limpon

Are there any downsides to disclosing the hashing algorithm they're using? Does a hacker have an advantage by knowing this information.

1. Ebola's rate of infection is ~1.5 - 2 new infections per infected persons [1] Even though this is an exponential rate, it does nowhere get near the rates of many other viruses. As such it is easier to restrict further infections than it is for most other infectious diseases.

2. The 1.4M people prediction from the CDS assumed no intervention or help from other countries and a collapse of the local healthcare systems. That's why I am saying that we should focus our efforts on helping the healthcare workers in West Africa.

> Who knows what the infection rate will be outside of West Africa Way lower than the rate in West Africa, that is for sure. Ebola doesn't spread through the air, you have to get in direct contact with body fluids. You don't get infected by sitting in a bus or plane with someone, who is infected. Most of the infected people are healthworkers in a setting without protective clothing, even gloves are rare to come by. Others are direct relatives who don't know much about ebola and who have burial rituals that are very different to the ones most of us are used to. It is very common in West Africa to wash out the mouth of dead persons and to kiss them goodbye. I am pretty sure this would not happen in the US or Europe, especially not if the deceased person died by bleeding out of all body openings.

A very large majority of ebola infected people in West Africa can't go to a hospital - there are no free beds at the moment. So they go back home to their families. THIS is how ebola spreads.

That's why we have to act, but not by panicking, but rather by sending well trained medical staff to help.

[1] http://www.nejm.org/doi/full/10.1056/NEJMoa1411100#t=article

Ebola is fairly difficult to spread, it is not very contagious, no matter what you might believe based on news reports. If you want to look at a contagious disease, look at flu. The 2009 flu pandemic lead to hospitalization of ~200,000 people in the US alone within a few weeks [1]. Talking about the flu, you can somewhat guess the number of infected people to be much much higher. The current Ebola outbreak lead to ~8,000 infected persons since its outbreak more than half a year ago in March. As you see, Ebola is not very contagious when compared to the flu. Yet flu pandemics are usually restricted fairly well once they take off and people are aware.

I'm constantly reading people being afraid of Ebola mutating to make people survive longer so the virus can spread better. Influenza (Flu) is very good with that, yet not even the very contagious flu was able to cause a significant thread to mankind in the recent history.

Ebola is the cause for a humanitarian crisis in West Africa and we should put all our efforts to helping the people who are affected by it, rather than worrying about ourselves for no good reason.

1) https://en.wikipedia.org/wiki/2009_flu_pandemic

Wow, it seems like you don't really know what you're talking about. It's not easy to move away if you're born and grew up in Africa. It's not like renting a U-Haul, pack your stuff and drive across the country.

You need a visa. But it's impossible to get a visa to work in US/Europe unless you have a job. And even trying and applying for a visa costs more than most people's monthly salary. And there is no money-back guarantee.

But finding a job is also not easy. Applying to some IT company in the US without being able to show of significant work experience? No college education from a well-known university? How can you get job experience that is sufficient to apply for an IT job when you live in a country that has the problems the article talks about?

And no, you cannot just apply to some junior entry-level job. You won't get a visa unless you are so qualified that the host country has a huge demand for people with your skills. And this is just one of the hundreds of problems you're facing when deciding to leave Africa.

So yeah:

>Get out of Africa. Africa will steal your life.

Thanks for that advice. Very helpful.

I've heard lots of people speculating that the big pharma companies would be better of if there would always be HIV and they can sell their ART pills for live. But on the other hand if one of them is the first one to create a HIV immunization, this alone will make them so extremely rich. An effective HIV immunization will become standard immunization for all people in the western world and the WHO and UN will take all in their power to immunize as many people worldwide as possible. Just imagine the amount of doses that will have to be produced. And you would be the only one company having this product. This has way more financial gain that being one of the dozens of companies that produce ART therapies. On top of that a few people working in high positions of big pharma companies are still "nice" people who would actually be proud of curing a disease. Not everyone just counts their dollars every day and hopes that more people get sick.

Hi Reid, as I said before, I wish you all the best but I simply don't understand how your experiment 2 is going to work. Did I understand correctly that you will immunize mice and then isolate CD4 T cells from the spleen. Then infect those cells and see if cells from immunized mice die slower/less/not at all and don't express p24 in high levels. I'm afraid this experiment will not work this way. CD4 T cells by itself can not be immunized against HIV. The immunizing effect comes from memory B cells that produce antibodies. These antibodies bind to HIV infected CD4 T cells and as such label them as evil to be killed by other cells. CD4 T cells alone will not show any effect in regards to susceptibility to HIV no matter how well your immunization works. As rgejman pointed out, it would be way better to infect the mice with HIV and do a CD4 T cell count there every week. This would be so much easier and it might actually show you something relevant.

I really really from all of my heart wish that your project will work. Seriously, the idea of a free HIV vaccine is amazing. But honestly, I believe that you might all be a bit naive when it comes to doing proper molecular biology experiments. There's a reason why most PhD students need several years to finish their studies and they mostly use just a few techniques. Doing experiments with humanized mice and HIV might sound easy on paper, but will turn out to be way more complicated than what you believe it to be now. Trust me, been there, done that. Anyways, I wish you all the best, I love it when people challenge old dogmas with new ideas. I'd appreciate it a lot if you could put some more information about the biology, especially the role if the immune system, online.

I'll try to give you a description of what transcription factors do and what the importance of Stamatoyannopoulos finding is. I hope it doesn't sound too weird.

Just noticed, how long my "brief" description is, so here is a TL;DR: Comparing cells to computer programs: A program figures out by itself which functions to call based on the byte sequence of the function in memory and changes these preferences based on the environment its running in.

As you know, the DNA in our cells encodes the blueprint for all proteins that exist in the human body. I'm trying to compare this to string encoding, but might be completely wrong, because string encoding is more difficult to me than DNA encoding ;) The DNA is our hard drive. This hard drive holds the information for all proteins. A protein will be a string. Our alphabet is made out of 21 characters, they are called amino acids. Each character (amino acid) is encoded as a 3bit sequence on the DNA, the so called codon. Opposite to the binary system, we have a base4 system, meaning each bit can have 4 different states (A,T,C,G), the nucleic acids. So, given a byte sequence from the hard drive (gene on the DNA), we always look at codons (three bits) and can then translate those codons into amino acids. ATG translates to Methionine, GGA translates to Glycine etc.... Having 4^3 (64) different codons but only 21 amino acids, some amino acids can be represented by several different codons. On top of that, some codons have a special meaning, such as "\n". Those special codons are called "stop codon", because it marks the end of a protein and the program stops decoding from this point on. In addition, there is also a "start codon" that marks the begin of a string.

When a cell wants to make a certain protein, it copies the byte-sequence from the DNA and translates it into the actual amino acid sequence and as such forms proteins (prints a string in our example).

The problem we're now facing is that every cell in your body (with a few exceptions, of course) has the exact same DNA sequence. But still, nature is able to somehow make different celltypes, such as a skin cell, blood cell, neuron, you get the point. The way how cells "know" which proteins to make is that the hard drive doesn't only hold encoded strings but also some byte sequences in between that don't encode any strings. These sequences are called regulatory sequences. These sequences attract so called transcription factors. Transcription factors are proteins that you could understand as a pointer. They will point to some genes, but not to others and thus instruct the cell which byte sequences should be translated into strings.

These regulatory sequences can not only attract transcription factors, but also suppressive factors. Those are proteins that prevent transcription factors from binding and thus ensure that certain proteins are not made.

There are hundreds of different transcription factors and repressors encoded on the DNA, but only a handful exist as protein in each given cell and they define the difference between celltypes. They come and go as the cell's environment changes as well.

So, going back to our string analogy, say you have saved thousands of strings on your harddrive but only want to show a subset of those to the user (eg language selection). You start your program by passing some information about which strings to choose. The same happens here as well, only that the information which strings to chose is somehow intrinsic but still different between celltypes. And on top of that you not only have distinct languages, but the languages overlap and language A uses string 1,2,3; language B uses string 2,5,6; and language C uses string 1,2,6 etc. Because of this complexity it is very difficult to understand how the cell "knows" which proteins are right.

Stamatoyannopoulos now for the first time proved that even though two different codons encode the same amino acids they might attract different transcription factors.

To get an understanding of the importance of this finding, imagine having a character encoding, such as DNA, where two different byte sequences encode the exact same string. Now imagine having a program that automatically chooses which strings to display based on which byte sequences encode certain characters.

And now, image that the DNA doesn't only encode strings, but also functions and closures, pointers, variables etc. So each time a part of the DNA is translated, the state of the program changes. Nature is vey complex and we're just at the beginning of understanding the code.

We have methods where we can out-comment some part of the DNA and see how the program changes (mutations). In addition, we recently learned how to see which part of the DNA is being used in certain cells. And in this paper, they refined this method by actually looking at all pointers in a cell and figuring out which part of the DNA they pointed at. And they did this for 81 different cell types to find networks that act together in certain settings.