nationwide survey finds that the common house sparrow is not so common any more.

Last year the Bombay Natural History Society (BNHS) conducted a survey that was endearingly named Citizen Sparrow.

The survey, using inputs from amateur naturalists, was conducted online and through hard-copy questionnaires in English and eight Indian languages. It reached out to rural and urban India, with 5,730 participants contributing information on the sparrow.

Over 25 per cent of the participants were from towns and villages and the rest from large cities.

According to the findings, sparrows are seen in fewer places now than they were before 2005. Where they are still found, the numbers are lower than earlier and fewer nests are seen as well. This suggests sparrows have indeed declined, and the low number of nests could indicate a continuing decline.

Sparrow populations through the country vary according to regions. A regional comparison showed that many reports of large sparrow flocks came from north-western areas such as Gujarat. Sparrows also seem to be doing comparatively better in north-eastern areas such as Assam and central India, including Maharashtra, Jharkhand and Chhattisgarh. These regions reported greater sparrow presence than other parts of India.

Among cities, Mumbai came out on top of the sparrow charts, with many more people reporting the presence of the bird than they did from Bangalore and Chennai, where a much higher percentage of participants said the bird was not found at all in their localities. ter Mumbai. Hyderabad and Delhi were intermediate in reporting the bird’s presence.

Bee venom-loaded nanoparticles kill HIV

NANOPARTICLES carrying a toxin found in bee venom can destroy the human immunodeficiency virus (HIV) while leaving surrounding cells unharmed, scientists at the Washington University School of Medicine in St. Louis have found. The finding is an important step towards developing a vaginal gel that may prevent the spread of HIV. The study appears in the current issue of Antiviral Therapy.

Bee venom contains a potent toxin called melittin that can poke holes in the protective envelope that surrounds HIV and other viruses. Significantly, by adding certain protective bumpers to the nanoparticle surface, the study has shown that melittin loaded onto these nanoparticles does not harm normal cells.

When the nanoparticles come into contact with normal cells, which are much larger in size, the particles simply bounce off. But HIV is smaller than the nanoparticle, so it fits between the bumpers and makes contact with the surface of the nanoparticle that harbours the bee toxin. Joshua Hood, one of the authors of the paper, says: “The melittin forms little pore-like attack complexes and ruptures the envelope, stripping it off the virus.” An advantage of this approach is that the nanoparticle attacks an essential part of the virus’ structure. In contrast, most anti-HIV drugs inhibit the virus’ ability to replicate, which does nothing to stop initial infection, and some strains of the virus have found ways to reproduce anyway. Hood also sees potential for using nanoparticles with melittin as therapy for existing HIV infections, especially those that are drug-resistant. Many viruses, including hepatitis B and C, rely on the same kind of protective envelope and would be vulnerable to melittinas well, according to the researchers. The paper’s lead author, Samuel A. Wickline, has shown that melittin-loaded nanoparticles are effective in killing tumour cells too.

H7N9

Only about 40 per cent of the 77 infected people had contact with poultry

The novel H7N9 avian flu virus that is currently circulating in certain regions in China has bewildered public health officials within and outside the country.

To start with, H7N9 is a product of reassortment of three avian influenza virus strains that “infect only birds.” Reassortment happens when gene swapping takes place between two or more viruses present at the same time in a host.

The influenza, which was initially restricted to Shanghai and neighbouring regions, has now reached Beijing — two people have so far been infected with the virus.

Till date, 77 people have been infected and 16 have died. But this number may be a gross underestimation of the actual spread of the infection. Therein begin the many puzzling and worrying characteristics of the bird flu.

Unlike the initial cases where the infection proved to be deadly, cases now being detected have wide ranging virulence. A 4-year-old boy has been tested positive for the virus on April 15, but shows no symptoms of infection. This is the first time that an asymptomatic case has been found. Unlike other avian flu infections and initial H7N9 infection cases, people appear to exhibit the entire range of infection — critical, mild and completely asymptomatic.

According to Gregory Hartl, Head of Media for WHO, the current H7N9 case fatality rate is “approximately 20 per cent,” and may end up even lower if the actual number of infected people is known.

Widespread?

But knowing the denominator is the biggest challenge. This is because, the presence of asymptomatic and mild cases raises the real possibility that the virus may be more widespread than believed and difficult to find. Though people with mild/asymptomatic infection may not be dying, such cases are, in fact, “very worrying,” notes Nature.

According to WHO, there is no way of knowing whether the number of cases identified represents “some or all of the cases actually occurring.” The occurrence of some “relatively mild cases” raises the possibility that there are “other such cases that have not been identified and reported.”

Reduced virulence may be facilitating “further genetic adaptation of the virus to infection of human beings — and thus greater potential to spread.”

According to a paper published on April 11 in The New England Journal of Medicine, genome sequencing of the first three cases of H7N9 infected people who died revealed that it is “better adapted” than other bird flu viruses to “infecting mammals.”

But the peculiar feature of the virus is that it causes only asymptomatic or mild disease even in birds. This allows the virus to silently spread among birds. The reason for this is now clear: the NEJM study indicated that the haemmagglutinin sequence data is associated with “low” pathogenicity in birds.

In the case of H5N1, birds falling sick after infection were clearly seen, and this helped in knowing the spread of the infection.

Exacerbating this enigma is not knowing which animals act as viral hosts. This is despite intense surveillance of animals to find out the reservoirs. “We can't be 100 per cent sure how anyone has contracted H7N9. Many patients had contact with poultry, but not all. So [it is] still a puzzle,” Hartl of WHO tweeted on April 13.

According to reports, about 40 per cent of infected people have had no contact with poultry.

The routes of transmission from animals to humans are not fully known either. But the NEJM paper provides certain clues. An amino acid substitution in H7N9 may facilitate transmission through respiratory droplets, just the way the highly pathogenic H5N1 bird flu spread from birds to humans.

Genome sequence of the first three cases showed that there have been “at least two introductions” from animals to humans.

Another peculiar aspect is that the number of people infected with H7N9 shot up from 24 to 63 within a short span of seven days. A reported increase of 14 infected cases on April 16 was the biggest ever for a single day.

Though sustained human-to-human transmission has not been found, two such “suspicious” cases have been found.

“We are not near a H7N9 pandemic yet but we need to understand better how the virus works in order to control the outbreak,” Hartl tweeted. “It is premature to dismiss the possibility of an H7N9 pandemic or to say the outbreak is under contrOL."

Coffee & the selfish gene

How did coffee become more popular in south India and tea in the north? History appears to give the reason. Legend has it that in the late 16th century while Haji Baba Budan was returning from Haj through Yemen, he found people boiling coffee beans in water and enjoying the “decoction”. He then smuggled a handful of the (forbidden to export) beans with him and planted them on the Chikamagalur hills in Karnataka and the locals took to it with elan. Soon, coffee plantations appeared in Kodagu and the Nilgiris, and we all were hooked on to the morning coffee. Tea, on the other hand, was introduced later (early 19 century) by the colonial British who copied it from the Chinese and planted it in Assam and Darjeeling. This colonial drink soon became popular among the subjects in the plains as well. Coffee and tea are thus external entrants into the Indian taste buds.

But why are we hooked on to coffee and tea? The answer comes from science, which tells us that they both contain the mood- altering and addictive drug caffeine. While this is a proximal answer, the ultimate question is why at all do these plants go to the trouble of making the molecule in the first place. After all, it takes metabolic energy to do so. The answer appears to be “to deter herbivores”, or as a defence chemical. Note that the raw bean or leaf is bitter to taste, and the animal would shy away, leaving the plant alone to grow and flourish.

Recent findings add another dimension to the tale. It has been found the caffeine is found not only in the bean or the leaves but also in the nectar that the plant produces and packs a drop or two in its flowers. And why it would do so and what this stored caffeine does in the flower nectar has been investigated by a group of researchers from U.K. and published in the March 8, 2013 issue of Science.

They note that while plant-derived drugs like caffeine and nicotine (the drug in the tobacco plant) are lethal in high doses, they do generate pleasant effects when taken in very low doses. But then why in the floral nectar? Is it in order to “hook on” bees and other pollinating insects? To understand this, the researchers first measured the levels of caffeine in the nectar of three plants, Coffee arabica, C. liberica and C. canephora, to which bees make a bee-line for (pardon the pun), and found the amounts to be less than a thousand-fold that of the sugar present in the bean — just a teasing touch.

They hypothesised that the caffeine in the nectar could affect the learning and memory of the foraging pollinators. Could it be that they would come to these flowers, enjoy the nectar and in the process take away and dispense the pollen, thus breeding these plants in preference to those that do not store caffeine in their nectar? In order to test this, the researchers took the trouble of training individual bees to associate a floral scent with sugar reward. In one set the bees would go to the containers with sugar solution, and in another set the sugar solution spiked with a bit of caffeine. And they found that the bees would consistently return to the caffeine sugar scent even three days later. In other words, caffeine acted as a memory enhancer. The bees were hooked onto caffeine.

The researchers went further ahead and investigated the biological mechanisms behind the mode of action of the caffeine. The bee brain contains what are called projection neurons or nerve cells that have a protein surface (a receptor) that normally binds to the molecule adenosine. When these nerve cells are adenosine-bound, the behaviour of the bee is one of quiet and calm. However when caffeine is brought in, it kicks out the adenosine and attaches itself to the receptors at the end of the sensory neurons. The effect is to stimulate the neurons, increase memory, and wake up and excite the insect.

In effect then, caffeine has two roles in the plant. One is defence against the predator goats and cows, while the other is to entice the pollinating insect by drugging it and tweaking its memory so that it pollinates this plant in preference to other pants that do not pack the drug in their nectar. The researchers conclude by stating that “our experiments suggest that by affecting a pollinator’s memory, plants reap the reproductive benefits arising from enhanced pollinator fidelity”.

In plainer English, one can say that the trick the coffee plants play is another example of the ‘selfish gene’ idea, namely, use any ruse to help propagate my genes over other competitors, and do so for generations; and if it takes caffeine to entice and tweak the memory of the pollinator, so be it.

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