As part of its lifecycle, HIV integrates its viral DNA into the DNA of the cell it infects. In a normal infection, the viral DNA is then processed by the infected cell's own gene expression machinery and the virus starts to replicate. However, sometimes instead of the virus being expressed and made, the DNA is "silenced" by the infected cell, meaning the viral DNA is there but not being actively expressed by the infected cell. These cells then harbor the latent virus for as long as these cells are alive, which for some memory immune cells can be for the rest of your life. This is the virus reservoir. If you take anti-retroviral therapy (ART) drugs, such as the NNRTIs mentioned before or protease or integrase inhibitors, these will inhibit active viral replication, but won't cause any harm to the reservoir viruses that are latent. Randomly* as well, these "silenced" virus DNAs in infected cells that make up the reservoir can become un-silenced, and the virus will start replicating. If you are still taking ART, then nothing happens. If, however, you stop taking the medication, these viruses that pop back up will re-start the HIV infection and within a few weeks you will be HIV+ with viral loads (amount of virus in your blood) the same as before the ART treatment was started. This is why the ART medication must be taken for the rest of the patient's life, not because big Pharma wants to make extra cash.

Interestingly, if you follow patients that have lapses in their ART treatment and sequence the viruses that repopulate the infection, they become more similar (clonal) over time, due in part to the reservoir cells! Since potentially a single virus will do the repopulating from a reservoir cell, you would expect the resulting population of viruses to be more similar to each other than in the original infection, and this is what is observed: Specific HIV integration sites are linked to clonal expansion and persistence of infected cells .

* Random by measurement, not necessarily by mechanism.

For the economics experts around, how much of these high rents and gentrification are being driven by wealth / income inequality ? In the Bay Area it seems that unless you are pulling a 6 figure tech job you are just playing a waiting game to be priced out. As a grad student in the area, I find this quite disheartening...

I understand the sentiment, but the major issue with vaccines, with respect to "parental choice", is that it is not a child-autonomous choice. Not vaccinating your child places others in danger. This is why we cannot have large numbers of people, children or otherwise, exempt themselves from vaccination that otherwise could receive it* without imposing a great danger to public health. Also, as a matter of fact, while we** don't mandate that children read particular books (that's religion's job), we do mandate that they, at least to a certain age, attend school - public, private, or home, so long as they are educated (again, for the betterment of society). And as a last point, we do have laws which set standards for how parents raise children; adding vaccinations to that list would not be a huge alteration of this societal notion.

* Exempting those who cannot have vaccinations for health-related reasons

** In the US

Long story short, it involves mutations in viral proteins that are responsible for counter-acting anti-viral proteins (termed restriction factors) in human cells, that differ slightly from the chimpanzee versions due to an ongoing genetic arms race between the host proteins that block viral infections, and the viral factors that counter-act them to retain virus infectivity. There are also changes in the viral envelope proteins to help evade adaptive immune responses (recognition by immune cells and antibodies)

That would be easy enough to test, provided we had archeological samples of Phoenicians / Romans who were infected with M. tuberculosis (Mtb). Then, one could do the same phylogenetic analysis done in the paper that claded with the seal / sea lion Mtb sequences. Of course, the sequence analysis data provided in the paper would probably argue against your hypothesis, as Mtb sequences obtained from infected members of those civilizations would probably clade with modern European Mtb sequences rather than with seal / sea lion Mtb, which it would have to do in order to fit the data in this study.

Wrong.

Step 1: Use public funds to do innovative research into expanding the genetic code in microbes.

Step 2: Patent everything to make sure no one else can build on your discoveries.

Step 3: Create a company that promises all the keywords for a biotech e.g. antibiotics, vaccines, etc.

Step 4: Get bought out

Step 5: ? Profit was Step 4.

Remember when science was about discovery and standing on the shoulders of giants?

Monsanto is, in part, doing exactly what you suggested. The genetic element that grants their crops resistance to glyphosate (Round-Up) was discovered in microbes growing in waste runoff containing glyphosate. The patent is on the plants that have been transformed / engineered to contain this naturally occurring resistance gene in their genome and express it to garner resistance to the herbicide.

The cDNA argument is much worse to ludicrous. The only thing one could imagine is patentable surrounding the issue of cDNA is the technique involved in its generation, but that ship has sailed long ago. The entire process of generating cDNA is by using materials all found in nature. The RNA template that is used to generate cDNA in these cases of naturally occurring genes is obviously naturally occurring* and the technology to even create cDNA in the first place is using a naturally occurring enzyme, reverse transcriptase (found in retroviruses like HIV to catalyze the conversion of their genomic RNA to DNA). Because all these elements exist in the natural world, it is certainly possible in say HIV infected humans that random gene mRNA molecules have been converted to cDNA, thus negating the argument of generating something that does not exist in the natural world. More importantly, the only facet of this whole process of generating cDNA that is artificial is placing the materials in a tube together, NOT inventing any novel chemicals or enzymes to catalyze the process!

* In cells, mRNA molecules are heavily modified, sections spliced out, nucleotides edited, the 5' end capped, the 3' end poly-adenylated, so with the arguments placed forth concerning cDNA, one can imagine in vitro transcription of a gene creates an RNA molecule that doesn't exist in nature and can therefore be patented. Ridiculous, right?

As far as I know, bacteria don't use epigenetics in the same way we would associate with eukaryotes. First off, bacteria don't have histones and are thus limited to DNA methylation in terms of types of epigenetic modifications they can employ (bacteria do have DNA-binding proteins that help package DNA, but I don't believe anyone has shown they are used to control gene expression in a heritable manner -- the definition of epigenetics). In terms of how bacteria use DNA methylation, there are two cases I am aware of: (1) distinguishing between newly synthesized and "template" DNA just after DNA replication to help fix errors (if the DNA repair machinary detects a mis-matching base-pair, it corrects based on the template, methylated strand; and (2) to distinguish between self and non-self DNA, particularly in anti-phage (viral) defense, so that enzymes that have evolved to destroy foreign DNA can avoid destroying the bacterial DNA.

In general, epigenetic markers are controlled by protein interactions, which can of course be very complex, including kinetic competitions between proteins that write the markers, and proteins that erase the markers. To build a genetic pathway that regulates epigenetic markers beyond simple sequence recognition (such as GAmTC methylation in E. coli that regulates the origin of DNA replication) is probably beyond the capability of current synthetic biology.

I'm not sure about influenza (BSL-3 requires a respirator, and since influenza is very easy to catch through aerosol, makes sense to protect against breathing it in), but HIV at the University I work at is considered BSL-2* (that's BSL-2 star). Basically BSL-3 minus the breathing apparatus, as you cannot contract HIV by breathing it in. So you double glove, no sharps, and bleach everything down, and make sure everything in there stays in there unless you are absolutely sure the virus is dead.

Mice aren't humans, human experimentation is still morally objectionable and illegal, and medical testing on primates / apes is much more expensive and considerably less ethical in most people's minds. It's important to note where mouse research fails to properly recapitulate human biology, but sensationalist journalism acting as though the animal rights crowd is finally vindicated in proving, through a few heroes in the scientific community, that animal testing is cruelty without merit is harmful to the field, both in terms of basic biological research and discovering new medical treatments. Mice are still the only mammalian model organism where gene knockouts and knock-ins are reliably possible (some new DNA modifying technology involving proteins called zinc fingers are changing this) and this study is only demonstrating that some aspects of mouse research cannot be translated into human medicine. And for those questioning how many drugs failed in mouse models that may work in human subjects, are you going to be the group / company testing drugs on humans that are toxic or otherwise not working in mice? Would you rather kill an equivalent number of chimpanzees as we do mice to get a more accurate model of human biology, ignoring the added cost of housing and longer time of maturity?

I'd only add:

Observation -> Hypothesis -> Theory -> Predictions -> Test -> Scientific fact.

Well, yes, the headline is misleading, but it's also a bit more than a "possible" ancestor.

The researchers in the study wanted to create a better phylogenetic reconstruction of the evolution of mammals than had been previously accomplished, to resolve whether divergence of placental mammals from non-plancental mammals (egg-laying / marsupials) occurred before or after the extinction of the Dinosaurs (the K-T boundary), and also to make predictions of the biology of that last common ancestor. Previous phylogenetic reconstructions had been done with molecular data (DNA or protein sequences), but molecular data is limited to extant species and makes a lot of assumptions about the rates of changes in DNA that get more unreliable the further back in time you go. This study combined molecular data with character traits they call 'phenomic' characters - from the paper: "4541 phenomic characters de novo for 86 fossil and living species." The resulting matrix of traits, both molecular and character, was used to generate a tree based on maximum parsimony - a method which minimizes the number of trait changes over time when building a tree. This resulted in a single, highest scoring tree predicting the evolution of these species and the changes in their traits over time. The resulting tree is then "clocked" (called 'time-calibration in the paper) to known rates of evolution for the molecular data (good for recent divergence of species) and by fossil data to give time ranges for the deeper sections of the tree. This last part is key, as you cannot get molecular data from fossils, and fossils allow you to map the existence of certain traits within a group to a certain point in the history of these organisms.

The result is a time-range in which the last common ancestor between placental and NON-placental mammals must have lived, given the data provided and the parsimony criterion. As the tree makes claims about when the phenomic characters evolved or were lost, it also predicts which phenomic characters the last common ancestor had.