In the Northern hemisphere, winter is the time for the flu. Every year 5% to 20% of us catch "the bug". So predictable is the influenza virus that "flu season" has entered the vernacular. This year, flu cases peaked around the end of February (see chart). Perhaps you've wondered "Why?".

Hypotheses for flu season are numerous and include:

1. Because people are indoors more often during the winter, they are in close contact more often, and this promotes transmission from person to person.
2. Cold temperatures lead to drier air, which may dehydrate mucus, preventing the body from effectively expelling virus particles.
3. The virus may linger longer on exposed surfaces (doorknobs, countertops, etc.) in colder temperatures.
4. Increased travel and visitation due to the holiday season.
5. Less sunlight promotes virus survival.
6. Our immune systems work poorly during the cold weather. (From Wikipedia).
   

I don't often see bacteriophage ecology and evolution papers in the open source literature, but there is a nice one in next month's American Naturalist (occasionally Am Nat selects papers for open access).

The paper by Rick Heineman and colleagues addresses the question of optimal foraging, a body of theory that seeks to explain the food choices of organisms in terms of how they maximize energy intake over time. As a model organism, the authors use the bacteriophage T7, a parasite of Escherichia coli.

Supposedly nanobacteria are cell-walled organisms much smaller than the generally accepted lower limits for cell size. The existence of nanobacteria has been a hot topic because of their putative roles in and heart disease and kidney stones.

There's even a company devoted to commercializing nanobacterial products: Nanobac. There's even a video of "nanobacteria" in action.

A new article in PLoS Pathogens says that's all balderdash. Here is the authors' summary:

In the US, most deaths are attributable to chronic afflictions, such as heart disease and cancer. Typically the medical community has attributed these diseases to accumulated damage, such as plaque formation in arteries or mutations in genes controlling cellular replication.

This view is changing.

Scientists are now beginning to recognize that many of these chronic illnesses are due to microbial infections. A recent report in the American Journal of Psychiatry suggests that schizophrenia, a mental illness leading to errors in perception, is associated with the pathogen, Toxoplasma gondii.

"Our findings reveal the strongest association we've seen yet between infection with this very common parasite and the subsequent development of schizophrenia," study investigator Dr. Robert Yolken of John Hopkins Children's Center in Baltimore said in a statement.

A favorite book of mine is Evolution: A Scientific American Reader, a collection of articles on astronomy, cell biology, paleontology and anthropology from the print magazine. One of my favorite chapters, "Skin Deep" by Nina Jablonski and George Chaplin, covers the evolution of human skin color.

Skin color results from the presence of the pigment melanin, an organic molecule that absorbs UV radiation and neutralizes free-radicals produced by UV radiation. Why do we need worry about UV radiation? UV radiation causes mutations in skin cells leading to skin cancer, and also destroys the essential B vitamin, folate, which is involved in DNA synthesis. The more melanin, the more protection against UV radiation and the darker the skin.

Hmm, if that is the case, why do not all humans have dark skin? Better to protect against cancer then, isn't it?

Did you know even bacteria get old? Scientists traditionally assumed that bacteria were immortal, since these single-celled organisms split into two apparently identical daughter cells, which in turn divide, and so on. We now believe that this is not true.

Eric Stewart of Northeastern University, and his colleagues took fluorescent images of individual E. coli cells over ten generations. Each generation the E. coli cells divide down the middle, giving each daughter cell one new tip and an old tip from its mother, or grandmother, or some older ancestor.

Using computer software, Stewart et al. identified and tracked the tips of each bacterial cell. The results (open access: PLoS) indicated that the cell that inherits the old tip suffer a diminished growth rate, decreased offspring production, and an increased incidence of death.

"The conflict between maternal and fetus genes is one of the weirdest ideas in the modern theory of evolution."* According to evolutionary logic, the fetus "wants" to milk the mother for all it can get; the mother "wants" to restrict the fetus to what it needs to survive and save something for future offspring. The reason is that the fetus benefits from every bit of help the mother gives, while the mother's return on her investment diminishes with increasing investment, (i.e. ever greater investment won't necessarily increase her fitness).

One example of this struggle is the regulation of the mother's blood sugar, which is much than normal higher during pregnancy. Well this makes sense, you might think, because the mother is now feeding a growing fetus. But look at the mother's insulin level, it also is much higher than normal, and insulin is used to down-regulate blood sugar levels. Huh, that's weird, she is secreting more insulin, yet her blood sugar level is ever higher. She must be responding less to insulin. Why should that be?