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I attended a fascinating talk today by biologist Shari Kaiser. She was presenting results of work she did that generated an interesting hypothesis about why humans are susceptible to HIV when other primate species are not. You can see an abstract of her paper on the subject here. Apparently this work is novel and interesting enough that it will soon be published in Science. I'll paraphrase the abstract and try to fill in some of the background science.

HIV is a retrovirus. Retroviruses work by making parts of the cellular genetic machinery work "backwards". Normally genes (sections of DNA) are transcribed into mRNA, which is then translated into proteins. But a retrovirus is a strand of RNA (plus a protein sheath called a capsid) that tricks the cell into reverse transcribing the virus RNA into DNA. That DNA can then sometimes insert itself into the genome of the host cell. Subsequently when that "gene" is expressed the resulting RNA is another copy of the virus.

One other piece of the story: there are two kinds of retroviruses: exogenous and endogenous. An exogenous virus is one that infects an organism from the outside, e.g. when a virus is passed from one person to another via transmission. But remember that successful retroviruses become incorporated in the genome of the host. Therefore, if the retrovirus infects a germ cell (sperm or egg) and becomes incorporated in that cell's DNA, the virus is then passed to offspring produced by the germ cell via normal DNA replication. Now it is a potentially permanent part of the genome of that family tree. Whether it becomes permanent, of "fixed", depends on whether and how it affects the selection outcome for the infected organism: for example if it kills the host before reproduction it cannot become fixed in the population. Once it becomes fixed in the genome it is an endogenous retrovirus. It is estimated that 8% of the human genome consists of (inactive) endogenous viruses. Compare that to the 1.2% of the human genome that comprises our genes.

Once can look for endogenous viruses in various species' genomes. It turns out that many primates, including our closest relative the chimpanzee, have multiple copies of an endogenous virus called PtERV, which appears to have become extinct as an exogenous virus approximately 4 million years ago. Humans do not carry PtERV, which may mean that early humans had resistance to the virus.

Cells have various defenses against viruses. One form is an antiviral protein that binds to the virus capsid and affects the virus in some adverse way. For example, it may disassemble the virus. Only two antiviral proteins have been discovered in humans so far, both were discovered coincidentally as part of HIV-related research. Kaiser's work focused on an antiviral protein named Trim5α. She was curious whether Trim5α may have protected early humans from PtERV. Trim5α is one of the set of genes that undergo the most dynamic mutation, presumably because it is responding to rapidly evolving viruses.
How do you test restriction of a virus that has apparently been extinct for 4 million years? You resurrect it. Remember, we have many copies of the DNA template for the virus sitting in all those primate genomes. So Kaiser identified the pertinent portions of the virus genome and used genetic engineering to make cat kidney cells produce them. She did this in three pieces so as not to actually recreate the whole virus - she really only needed the capsid for her work.
It turns out that the human Trim5α protein is quite good at restricting the resurrected PtERV virus. A whole bunch more work with Trim5α from various primate species essentially showed that Trim5α can either be good at restricting PtERV or it can be good at restricting HIV-1 but generally not both. Rhesus macaque monkeys, for example, are essentially immune to HIV-1 because their form of Trim5α is good at restricting the HIV-1 virus.

So her hypothesis after all of this: humans suck at fighting off HIV-1 because we were good at fighting off PtERV 4 million years ago.

Along the way, she made a lot of discoveries that could be helpful in fighting HIV-1. For example, could we enhance human resistance to HIV-1 by modifying the human Trim5α gene? Time will tell.

Now we turn to some real science. Scientists from the University of California, Berkeley and the University of Texas recently described observations of a very large supernova. The New York Times has a good article about it. It is apparently the largest supernova ever observed and was a star about 150 times the mass of our Sun.

A press release from UC Berkeley points out:

Unlike typical supernovas that reach a peak brightness in days to a few weeks and then dim into obscurity a few months later, SN2006gy took 70 days to reach full brightness and stayed brighter than any previously observed supernova for more than three months. Nearly eight months later, it still is as bright as a typical supernova at its peak, outshining its host galaxy 240 million light years away.

The NY Times article describes what we might experience if a very similar star in our own galaxy, Eta Carinae, were to die in a similar fashion:

Eta Carinae could blow up sooner than we thought, Dr. Smith said, noting that it could be tomorrow, it could be thousands of years from now. Astronomers have no way of telling.

Even if it did blow as the new supernova did last fall, at a distance of around 7,500 light years, Eta Carinae would be unlikely to cause any serious harm to Earth, astronomers said. The explosion would be visible in the daylight and at night you would be able to read a book by its light.

The Improbable Research blog (from the folks who hand out the Ig Noble Prizes), today brought my attention to a New Yorker article about the Large Hadron Collider. The LHC is being built at CERN on the French/Swiss border near Geneva, and when it comes online will be the largest particle accelerator ever built.

Out of curiosity, I asked Wikipedia how the LHC compared to the Superconducting Super Collider, which was partially built in Texas before being canceled by Congress in 1993. The answer: the LHC will achieve energies of 7 TeV (trillion electron volts). The SSC was designed to achieve 20 TeV.

The New Yorker piece is the most recent in a string of articles that ponder the question of whether the LHC will accidentally create a mini-black hole that will swallow up the Earth and presumably our neighborhood of space.

The subject is fascinating, but in my opinion completely pointless. Humorously:

'...CERN officials are now instructed, with respect to the L.H.C.’s world-destroying potential, “not to say that the probability is very small but that the probability is zero.”'

Regardless of the PR, there is still a small chance that this could happen. But if it did, we wouldn't be around to care. So why care now? Humanity, from a big enough context, consists of a hair on a wart on a frog on a bump on a log on the bottom of the multiverse. We wouldn't even merit a paragraph in the obits of the Universe Gazette.

This post is about a year out of date, but hey, I’ve been a busy graduate student! I can only claim to understand the underlying mathematics at the shallowest level but I am fascinated by modern physics. I recall reading articles about the observations of the Bullet Cluster in the popular media a year or so ago but at the time the implications and importance of the discovery were not obvious (at least to me). I’ve taken advantage of my summer vacation by spending a lot of time reading and today I discovered this blog entry that describes the observations of the Bullet Cluster and the cosmological implications. This particular entry is one of the most accessible descriptions of the connection between astronomical observations and theoretical cosmology that I’ve encountered (be sure to check out the cool animation!). Observations of this sort are largely possible because of orbiting platforms, of which the Hubble Space Telescope is the most well known. These satellites can be developed and launched for a fraction of the cost of manned space missions. They indisputably provide insight into some of the most profound questions of science. And yet, many of these missions will be sacrificed in order to repeat a visit to the moon. Under the unlikely assumption that a new moon mission is not simply election-year rhetoric, what’s the point? Read here about some of the basic science that won’t happen as a result.