little as a single copy of the DNA segment or gene can be cloned into millions of copies, allowing detection using dyes and other visualization techniques.

We will now look at a short clip to understand how PCR works.

Immunofluresence

Immunofluorescence
How to use immunofluorescence to stain the different parts of a cell? This clip will tell you more.

Direct ELISA

Direct ELISA

a) Antigen is added in buffer. The protein attaches passively to the plastic surface of microtitre plates well. After a period of incubation the non-adsorped protein is washed away.

b) Antibodies with enzyme covalently linked (conjugate) is added in a solution containing inert protein and detergent (to prevent non-specific attachment of the antibodies to plastic wells). The antibody binds to the antigen on well surface. After incubation, non-bound antibodies are washed away.

c) Add substrate and chromogenic dye solution. Substrate interacts with enzyme to affect dye solution to give a colour reaction.

Plaque assay!

Plaque Assay - Determining viral concentration of a sample
Definition: Assay for virus in which a dilute solution of the virus is applied to a culture dish containing a layer of the host cells, convective spread is prevented by making the medium very viscous. After incubation the plaques, areas in which cells have been killed (or transformed), can be recognised and the number of infective virus particles in the original suspension estimated.

Let us recap the process of performing a plaque assay with the following clip.

small pox again!

Smallpox is an infectious disease caused by two virus virant Variola major and Variola minor .The disease also is known by its Latin name Variola or Variola vera . Smallpox localizes in small blood vessels of the skin and in the mouth and throat. In the skin, this results in a characteristic maculopapular rash, and later, raised fluid-filled blisters. V. major produces a more serious disease and has an overall mortality rate of 30–35%. V. minor causes a milder form of disease (also known as alastrim, cottonpox, milkpox, whitepox, and Cuban itch) which kills ~1% of its victims
After recover, it causes long term scarring , 65-85% blindness from corneal ulceration and probably limb deformities due to arthritis and osteomyelitis.
Its is said to be discovered at about 10000 BC. Small pox killed about 400,000 people in Europe every year in the 18th century and almost 1/3 of the people were blinded.
During the 20th century, it is estimated that smallpox was responsible for 300–500 million deaths. In the early 1950s an estimated 50 million cases of smallpox occurred in the world each year.] As recently as 1967, the World Health Organization estimated that 15 million people contracted the disease and that two million died in that year. After successful vaccination campaigns throughout the 19th and 20th centuries, the WHO certified the eradication of smallpox in December 1979. ]To this day, smallpox is the only human infectious disease to have been completely eradicated.

SMALL POX!

Small pox àorthopoxvirus from poxviridae
Variola virus is a large brick-shaped virus measuring approximately 302 to 350 nanometers by 244 to 270 nm , with a single linear double stranded DNA genome 186 kilobase pairs (kbp) in size and containing a hairpin loop at each end.
Poxviruses are unique among DNA viruses in that they replicate in the cytoplasm of the cell rather than in the nucleus. order to replicate, poxviruses produce a variety of specialized proteins not produced by other DNA viruses, the most important of which is a viral-associated DNA-dependent RNA polymerase. Both enveloped and unenveloped virions are infectious.
Transmission of smallpox occurs through inhalation of airborne variola virus, usually droplets expressed from the oral, nasal, or pharyngeal mucosa of an infected person. It is transmitted from one person to another primarily through prolonged face-to-face contact with an infected person, usually within a distance of 6 feet, but can also be spread through direct contact with infected bodily fluids or contaminated objects (fomites) such as bedding or clothing. Rarely, smallpox has been spread by virus carried in the air in enclosed settings such as buildings, buses, and trains. The virus can cross the placenta, but the incidence of congenital smallpox is relatively low.
Small pox can be transmitted throughout the course of the illness, but is most frequent during the first week of the rash, when most of the skin lesions are intact. Infectivity wanes in 7 to 10 days when scabs form over the lesions, but the infected person is contagious until the last smallpox scab falls off.
It is highly contagious but usually spread more slower than other viral disease.
Variola major is the severe and most common form of smallpox, with a more extensive rash and higher fever. There are four types of variola major smallpox based on the Rao classification: ordinary, modified, flat, and hemorrhagic. Historically, variola major has an overall fatality rate of about 30%; however, flat and hemorrhagic smallpox are usually fatal. In addition, a form called variola sine eruptione (smallpox without rash) is seen generally in vaccinated persons. This form is marked by a fever that occurs after the usual incubation period and can be confirmed only by antibody studies or, rarely, by virus isolation.
The incubation period between contraction and the first obvious symptoms of the disease is around 12 days. Once inhaled, variola virus invades the oropharyngeal (mouth and throat) or the respiratory mucosa, migrates to regional lymph nodes, and begins to multiply. In the initial growth phase the virus seems to move from cell to cell, but around the 12th day, lysis of many infected cells occurs and the virus is found in the bloodstream in large numbers (this is called viremia), and a second wave of multiplication occurs in the spleen, bone marrow, and lymph nodes. The initial or prodromal symptoms are similar to other viral diseases such as influenza and the common cold: fever (at least 38.5 °C (101 °F)), muscle pain, malaise, headache, prostration, and as the digestive tract is commonly involved, nausea and vomiting and backache often occur.

Poxivirdae introduction

Poxviridae

•Can affect both vertebrates and invertebrate animals.


Structure
-Has an enveloped virus particle
-Generally shaped as an oval or brick
-Virion has a diameter of 200 nm and length of 300 nm
-Genome is carried in single stranded (ss) linear DNA.


Smallpox Virus
•Cure invented by Edward Jenner
•Found out that cowpox is the vaccination to small pox.
•Tested by pricking a boy with milkmaid affected by cowpox virus and exposing him to smallpox virus.
•Amazingly few scares were seen and he recovered quickly.
•It is the largest virus cell and it can be seen through a light microscope.

New researches on dengue fever?

Australian researchers claim breakthrough on dengue fever

SYDNEY : Australian researchers funded by US billionaire Bill Gates Friday claimed a breakthrough which could help in the fight against dengue fever by stopping the often deadly disease in its tracks.

University of Queensland researchers said they have successfully infected the mosquito which spreads the tropical disease with a bacterium which halves its 30-day lifespan, thereby reducing its ability to transmit dengue to humans.

Scientists hope their work will help halt the spread of the painful and debilitating disease which affects millions of people each year.

"The key is that really only very old mosquitos are the only ones that are able to transmit the disease," said researcher Professor Scott O'Neill.

"What we've done is put this naturally occurring bacteria into the mosquitos that actually halves their adult lifespan so they don't live long enough to be able to transmit the virus."

The research published Friday in the journal Science is the result of injecting 10,000 mosquito embryos with a bacterium that occurs naturally in fruit flies but has never been detected in dengue-carrying mosquitoes.

O'Neill said the test was designed to see whether the bacterium reduced the lifespan of the insects without killing them or preventing them from breeding and was able to be passed on to offspring.

He said while the laboratory tests, which involved researchers allowing the bacteria-infected mosquitoes to bite their arms because the species needs human blood to breed, had been successful, it would be several years before the technique would be tested in the wild.

"It's really a preventative strategy for preventing dengue fever outbreaks and what we've done is show that it's possible to be done in a laboratory," he told AFP.

"The next stage is now to move it into a more realistic field setting."

There is no known cure or vaccine for dengue fever, which is transmitted by mosquitos and kills more than 20,000 people each year. Also known as "breakbone fever," symptoms include high temperatures and muscle aches.

The Bill and Melinda Gates Foundation donated 10 million dollars to an international research team led by the University of Queensland into a means of defeating dengue fever in 2005.


Source: http://www.channelnewsasia.com/stories/afp_asiapacific/view/399799/1/.html

With a new year new hope and new cure in the future more life can be saved.
by Amas goh chun kiat