arthenice – BioQuakes

Kid Cured from HIV

On March 12, 2013

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)

Telomere the Tell all?

By arthenice

On March 12, 2013

In Student Post

Scientists have recently discovered that they can predict life expectancy based on the length of the telomere in patients with heart disease. Telomeres which are protective, non coding regions at the ends of chromosomes get shorter over time due to cell division. The replication of DNA shortens our telomeres and our chromosomes. This makes us more susceptible to age-related “diseases such as heart disease or cancer, as well as exposure to oxidative damage from stress, smoking, air pollution, or conditions that accelerate biologic aging.” (http://www.sciencedaily.com/releases/2013/03/130310164232.htm)Telomere length used to be used to show age in a person but recently it also seems to be correlated with their chance of survival with heart disease. In a study conducted with 3,500 heart attack and stroke patients, researchers stated that those with longer telomeres had a greater chance of survival. In the future doctors believe that judging from the telomeres in patients, they could increase their effectiveness in treating heart disease.

How the “guardian of the genome” falls:

By arthenice

On February 10, 2013

In Student Post

p53 is a protein that plays a vital role in the G2 checkpoint phase before mitosis begins. This checkpoint “ serves to prevent the cell from entering mitosis (M-phase) with genomic DNA damage.” (http://www.cellsignal.com/reference/pathway/Cell_Cycle_G2M_DNA.html) The role of p53 is to trigger repair for damaged DNA if possible and to hold the cell in the G1/S checkpoint until it is repaired and if the repair of the DNA is not possible p53 triggers apoptosis. Therefore, p53 plays a large role is preventing cancer because a cancerous cell starts with a mutation in DNA. However mutant p53 allows cells who have DNA damage and have “tranformed” to be cancerous to enter into M-phase and proliferate thus forming a tumor.

Biologists, chemists and computer scientists at UC bolder however have discovered a “an elusive binging pocket” in the quaternary structure of p53 which is open “5 percent of the time.” (http://www.sciencedaily.com/releases/2013/01/130131121312.htm) The reason the pocket is only open 5 percent of the time is because the p53 protein undulates, meaning it sways so this pocket was hard to find and target. Their team then screened almost 2,500 molecules and tested out 45 molecules to see if any of them could fit into this pocket and trigger the normal tumor-suppressing abilities found in p53 in a mutated p53 molecule. They found that stictic acid fit and triggered the tumor-suppressing abilities. Although stictic acid is not able to be used as a drug, they can now scan other molecules that have similar properties as stictic acid making this a large step in cancer research because mutated p53 is found in over 40 percent of diagnosed cancer cases. (http://www.sciencedaily.com/releases/2013/01/130131121312.htm)

Sources:

http://www.sciencedaily.com/releases/2013/01/130131121312.htm

http://www.cellsignal.com/reference/pathway/Cell_Cycle_G2M_DNA.html

Gerbils Can You Hear Me?

By arthenice

On October 8, 2012

In Student Post

80 to 90 percent of people suffer from inherited deafness. In a study, scientists have reversed deafness in gerbils. This is a huge step in gene therapy research this month making the possibility of using gene therapy as a cure for deftness one step closer. Genetic therapy is the use of genetic material such as DNA to manipulate a cell and is generally used to treat inherited diseases; in this case scientists used human embryonic stem cells. The gerbils in the study were born deaf. This type of deafness is a birth defect caused by damage to hair cells in the inner ear. These inner ear hair along with auditory neurons which translate sound vibrations from the inner-ear cells to electrical signals are how you can hear. Scientists specifically worked on gerbils whose deafness was caused by a mutation in a gene coding for a protein called vesicular glumamate transporter-3. Even minor alterations to a protein’s primary structure ,such as the movement of a double bond, will cause major defects in the tertiary structure and the function of the protein. The mutated protein in this study vesicular glutamate transporter-3 controls the consumption of glutamate (neurotransmitter) into synaptic vesicles, which join two nerve cells, of the neural cells. This is clearly groundbreaking news this month and has proved the various use of stem cells. How do you feel about the use of embryonic stem cell research? Feel free to comment!!

BioQuakes

AP Biology class blog for discussing current research in Biology

Author: arthenice

Kid Cured from HIV

Telomere the Tell all?

How the “guardian of the genome” falls:

Gerbils Can You Hear Me?

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