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Genome and Structure:

HIV’s genome is a 9.7 kb linear positive-sense ssRNA.1 There is a m7G-cap (specifically the standard eukaryotic m7GpppG as added by the host’s enzymes) at the 5’ end of the genome and a poly-A tail at the 3’ end of the genome.2 The genome also has a 5’-LTR and 3’-LTR (long terminal repeats) that aid its integration into the host genome after reverse transcription, that facilitate HIV genetic regulation, and that play a variety of other important functional roles. In particular, it should be noted that the integrated 5’UTR contains the HIV promoter called U3.3,4

HIV’s genome translates three polyproteins (as well as several accessory proteins). The Gag polyprotein contains the HIV structural proteins. The Gag-Pol polyprotein contains (within its Pol component) the enzymes viral protease, reverse transcriptase, and integrase. The Gag-Pol polyprotein is produced via a −1 ribosomal frameshift at the end of Gag translation. Because of the lower efficiency of this frameshift, Gag-Pol is synthesized 20-fold less frequently than Gag.5 The frameshift’s mechanism depends upon a slippery heptanucleotide sequence UUUUUUA and a downstream RNA secondary structure called the frameshift stimulatory signal (FSS).6 This FSS controls the efficiency of the frameshift process.

Small amounts of nanometer-thin metal-organic layers efficiently protect red blood cells during freezing and thawing, as a team of researchers writing in the journal Angewandte Chemie International Edition has discovered. The nanolayers, made from metal-organic frameworks based on the metal hafnium, prevent ice crystal formation at very low concentrations. This effective novel cryoprotection mode could be used to develop new and more efficient cryoprotectants for the biosciences.

Cryoprotectants prevent ice crystals from forming when samples are frozen. Growing crystals can damage delicate cell membranes and cell components and disrupt cell integrity. Some solvents or polymers make good cryoprotectants; they keep ice in check by binding and disrupting their ordered assembly during ice formation.

Synthetic chemistry has yet more tricks up its sleeve for targeting and influencing ice formation in a more effective way. Metal-organic frameworks (MOFs) are three-dimensional crystalline networks of metal ions linked by organic ligands. These ligands can be tailored to bind such as water, allowing the assembly of the water molecules into ice crystals to be very precisely tuned.

Researchers at universities in New York and Ningbo, China, say they have created tiny robots built from DNA that can reproduce themselves.

Such nanorobots could one day launch search-and-destroy missions against within a human’s bloodstream without the need for surgery or collect toxic waste from the ocean.

The tiny mechanism is so small that 1,000 of them could fit into the width of a sheet of paper.

I like the chapter “would you want to be”.


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Ah, immortality, previously only for the gods and individuals with a fetish for chopping each other’s heads off. In more modern times, science is coming closer and closer to both identifying the tapestry of things that cause humans to grow old, and slowly but surely taking the first steps into finding ways to delay and even reverse this process for fun and profit. So, just what causes individuals of the human persuasion to grow old and die, who was the oldest confirmed human, are there any living things that are biologically immortal, and if there was an option to become biologically immortal, would you take it?

An MIT study suggests 3D folding of the genome is key to cells’ ability to store and pass on “memories” of which genes they should express.


Every cell in the human body contains the same genetic instructions, encoded in its DNA. However, out of about 30,000 genes, each cell expresses only those genes that it needs to become a nerve cell, immune cell, or any of the other hundreds of cell types in the body.

Each cell’s fate is largely determined by chemical modifications to the proteins that decorate its DNA; these modification in turn control which genes get turned on or off. When cells copy their DNA to divide, however, they lose half of these modifications, leaving the question: How do cells maintain the memory of what kind of cell they are supposed to be?

A new MIT study proposes a theoretical model that helps explain how these memories are passed from generation to generation when cells divide. The research team suggests that within each cell’s nucleus, the 3D folding of its genome determines which parts of the genome will be marked by these chemical modifications. After a cell copies its DNA, the marks are partially lost, but the 3D folding allows the cell to easily restore the chemical marks needed to maintain its identity. And each time a cell divides, chemical marks allow a cell to restore its 3D folding of its genome. This way, by juggling the memory between 3D folding and the marks, the memory can be preserved over hundreds of cell divisions.