BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: HIV

HIV Resistance to CRISPR/Cas9

A recent study, described in the Science Daily, shows that researches who used the CRISPR/Cas9 to mutate HIV-1 within cellular DNA found that the mutation led to unexpected resistance.

When HIV enters a cell, its RNA genome is converted into DNA and becomes intertwined with the cellular DNA. So the goal for the CRISPR/Cas9 is to target a DNA sequence and cleave viral DNA. The problem is HIV is too good at surviving and thriving despite new mutations, making it more difficult for the CRISPR/CAS9 to target.

PDB_1wj9_EBI

Photo Source

Chen Liang, Senior Investigator at the Lady Davis Institute at the Jewish General Hospital, noted that when they sequenced the viral RNA of escaped HIV, they were surprised to see that majority of the mutations the virus had, instead of resulting from the errors of viral reverse transcriptase, were rather introduced by the cellular non-homologous end joining machinery when repairing the broken DNA.

The mutations to the sequences caused by the HIV were unrecognizable to the Cas9. Thus the resistant viruses just continued to replicate.

This study serves as a cautionary tale for scientists hoping to apply CRISPR/Cas9 as an antiviral. Liang does not believe these efforts are useless, however, as he is hopeful about strategies that could overcome this roadblock. One such strategy would be to target multiple sites with CRISPR/Cas9 or use other enzymes besides Cas9. After the solution is identified, the next step will be figuring out ways to deliver the treatment to patients. Liang is confident that CRISPR/Cas9 will open doors for finding a cure for HIV-1 and many other viruses.

More Info:

http://www.genengnews.com/gen-news-highlights/hitting-hiv-with-crispr-cas9-can-arouse-resistance/81252590/

http://www.techtimes.com/articles/148378/20160409/crispr-cas9-gene-editing-is-not-good-enough-to-beat-hiv-whats-next-in-humanitys-fight-against-the-deadly-disease.htm

 

 

How CRISPR/Cas9 could one day prevent AIDS

CRISPR/Cas9 is a new gene editing tool that can target and modify DNA with great accuracy.  This new tool has many scientific uses, including treatment of many diseases.  Recently, several breakthroughs have been made in treating HIV with CRISPR Cas9.  However, a number of issues with the tool have come up at the same time.

To understand how CRISPR eliminates HIV, one must know how HIV replicates. HIV replicates by taking over a host cell and injecting its RNA into the cell.  This RNA becomes DNA and joins together with parts of the host cell’s DNA.  After entering the cells, the virus can lay dormant for several years, but will eventually start replicating and taking over other cells.  The standard form of treatment for HIV is an antiretroviral.  While antiretrovirals can be very effective at limiting the spread of the disease, it cannot fully remove it or stop it forever.

HIV virus

image source: http://bit.ly/1S4bcWY

The CRISPR Cas9 could potentially be used to inhibit the spread of HIV by editing the virus out of a cell’s DNA.  Researchers at The University of Massachusetts Medical School have been developing a technology to perform this impressive task.  While there have been several successful trials in preventing HIV from spreading, several trials have lead to increased resistance for the HIV.

“When we sequence the viral RNA of escaped HIV, the surprise is that the majority of the mutations that the virus has are nicely aligned at the site where Cas9 cleaves the DNA, which immediately indicates that these mutations, instead of resulting from the errors of viral reverse transcriptase, are rather introduced by the cellular non-homologous end joining machinery when repairing the broken DNA,” says Chen Liang, a senior investigator at the Lady Davis Institute at the Jewish General Hospital and the Associate Professor of Medicine at the McGill University AIDS Centre.

These mutations alter the strand of DNA, preventing the CRISPR Cas9 from recognizing it.  If the CRISPR Cas9 cannot recognize the virus, it cant remove the viral DNA, allowing the virus to create more copies of itself.  Despite these limitations, researchers like Liang are confident that they can succeed.

article: http://esciencenews.com/articles/2016/04/08/hiv.can.develop.resistance.crisprcas9

A Cure to HIV is Near, But Not Here Yet

The study of genetics, specifically gene editing, has taken monumental leaps over the past few years. One of the biggest achievements of late is the discovery and further research into CRISPR/Cas9. Being able to use CRISPR/Cas9 to edit the genome sequences of living cells far has been the efficient tool geneticists have dreamed of. However, a recent study proved that CRISPR/Cas9 is not yet able to work as the perfect antiviral mechanism.

Image courtesy of AJC ajcann.wordpress.com, https://flic.kr/p/c9ktfQ

Image courtesy of AJC ajcann.wordpress.com, https://flic.kr/p/c9ktfQ

Scientists from McGill University, the University of Montreal, the Chinese Academy of Medical Sciences and Peking Union Medical College did a study where CRISPR/Cas9 was inserted to the replicative process of the HIV invested cell. After HIV enters a cell it’s RNA is converted to DNA which attaches to a cell’s pre-existing strand of DNA. This is when CRISPR/Cas9 is used, it breaks up these two DNA strands. The study found that many of the targeted viruses were killed, however the others viruses developed mutations on even just one nucleotide that made them more resistant and impossible for Cas9 to identify. In conclusion, scientists realize they may need to target more than one region of the DNA at once to effectively kill viruses like HIV.

This topic is very interesting to me because it reflects how we are on the cusp of some incredible biological achievements. I am particularly interested in this study because the effect of HIV/AIDs has devastated not only our country, but also the world, and this study seems like an important step in finding the cure that could save millions of lives. CRISPR/Cas9 seems to offer amazing possibilities, and this is one specific area that grabbed my attention. Do you think a solution to currently incurable diseases is near? Why/Why not? Let me know in the comments below.

Sources:

https://www.sciencedaily.com/releases/2016/04/160407132307.htm

 

Evolution: 1, Humans: 0 – HIV Virus has evolved to evade latest gene-editing treatments.

The Human Immunodeficiency Virus (HIV) is notorious for its rapid evolution and elusiveness to our treatments.  Our latest attempt to beat it has been foiled, yet again. As explained in this article, researchers have attempted to eliminate the virus through a genome editing technique called CRISPR-Cas9.  This technique allows scientists to target a specific genetic sequence in a cell to cut, using the Cas9 enzyme and a guiding sequence, and change the function of the gene by inserting corrected/modified sequences.

HIV budding from a Lymphocyte http://https://en.wikipedia.org/wiki/HIV/AIDS#/media/File:HIV-budding-Color.jpg

HIV budding from a Lymphocyte
[Picture Source Link]

This highly versatile technique was recently applied to HIV, in an attempt to disable it and prevent further infection from it.  The technique would theoretically delete HIV genetic sequences in an infected cell and prevent further virus production; however, a recent study  shows that the virus evolves rapidly to avoid this treatment.  The fault lies in the fact that the gene-editing technique targets a specific locus on the DNA to modify.  The treatment was successful in destroying HIV genes in that area of the DNA, but the cell’s repair mechanisms allowed the removed HIV genes to be repaired with new sequences.  This means that the new HIV genes will not be targeted by the CRISPR mechanism, because it contains a different marker, and the virus will live long enough to reproduce.  This rapid microevolution demonstrates the power of natural selection: a predator destroys the majority of the population, but those that are adapted to survive the conditions will live long enough to reproduce and pass on its traits! HIV has eluded us once again, but we now know that the gene-editing CRISPR-Cas9 system will work, provided that we don’t miss any HIV loci…

The research looks promising, but will this be our golden ticket?

 

Original Article: “CRISPR/Cas9 Gene Editing Is Not Good Enough To Beat HIV: What’s Next In Humanity’s Fight Against The Deadly Disease” (Tech Times)

Original Study & Further Reading: “CRISPR/Cas9-Derived Mutations Both Inhibit HIV-1 Replication and Accelerate Viral Escape” (Cell Reports Journal)

Image Source: Wikimedia Commons

 

HIV > CRISPR-Cas 9

https://commons.wikimedia.org/wiki/Category:HIV#/media/File:HIV-infected_H9_T_Cell_(6813314147).jpg

HIV Infecting a Cell

CRISPR-Cas 9 is an extremely advanced gene editing tool. This tool has efficiently created ways to make precise and targeted changes to the genome of living cells. However, in a study in the journal Cell Reports, scientists from the McGill University AIDS Center in Canada discovered drawbacks in using CRISPR to treat HIV. Instead of simply removing the virus from affected cells, the process of using CRISPR can also strengthen the infection by causing it to replicate at a much faster rate.

HIV has always been a popular disease to conduct research on. Scientists are constantly attempting to come up with ways to kill HIV. Several cures to HIV have been developed such as various as antiretroviral drugs, however, these medicines stop being effective after the patient has ceased to take them. As scientists have started to utilize gene editing tools to remove HIV they have been noticing the huge drawback. They realize that while the gene alteration allows the virus to be killed off in some cases, the resulting scar tissue can lead to the infection becoming stronger! Kamel Khalili, a scientist at Temple University, pointed out that the key to eliminating HIV could lie in attacking the virus at different sites using CRISPR.

Link to Original Study

Link to Original Article 

Link to Original Photo

Can Cats Help Fight AIDS?

Cat

Cats can in fact, unfortunately, get AIDS as well.  Their version of the HIV virus, FIV, is quite similar to the HIV virus. FIV and HIV are the same shape and have the same contents. This new discovery in cats may lead to new discoveries with anti-HIV drugs.

In an article titled “Cats lend a helping paw in search for anti-HIV drugs”, the American Technion Society explains how studying FIV can help scientists discover anti-HIV drugs. FIV and HIV use a protein, integrase, which puts the virus’ DNA into an infected cell’s DNA. Scientists and Professors can now study the Feline FIV virus and its interactions with integrase within cats to figure out important reasons how this deadly protein works. Through studying FIV and integrase, an amino acid change was found that tells us how integrase builds in its primary stages. Now those scientists know about this early assembly process, and can further learn how to terminate this process all together. About 40-45% of the proteins on the amino acid level are the same between FIV and HIV, allowing them to use this discovery on the human counterpart.

The feline virus, FIV, is a lot easier to study and researchers have already found a simpler form (than its HIV counterpart). By studying their 3-D model, they found that integrase’s simple and complex backbones are almost identical. These near identical backbones allow a much easier research path in FIV that will assist similarly with HIV integrase research.

HIV_attachment

 

Image of HIV Virus working

 

FIV and HIV are almost the same in how they work, but the more simple research on the feline version of the virus and integrase will greatly help the fight against AIDS. Who would’ve thought that cats could help fight such a deadly virus?!

 

More Information:

https://www.scripps.edu/newsandviews/e_20030414/elder.html

 

Pics:

http://commons.wikimedia.org/wiki/File:Cat_Cute.JPG

http://en.wikipedia.org/wiki/CCR5_receptor_antagonist#mediaviewer/File:HIV_attachment.gif

Possible HIV Remedy?

There wide array of deadly diseases that affect millions of people worldwide. Do you ever wonder if there could be a cure for just one? A team of researchers led by Dr. Caroline Goujon and Professor Mike Malim at the Department of Infectious Diseases in King’s College London has recognized a new gene that may have the ability to prevent HIV (Human immunodeficiency virus), a virus that slowly replicates and eventually causes AIDS. AIDS is a human condition that causes continuous failure of the immune system that could potentially lead to life-threatening infections and cancers. The research team has concluded that the human MX2 gene could play a major role in the path to finding an official cure for the deadly virus.

The MX2 gene is the Interferon-induced GTP-binding protein MX2. The protein encoded in this gene has nuclear and cytoplasmic forms. Researches have concluded that this protein could “lead to the development of new, less toxic treatments where the body’s own natural defense system is mobilized against the virus.” The scientists began the experiment by presenting the virus to human cells where the HIV virus had an encounter with two different cell lines and observing effects. After an intense study of the experiment, they detected in one cell line the MX2 gene was “switched on” and in the other cell line the gene was “silenced”. In the cell where the MX2 was switched off the virus duplicated, but in the cells were the gene was switched on no new viruses were produced or continued. In this way, the gene tested positive for its ability to fight off the virus.

The recent finding by the researchers brings way for other researches and scientist to continue to advance their knowledge about the virus. The goal would be to allow the 34 million people worldwide who are infected with HIV to lead a life free of the virus.hiv

 

Kid Cured from HIV

For the first time an infant was cured from HIV virus as in, the child does not have “detectable levels of virus” and there are “no signs of disease without the antiretroviral therapy.” The child’s mother with diagnosed with HIV gave birth to her child that also had HIV which was confirmed when she was born. Doctors immedietly began a regiment of a “liquid antiretroviral treatment consisting of a combination of three anti-HIV drugs: zidovudine, lamivudine, and nevirapine.” This treatment was continued for 18 months. It is also noted that by day 29 the amount of infant’s viral load had fallen to less than 50 copies of HIV per milliliter of blood (copies/mL).

HIV is spread via blood, semen and vaginal fluids and breastmilk making children with HIV infected mothers extremely susceptible to the virus. HIV is a retrovirus meaning the virus does transcription in reverse, transcribing DNA from RNA. During infection, the HIV virus attaches to a compatible receptor on the host cell’s surface. The virus  and injects its RNA and proteins into the host cell. The enzymes reverse transcriptase, integrase and protease are used to transcribe the virus from RNA to DNA and to integrate it into the host cell’s genome. The host cell then becomes a production house for the HIV virus producing the needed enzymes and genetic material to produce many more viruses. These newly formed viruses leave the cells in vesicles via exocytosis damaging the cell. This persistent damage to CD4 lymphocytes and the immune system eventually cases AIDS or acquired immunodeficiency syndrome. This diagnosis is determined through the person’s blood and their CD4 count.

18 months later the treatment was discontinued for unclear reasons.” After, blood samples were taken which revealed that there were undetectable HIV levels in the child’s blood. The child continues to thrive with no detectable levels of HIV in the the body without antiretroviral therapy. What doctors and scientists have taken from this case is that if antiretroviral therapy is started on “infants who are infected with HIV through their mothers via pregnancy or delivery” it may “prevent HIV from establishing a reservoir or a hiding place.” (http://www.biologynews.net/archives/2013/03/04/toddler_functionally_cured_of_hiv_infection_nihsupported_investigators_report.html)

Can HIV finally be cured?

While the answer to this question is very broad, there is hope that the number of people living with HIV throughout the world will significantly decrease in the near future due to a toddler who was cured of the virus.

About 1000 infants are born with HIV every day, that’s about 330,000 children each year. While most of the infections are in the developing world, there is still a vast number of people living with HIV in first world countries. An example is the Mississippi mother who had no idea she had HIV until a few days before she gave birth to her baby. Once the doctors learned she was infected with the virus, they took precautionary measures to ensure they could prevent the transfer of HIV during birth, a very common way of HIV transmission along with breast feeding. Once the baby was born Dr. Hannah Gay administer three drugs to the baby within thirty hours of birth. Typically, babies born from mothers with HIV are given two drugs as a prophylactic measure, however Dr. Gay said “her standard is to use a three drug regimen to treat an infection. She did this on the infant without waiting for HIV test results” (CNN.com)

Gay believes that the timing of the drug treatment was extremely crucial, and is key to effectively treating HIV in children/newborns. Currently, researchers are trying to see if this “cure” is an anomaly for a short period of time, or if the cure is permanent. In addition, physicians and scientists are optimistic, hoping that this cure will prevent many children from living with HIV throughout the world. Although the antiviral medications are very costly, doctors believe that it is not a stretch to offer these medications in third world countries and are hoping to soon make these medications available to many clinics throughout the world, assuming the “cure” was a success.

Read more at: http://www.cnn.com/2013/03/05/health/hiv-cure-global-hope/index.html?hpt=he_t3

Cute Baby
Photo By: Christopher Lance
http://www.flickr.com/photos/ninedragons/4822437519/

 

Protein Might Help Fight Deadly Diseases

The enzyme “Cholesterol-25-Hydroxylase,” or CH25H, might help fight against human viruses such as Rift Valley Fever, Niphah and HIV. CH25H converts cholesterol to an oxysterol called 25HC, which can permeate a cell’s wall to prevent a virus from getting in. The CH25H enzyme is activated by interferon, an anti-viral cell signaling protein produced in the body.  Researchers have known that interferon has been part of the body’s defense mechanism against viruses, though it does not have any antiviral properties itself.

This discovery is revolutionary because other antiviral genes have not been able to be used for treatment of viruses in humans. According to Yang Lui, a student at the David Geffen School of Medicine at UCLA, most antiviral genes are difficult to use in therapy because the genes are difficult for cells to express. However, CH25H is different because it is naturally synthesized.

HIV Replication within a cell

The discovery of CH25H is relevant to the efforts to develop broad antivirals against an increase of emerging pathogens. In a collaboration with Dr. Lee, another UCLA professor, it was discovered that the 25HC produced from CH25H can inhibit HIV growth in vivo. The researchers initially found that 25HC inhibited HIV growth in cultures. When implanted mice with human tissues, the 25HC reduced the HIV in within 7 days and reversed T-Cell depletion caused by the HIV. It was also discovered that 25HC inhibited the growth of other diseases such as Rift Valley Fever Virus and Ebola.

There are still some weaknesses with the study. It’s difficult to deliver 25HC in the large doses needed to fight viruses. Researchers also need to compare 25HC to other antiviral HIV treatments.

Bees and HIV

 

By PaulSteinJC. Photo from Flickr. http://www.flickr.com/photos/kapkap/2632994523/

 

30 million people have died due to AIDS.

However, a cure is yet to be found.

HIV is a retrovirus that manages to evade detection from the immune system because the virus hides in latency, incorporated into your DNA.

Instead, doctors give patients a “drug cocktail” that slows the replication and action of HIV enzymes. However, this treatment does not stop the initial infection.

A recent study had found that nanoparticles carrying a toxin found in bee venom can destroy HIV.

Bee venom contains melittin, which can “poke holes in the protective envelope that surrounds HIV,” thereby destroying the virus.

The researchers believe that this discovery can help them develop a vaginal gel that may prevent the spread of HIV.

A researcher Joshua Hood hopes “that in places where HIV is running rampant, people could use this gel as a preventive measure to stop the initial infection.”

Hood also thinks that these nanoparticles could be used to treat existing HIV infections. The nanoparticles could be injected into the blood, clearing HIV from the blood stream.

This is truly a wonderful discovery. Hopefully, this is the first step towards ending the AIDS epidemic.

To read more about HIV visit these sites:

http://www.thesun.co.uk/sol/homepage/news/4831508/Bee-stings-could-prevent-the-spread-of-HIV-doctors-claim.html

http://www.plannedparenthood.org/health-topics/stds-hiv-safer-sex/hiv-aids-4264.htm

 

Understanding HIV, one protein at a time

By NIAID/NIH (NIAID Flickr’s photostream) [Public domain], via Wikimedia Commons

In a recent study, scientists at Johns Hopkins University have narrowed down a list of 25 human proteins that HIV viruses target the most. The scientists started by studying the HIV-1virus, which is the most infectious and most common type of HIV. They knew that the virus clings to proteins and membrane as it emerges from an infected human cell in order to disguise itself from the human immune system, but inquired as to whether it was a random process or not. They then searched for types of proteins that they targeted the most, using the HIV-1.

They virus tends to target the CD4+ T cells and microphages which both migrate to sites of inflammation. This makes sense because HIV targets the immune system and  the virus can wait to attack while disguised by these cells. They originally identified 279 proteins that this virus in particular targeted when isolating the HIV-1 with CD4+ T cells, but when they crossed the data from two different cell types, they found that only 25 proteins were shared by viruses from both cell types!

This is an extremely interesting and groundbreaking discovery because of the possibilities behind this discovery. If we can figure out the types of proteins these HIV viruses are hiding behind, we could target and destroy them which could possibly lead to the abolition of HIV.

A True Medical Miracle!

Baby

Flickr
Photo By: Espen Faugstad

What would you do if your newborn baby had been HIV positive? Well this sad truth was given to more then 330,000 parents last year alone. Up until now there had never been a way of curing infants with this deadly disease, but due to a new radical treatment there may be hope for these babies. Thanks to Dr. Deborah Persaud this is now a possibility. She had a patient whose baby had been born with HIV. After the child had only been alive for about 30 hours her team started an aggressive treatment with antiretroviral drugs. After months of nonstop treatment the baby was no longer HIV positive. Dr. Deborah said,”It’s proof of principle that we can cure H.I.V. infection if we can replicate this case.” Although this is a breakthrough case for HIV doctors, there are still some people who are suspicious of the results. Dr. Daniel R. Kuritzkes, chief of infectious diseases at Brigham and Women’s Hospital in Boston, was quoted as saying, “The one uncertainty is really definitive evidence that the child was indeed infected.” One hypothesis of way the treatment worked for the child is that the drugs killed off the virus before it could establish a hidden reservoir in the baby’s body. One reason older people cannot be cured now is that the virus hides in a dormant state, out of reach of existing drugs. When drug therapy is stopped, the virus can emerge from hiding. Although HIV is far from being cured altogether, this new information and research is a step in the right direction of a world where no one has to die of HIV or AIDS.

For more information on this subject please visit: http://www.nytimes.com/2013/03/04/health/for-first-time-baby-cured-of-hiv-doctors-say.html?pagewanted=1&_r=0&ref=science

 

Can we fight off AIDS?

AIDS is a tragic epidemic world wide. More than 34 million people are affected by AIDS and in 2011 alone, 1.7 million people died from AIDS. The people affected by AIDS are largely from regions in Africa and Asia, but more than one million people in the US are living with AIDS.

Obviously such a prevalent disease attracts scientists looking to help find a cure from all over the world. There have been significant advances in medications that can prevent symptoms and prolong life, but there is yet to be a cure.

A new discovery in treatment for AIDS gives hope for a long term or even permanent control over the HIV. The treatment includes a vaccine with a disabled version of the virus. The heat-inactivated version of HIV “awakens immune protection in some patients”. This means certain patients didn’t have to take their medication for weeks or even months. Thought the affects of the vaccination are temporary, this method of treatment shows promise.

Even if scientists don’t come up with a more permanent treatment for HIV in the near future, the temporary suppressing of the virus results in “knocking the virus down to extremely low levels would mean many patients wouldn’t need drugs, wouldn’t show disease symptoms and wouldn’t be likely to transmit HIV to others.” This is a significant accomplishment. It could lower the amount of people infected with AIDS world wide by stopping the transmission between people and would also improve the quality of life for AIDS infected people.

 

Sources:

main article:

http://www.sciencenews.org/view/generic/id/347357/description/Inactivated_virus_shows_promise_against_HIV_

extra articles:

http://www.amfar.org/about_hiv_and_aids/facts_and_stats/statistics__worldwide/

http://aids.gov/hiv-aids-basics/hiv-aids-101/statistics/

photo:

Earth taken by Galileo after completing its first Earth Gravity Assist

The True Origins of HIV

There’s no doubt you’ve heard of HIV, or Human Immunodeficiency Virus. The HIV virus, if left untreated can lead to AIDS, or Acquired Immunodeficiency Syndrome, which leads to progressive immune system failure (http://en.wikipedia.org/wiki/HIV#Discovery). HIV didn’t become a problem in the United States until the 1980s, but was around long before then. Alfred Roca, an assistant Professor at the University of Illinois believes HIV was around for much longer than we believe.

 

The Origins 

HIV was thought to be originated from SIV, or Simian Immunodeficiency Virus, that infected Chimpanzees in Central Africa. About ninety percent of humans infected with HIV are infected with a strain called HIV-1 Type M, which was believed to have crossed the species barrier anywhere between 1884 and 1924. However, believes that HIV crossed the species barrier many times before 1884, but was most prevalent in rural areas, so it remained undetected.

 

Why it was a mystery

If HIV was around long before we initially thought, why did it remain undetected. According to Roca, “the persistence of HIV in humans requires population densities typically of larger cities that appeared in West Central Africa during the colonial period.” HIV didn’t spread amongst humans pre-1884 because the population was not dense enough. In addition, diseases spread much faster. Many people would have died early from diseases such as smallpox, and those with compromised immune systems would have been hit first, thus the disease couldn’t spread.

Map of the prevalence of HIV in the world, according to the 2008 UNAIDS Preport

Roca also believes that different strains of HIV could affect people with different genes. Using data from The Human Genome Project, Roca was able to analyze the DNA of the Biaka people, who live in the forests where the chimpanzees responsible for our current HIV pandemic reside and 4 other African populations which live outside the chimpanzees’ range. Research done in the 1980s concluded there are 26 genomic locations that help resist HIV.

The results of the research were astounding. Roca and his team identified four genes that code for proteins that affect the ability of the HIV to affect the host or the progression of the disease. Several of these genes were common among the Biaka people. Though the results aren’t definitive, they show that natural selection does play a part in the transfer of HIV to human populations, which is why the disease didn’t thrive earlier.

 

 

Tricky Viruses

Photo Credit: Foto_di_Signorina Flickr

           Strong viruses, such as HIV, make the body work for them. Researchers in Copenhagen have been studying how these viruses manage to take over the body. The virus takes over one cell and then uses the RNA to influence the DNA, giving the virus complete control over the cell. The RNA of the virus is similar to the RNA of the cell. Therefore, the ribosomes of the cell copy the sequence from the virus instead of the actual RNA. This causes the cell to produce the virus’ proteins.

                The RNA of the virus has what is called a pseudoknot. Pseudoknots are places on the RNA that the ribosomes must decipher before it can move on. The pseudoknot holds the sequence for key destructive proteins of the virus and once the ribosome deciphers it, those proteins are produced. This is how HIV can spread so rapidly in the body and can take such a hold over the host; it doesn’t do any of the work.

Antibodies to the Rescue!

Photo Credit: RambergMediaImages Flickr

 

 

HIV is an extremely dangerous virus because our own antibodies cannot effectively attack it. HIV uses a coat of sugars to hide itself from our antibodies. Although the body cannot effectively fight HIV, it does its best by making new antibodies to try and attack this powerful virus. These new antibodies attach to different spots on the sugar coating of the virus. It uses the sugar coat to bind to a site on the virus where amino acids are exposed. Then the antibody attacks the virus from that site, disabling it.

 

The discovery of this antibody and the way it binds to the virus is important because it can lead to advances in a cure and a vaccine. It gave scientists key information about binding sites made out of sugars and amino acids. They can use this information, as well as information from other projects and discoveries to make a more effective vaccine. In fact, some recent tests have shown that the antibodies play an important role in the health of someone infected with HIV.

New HIV Prevention Technique

CC licensed by photo Micro World (flickr)

An exciting, cutting-edge approach to HIV prevention is quickly gaining support, as researchers  have been learning about special antibodies that have destroyed HIV in the lab.  Now, biologists at Caltech have taken the next step, as they have discovered a way to insert these antibodies into mice, thus protecting them from HIV infection.

This new approach to HIV prevention — called Vectored ImmunoProphylaxis, or VIP — is outlined in the November 30 advance online publication of the journal Nature.

This new technique in HIV prevention is revolutionary, as supposed to traditional methods that centered on developing a vaccine that would provoke the formation of antibodies or T cells in the body, VIP provides protective antibodies directly.

Mice treated with VIP have been shown to produce high concentrations of the protective antibodies throughout their lives, and remain protected from HIV when it is administered intravenously.

Still, researchers must make the next step and show that the antibodies produced from VIP work to destroy HIV in humans.  According to researchers however, the problem will not be whether the antibodies work, as they are relatively sure of its effectiveness.  Rather, experiments will have to be conducted to see if VIP produces enough of these antibodies.  According to Alejandro Balazs, lead author of the study and a postdoctoral scholar, “In typical vaccine studies, those inoculated usually mount an immune response — you just don’t know if it’s going to work to fight the virus.  In this case, because we already know that the antibodies work, my opinion is that if we can induce production of sufficient antibody in people, then the odds that VIP will be successful are actually pretty high.”

For more information on this revolutionary new technique, visit the page http://intelwars.com/2011/11/30/gene-therapy-turns-muscles-into-hiv-antibody-factories/ 

What do you think?  Will the VIP method be successful in humans, and will HIV and AIDS finally be conquered?

 

 

 

 

 

 

 

 

 

Can timing change everything?

A Map of Cambodia: Cambodia Map from CIA World Factbook

Amongst individuals living with HIV, twenty to thirty percent die because of an additional tuberculosis infection. This co-infection is extremely common in Cambodia, a nation with 63,000 out of 13.2-million individuals living with just the HIV diagnosis, which eventually leads to AIDS. The HIV/Tuberculosis co-infection makes up 6.4% of Cambodia’s 5% HIV diagnosed population.

Dr. Anne Goldfeld, who has done studies on this trial as a Harvard Medical School employee and as President of the co- founder of the Cambodian Health Committee, says,


“Tuberculosis claims the lives of more than half a million people with HIV worldwide every year…”

 

She also says,


“This is a tragedy, because TB is completely curable when diagnosed and treated properly even in a patient with advanced HIV, especially if the patient also receives anti-retroviral therapy.”

 

In the past, the treatment for the co-infection has been very consistent. The treatment for Tuberculosis has been given to a patient immediately upon diagnosis. Two months later, anti-retroviral (ART) therapy for HIV would be given. However, recently, a trial entitled CAMELIA , >Cambodian Early versus Late Introduction of Antiretroviral Drugs, has helped give hope to HIV patients. The trial, which was created by Cambodian, French, and

 

American doctors, began in 2006 and lasted until 2010, encouraged five Cambodian hospitals to give HIV treatment to co-infected diagnosed patients only two short weeks following anti-tuberculosis treatment. The five hospitals are Calmette Hospital, Khmero-Soviet Friendship Hospital, and three provincial hospitals in the Siem Reap, Svay Rieng, and Takeo regions. This trial cut down the waiting time for HIV treatment by six weeks and overtime, the trial increased the survival rate of co-infected individuals by 33%.  Could six weeks really change the chance of survival for tuberculosis and HIV co-infected patients by such a great percentage? The answer is: absolutely! Did all medical physicians involved in this field of medicine agree with these techniques used to aid co-infected individuals? The answer is: definitely not.

 

Many of those who were opposed to the trial’s process said that the two treatments of Tuberculosis and the HIV  would wear the body down if done at similar times. Additional difficulties could be created for the body, which could already face toxicity with the required seven pills a day. The treatment was not risk-free either. It was possible that the immune system could become increasingly inflamed as it “rebound[ed] from HIV’s suppressive influence.” This trial was also available to patients who had an extremely strong immune system (given their diagnosis) at the time of treatment. Nevertheless, the benefits of the treatment have been much greater and more substantial than those doctors’ fears holding co-infected individuals from getting treated.

Doctors are still learning how the CAMELIA treatment can be improved and altered for the future. However, there has been enormous success with moving the treatments of co – infected Tuberculosis and HIV patients closer by six weeks. In just Cambodia, 661 patients participated in the CAMELIA trial, and less than one percent of the population participating, missed an appointment of the 8,955 scheduled for the population at the five separate hospitals. Many doctors, Cambodian citizens, and observers wanted this trial to work, and it was happening! The World Health Organization (WHO) should be encouraging this treatment more! Thirty three more percent of the initially co-infected patients of Cambodia are living! So where will the trial go next to help co – infected Tuberculosis and HIV patients? Ethiopia.

Killing Two Birds with One Stone

Credit: Fillmore Photography Flickr

Can you imagine having TWO life threatening diseases? Well, for some in Cambodia, that is the case. HIV and TB are two very common diseases that plague Cambodia, as well as other countries. Typically, a patient would go through TB treatment for two months and then begin HIV treatment. However, a new study done by Dr. Anne Goldfeld, the Program in Cellular and Molecule Medicine at Children’s Hospital Boston, and the CAMELIA (Cambodian Early versus Late Introduction of Antiretrovirals) shows that people with HIV and TB can benefit by being introduced HIV Treatment two weeks, instead of two months, after TB treatment was started. 

Doctors and researchers used to believe that the two medicines too much for the body to handle. Combining these two treatments would include taking seven, yes seven, pills a day. In addition, the pills would actually work against each other, the TB pills would work up the immune system to attack the TB and the HIV pills would suppress the immune system to stop the HIV from getting worse. This would put a massive strain on the body. However, this new study shows that the combination of the treatments can actually benefit the patient.

As of now there is no specific research or answers as to why the combination of the TB treatment and the HIV treatment is so effective. However, the study’s results are definitive. The patients that started the HIV treatment two weeks after starting the TB treatment had a better survival rate than those that started the HIV treatment later, 33% greater, to be exact.

Although the study did not give the exact reason behind this beneficial combination, it opened the door to a multitude of possibilities for HIV and TB sufferers around the world.

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