Research on the efficacy of HIV vaccines in humans is close to its inception; and there are others that may emerge in 2017!
HIV vaccine is currently in the field of research in 2016, probably in its most fertile and diversified, copious and prolific period these days, year 2016, in the search for vaccine against the Human Immunodeficiency Virus, in the II Research for Prevention conference (HIVR4P) as was said in Chicago last week. A high proportion of presentations was devoted to the multiplicity of different approaches that scientists are using to make a vaccine reliable and effective. At the opening of the plenary, Georgia Tomaras Duke University, North Carolina, USA, gave an overview of the field. It was a long way for effective, even partial, vaccine development: the first test of any vaccine species was on 1987 and the first major efficacy test - failed - It was 2003. But the RV144 vaccine, which in 2009 showed limited effectiveness, reducing infections by 31% of subjects, injected new mood into the field. This was not lower because its effect It appears to conduct an unexpected immune response to HIV.
During the International AIDS Conference (AIDS 2016) held in Durban in July, a pilot study, HVTN100, of a Type-RV144 vaccine adapted for the predominant strain in South Africa presented evidence of a stronger immune response to the presence of HIV. This meant that the initial target had been met, meeting the criteria to move toward a larger study to verify this effectiveness in more people, this will start in November two thousand and sixteen – the first efficacy study to last seven yearsSince HVTN 505 which was started in July 2009. (Translator's note: You have to have hope, but we also need to act with caution A staggered information can take hundreds, even thousands of people to an unwanted destination.).
How immune responses always surprise us!
There is a vaccine that surprised and greatly surprised the researchers, and yet it was found that the immune response seen in HVTN100 presented a type of response that was not seen in RV144. In this study, antibodies of the type called immunoglobulin G (IgG) appeared protective, although they did not do the work of attacking HIV or infected cells, but interestingly, by stimulating antibodies that did not neutralize HIV, on the other hand it induced the system immune to mounting a widespread attack on HIV.
A second type of antibody, of the immunoglobulin type A (IgA), proved decidedly unhelpful and eventually become a factor correlated to an increase in infection rate. Editor's note: In short, it worked against us, "delivering", as they say on the streets and in life, "gold for the bad guys."
Now researchers have discovered a subtype of IgG called IgG3 that further enhances immunity by reacting against two specific parts of two "tips" of the "viral envelope" protein. This type of response It has not been seen in RV144 but was observed in HVTN 100 - and this is a very positive signal.
However, when the research subjects with RV144 were revaccinated, a dose of the vaccine was given to them.
to make observations and studies for up to six years, IgG3 reactions began to appear. With what has been reported here and with the cytomegalovirus (CMV) vaccine (see below), it implies that an effective HIV vaccine could involve the onset of childhood immunity against HIV, which could be enhanced with another dose in adolescence.
Tomaras, the researcher, stressed the complexity of multidimensional type of immune response that researchers intend to induce. There are three spectra of immune response, the antibody response, the cellular response and the innate response and in each case these responses may vary by typeBy force and crafts relating to the scope of these responses; vaccine would need to work against the most different strains of HIV).
"Vector, Primary and Amplificantes"
There are a large number of choices facing vaccine manufacturers. RV144 and subsequent studies show that an HIV vaccine may work best if it is applied as two types of jab (Jab is, in the box, an art almost forgotten because of the current spectacles of brutalities and monstrosities within a "Octagon".), A "primary (Jab)"Usually consist of HIV genes incorporated into the capsid"a kind of another virus envelope"Followed by an" enlarger "(the Hook), usually made up of" naked "and harmless HIV proteins. If you want to learn more, watch the video on YouTube: Box Basics (Opens in another tab); and if you would like to see how I mentalizo, for one day, our MH antibodies that finish with this virus, invest 5 minutes of its life and see the above antibody here The link opens on another tab. (I.e.
So far these have been applied in some dosages of three to four doses over the course of a year, although it is clearly seen that it would be better to find a vaccine that is effective in a smaller number of doses.
The pharmaceutical company Janssen, a subsidiary of Johnson & Johnson, has an ambitious research program to develop a vaccine prime-boost that can act against a wide variety of HIV strains. The company Hanneke Schuitermaker told the conference that Janssen would apply two or more doses of a vaccine first of an osaic antigen "(Note from the translator: there is nothing about the entry OSAIC: Research - osaic antigen - does not match results) consisting of gene sequences from a wide variety of different HIV strains in a viral capsule (usually an adenovirus similar to the common cold) and follows with two doses of amplification containing protein from capsid. So far their best vaccine scheme has produced an 94% reduction in viral infections in one study with monkeys and 66% from six viral attacks.
Janssen has a study called APPROACH (another window automatically translated) (approach) of seven different vaccine schemes, ongoing in 400 volunteers in the US, Rwanda, Uganda, South Africa and Thailand. And there are also two other trials called TRAVERSE and the ASCENT with 348 volunteers altogether, which compare two different spectra of HIV viral strains. These are pilot trials and, as with HVTN100, if there are good immune responses by the end of this year from the APPROACH study and mid-2017 from APPROACH and TRAVERSE, decisions will be made as to which of these studies could generate a vaccine with the study, in which case, which one. (HUH)
"Teaching the body to manufacture antibodies"
This is a Infographic the human body. Take a look at this, it might be interesting
The strategy vector-> primary-> e-> amplifiers is not universal. Some "primary" vaccines with DNA exposed to HIV, which would be easier and cheaper than a vector vaccine, the challenge here would be in which cells. Other vaccines would do the prime / push scheme that could represent a fully effective strategy.
A major problem with antibodies is that although the body produce, in many cases, highly adapted and unusual antibodies, which are called "broadly neutralizing" and eliminate viruses that infect people and
can therefore be used as a kind of "high tech weapon", as "Long term prep", applied via infusion) once in the body would develop immunity to them, the various strains of HIV, within a few weeks, and would be like trying to stay ahead in an arms race that, generally, HIV has expired since it started , in the middle of 1996, the application of Antiretroviral Therapy - ART – .
Dennis Burton of the Scripps Institute in La Jolla, California and Stephen Kent of the University of Melbourne both spoke in separate presentations on the development of versions mais immunogenic HIV which involve the strictest exposure of proteins that mimic which the immune system actually "sees" in an infection. This has only been possible in recent years using microorganism manipulation techniques to obtain the surface protein gp120 (viral) to actually fold into pairs and triads of proteins called "dimers and trimers", which is what receptors on the surface of the That the immune system has to "look"Instead of using unfolded protein capsid of HIV.
The researchers induced broadly neutralizing antibody responses using these techniques, but the antibodies have shown a frustrating tendency to react against "wrong spots" of the protein envelope, the capsid, and connect to "holes" in the protection of glucose molecules which surround the protein rather than evolve directly to attach to the protein itself. But getting cells that can produce broadly neutralizing antibodies to all HIV strains, such as a response to a vaccine, is already a breakthrough.
Another strategy is to get ahead of the arms race and make a vaccine that 'mimics', before the immune system, the actions of visa adapted viruses in chronic infection, Thereby inducing the body to manufacture broadly neutralizing antibodies without the provision of HIV infection.
Christopher Parks of the International AIDS Initiative (IAVI) introduced programs to develop HIV-like particles that would be like 'living vectors' that would spread from cell to cell and generate what would seem to the immune system as a ongoing HIV infection. So far, they have used a benign virus called VSV (vesicular stomatitis virus) as the protection of their living vector. Studies in monkeys have only demonstrated a "short delay" in HIV infection and there is, however, a correlation between poor antibody response and very rapid infection.
But they are trying to develop virus particles and "stronger", including coated with the HIV protein
itself and a coated envelope, with a capsid from the Ebola virus. As these are not really viruses, they would probably be harmless, although clearly and clearly, biosafety studies will have to be done.
The vaccine that nobody expected and surprised!
Although most researchers since have focused on increasing RV144 antibodies, which should prevent infection in the first place; at least one conventional vaccine based on a vector of CMV virus that aims to produce a strong response of the immune cells, which would not necessarily stop stop HIV infection, but to contain it or even put it into permanent remission.
This is based vaccine in CMV - opens on another tab - produced by Louis Picker in Oregon, USA, which caused great excitement three years ago, when it seemed to have healed completely, 55% of a group of monkeys placed as subjects of the surgery. CMV is another "live" vector that mimics the spread of a true HIV infection. Monkeys developed infections when infected with SIV, the simian HIV equivalent, but responded strongly to the presence of the infection and the peak of the viral load of these monkeys were very low and eventually the virus completely disappeared. Picker said that they now have reproduced the same results on many other monkeys. Moreover, the effect seems quite persistent; when reexposed with new SIV infections in periods from 2 to 6 years after their initial infection and from 3 to 7 years after vaccination, 80% of the monkeys that originally offered a good response were still protected from SIV through vaginal delivery and 56 % by rectal route.
You can skip the whole stretch in green. It is my explanation of certain "editorial policies that I would classify as, when little,"stunt ".
I make an aside here: Note that all these exams speak in terms of at least 6 years. This already dismantles AmFar's "promise" of a cure for 2020!
It is reckless (with forgiveness for the bad word) to throw yourself into unprotected sex of any nature, to believe that "healing will appear soon" and, with that, to return to share "equipment" for injecting drug use. I think the ideal is not to use drugs, with this and other "Exceptions" correlated, and in the meantime, if you are going to use injectable drugs, please !!!!! Do not share needles and syringes!
People who come to this site, I know what I hear and read every day from people who, for one reason or another, being that, in general, the majority are people of both sexes and with a sexual desires, in great desperation for not knowing if they can or can not believe that their "non-reagent" is real and other doubts, and especially those who find themselves opportunistic diseases in situations that are several times definitive (test yourself, ignoring a problem does not solve the problem and, on the contrary, only tends to worsen it) ...
The CMV-based vaccine does not work by producing antibodies: it stimulates cells that kill infected cells, which is why it "sniffs" ongoing infections, unlike others, that prevent infection. When Parker's team analyzed the results, they found an entirely new type of immune response. Infected cells usually display the viral protein spots that they contain on their surface, as distress flags. The "hoisting". (Translator's note: The original is flagpoles, it seems to be an idiomatic expression and the best response I received came from the Google translator who replied with "masts." I decided to "hoist", which is what seems to happen with cell, which hoots a "flag" and shows the identity of the attacker or attacker). This consists of an enormous recognition of strange variable proteins, called MHC 1a or MHC 2 (MHC means class of histocompatibility). These classically alert CDXUMUMX cells to send "reinforcements" to kill compromised cells, as well as a warning system composed of proteins that attract CD4 cells to kill the virus directly in infected cells.
The vaccine, which is making use CMV vector as produced responses 2 MHC class, and also raised a completely different type of immune response to molecules MHC class E. These alert the innate immune system and natural killer cells (NK is a cell of the immune system that acts as a state agent that systematically checks every cell in the body for problematic or potentially dangerous cells - such as those that can arise as a polyp in the gut that could lead to cancer - and kills them or order them to commit suicide in a apoptosis (opens in another tab). This response has never been seen until this day - either in a vaccine or, strangely, in the natural CMV infection.
What the researchers found was that fortunately the CMV strain used to make the vector had two crucial genes absent. It was only when both genes were excluded that CMV stimulated the response with MHC-E. In addition, although MHC responses varied from the natural of an animal compared to another animal, there were some responses to the specific genes of the SIV itself in all animals - what is wanted from a "broad spectrum vaccine ". Translator's note: The original text refers to broad-brush vaccine, and the broad-brush expression is practically untranslatable, probably an idiomatic expression whose best definition was: very general and without many details, which in free translation would be "very widespread and without many details ". I found myself forced to interpret and, for better understanding, think of a US citizen who was learning to speak Portuguese and were called "to participate in a kitty ...")
Parker's team is trying to develop vaccines with human CMV range. Human CMV has genes that are analogous to the two missing genes in CMV that infects rhesus monkeys and the big question is whether the human vector will produce the same immune response, with such effective action. A dose escalation study is scheduled and will seek to obtain, with the CMV acting as a vector and it is expected that produces a more conventional response of responses with MHC-1a and 2, and if this attempt is successful will to seek by stimulating a response of an MHC-E.
A major problem remains: the vaccine only worked consistently at about 55% of the monkeys, and so far there seems to be no way to tell which monkeys will have this response and which will not. Louis Picker told AIDSMAP.COM that the difference is probably caused by the way CMV generates a rapid immune response and whether it is able to stop SIV / HIV before the infection becomes systemic and spreads throughout the body. What determines the rate of response is still unknown, but may mean that the CMV-loaded vaccine, which would have to be combined with an antibody vaccine to obtain a response with better efficacy. As with other vaccines, the difference between success and failure is whether the immune response can remain one step ahead of HIV the arms race between the virus and the human organism.
Reviewed by Claudio Souza (if any typos or spelling, consider my dyslexia accompanied a rather long peripheral neuropathy ... and tell me this Claudio Souza - Note that your email client will create a message already with the subject. Please keep this in mind as I have a specific rule in my email client and iao allows a sound to be played and a visual warning as well. This way I will be able to solve "the thing" as soon as possible. Thank you )
A very interesting video for those interested in the body. On the basis of my survival and also with regard to the Mara, is the knowledge we have of our bodies and a constant and diurnal observation of the behavior of our bodies (...)
This is just a brief summary of some of the presentations on the development of a vaccine at the HIVR4P conference. Many more studies can be explored by previewing the book summary here, two webcasts here, posters here.
Tomaras G. Overview of the humoral and cellular immune response to HIV vaccination. Plenary explanation session. Conference for HIV Prevention Research (HIVR4P 2016), Chicago, 01 / 02, 2016 Presentation Plenary Session. See the webcast here.
Schuitermaker H. Towards an HIV vaccine: (pre-) clinical evaluation of Prime-Boost schemes Using Ad26 and MVA with mosaic antigens and soluble proteins Gp140 ... Explanation session to plenary. Conference for HIV Prevention Research (HIVR4P 2016), Chicago, SY01.03 presentation plenary, 2016. see the webcast here.
Burton D. Progress Based on Neutralizing Antibodies to HIV Vaccine. Conference on HIV Prevention (HIVR4P 2016), Chicago, plenary presentation at 03.01, 2016. See the webcast here.
Parks C et al. Protection against SHIV rectal infection induced by mucosal vaccination with a replication-authoritative VSV-HIV Chemotherium showing Env Envers to the immune system. Conference for HIV Prevention Research (HIVR4P 2016), Chicago, presentation at symposium SY01.02, 2016. See the webcast here.
Picker L. Development of a vaccine based on the action of cytomegalovirus as an "organic delivery vehicle. Conference on HIV Prevention Research, Chicago, Symposium presentation SY06.03, 2016.See the webcast here.