Gene therapy may kill HIV

Gene therapy may have the potential to eradicate HIV in people infected with the virus, new animal research suggests. The science centers around the use of "chimeric antigen receptor" (CAR) genes. In laboratory work with monkeys, these engineered cells have destroyed HIV-infected cells for more than two years, scientists reported.

T-cells are the cells that are largely responsible for human ability to fight off pathogens and get rid of infections in the body. Every T-cell has a unique receptor, or molecule, on it. That receptor allows the cell to recognize a specific target-a bacteria, or fungus or virus. And when it recognizes that target, it's called into duty to clear it from the body. Taking artificial receptors- CAR that can go on to these cells and allow them to recognize what we want them to recognize," he noted. "In this case that's HIV."

First, the team genetically engineered CAR to find and bind to simian/human immunodeficiency virus (SHIV), a lab-engineered HIV hybrid composed of human virus and monkey virus. Then the researchers modified the DNA of certain blood-forming stem cells so they would carry SHIV-killing CAR. The resulting cells were introduced into the bloodstream of four male juvenile SHIV-infected macaque monkeys.

The engineered cells successfully took up residence in each monkey's bone marrow. The cells moved widely throughout the body, targeting and killing SHIV-infected cells, without producing any notable adverse side effects. The advantage of the stem cell-based approach is that once these cells are grafted into the body, they continuously produce new T-cells that have this gene in them that can target HIV cells.

Plans are underway for a human trial, this study shows both that these cells will respond to HIV and that it's safe. This strategy is unlikely to fully work on its own, CAR will most likely need to be used with antiretroviral therapy. CAR therapy is already leading to impressive results in cancer and holds promise for HIV eradication.
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ADHD drugs can prevent STI

Attention-deficit/hyperactivity disorder ADHD increases the risk of subsequent sexually transmitted infections STIs among adolescent and young adult populations, short- and long-term use of ADHD medication reduced the risk of subsequent STIs among men. ADHD is the most common neurodevelopmental disorder. Increasing evidence supports an association between ADHD and various health-risk behaviors, such as risky driving, substance abuse, and risky sexual behaviors.

Focusing on the occurrence of risky sexual behaviors and the risk of STIs among patients with ADHD, and emphasizing the treatment with ADHD medications may be a protective factor for prevention of STIs. The findings are based on the Taiwan National Health Insurance Research Database, which is a nationally representative database of medical claims and healthcare data from > 99% of the entire Taiwan population.

A cohort of 17,898 adolescents and young adults who were diagnosed with ADHD and 71,592 age and sex-matched non-ADHD controls who did not have STIs prior to enrollment were studied. Adolescents aged 12-17 years and young adults aged 18-29 years were followed from January 1, 2001 through December 31, 2009. The researchers tracked data related to risk of STIs, including HIV, syphilis, genital warts, gonorrhea, chlamydial infection, and trichomoniasis, psychiatric comorbidity, and pharmacologic treatment for ADHD (methylphenidate or atomoxetine).

The researchers found that adolescents and young adults with ADHD had greater incidence of any STI (1.2% versus 0.4%), and developed STIs at a younger age (20.51 ± 4.48 versus 21.90 ± 4.49) as compared to age- and sex-matched peers. They also found that those adolescents and young adults with ADHD had a higher prevalence of psychiatric comorbidity, including disruptive behavior disorder (13.5% v. 0.3%), alcohol use disorders (1.1% versus 0.5%), and substance use disorders (2.5% versus 0.8%). Male short-term (HR 0.70) and long-term (HR 0.59) ADHD medication users had a significantly lower risk of developing any STI during follow-up.
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Using viruses to fight viruses

Researchers at The Ottawa Hospital and the University of Ottawa have discovered that the Maraba virus, or MG1, can target and destroy the kind of HIV-infected cells that standard antiretroviral therapies can't reach. Daily medications keep the level of HIV virus in the blood low, there is currently no way to totally eliminate dormant HIV-infected cells from the body. If a person living with HIV stops taking antiretroviral medications, these hidden viruses rapidly rebound.

These latently HIV-infected cells are hard to target because they are not distinguishable from normal cells. Dr. Jonathan Angel and his team tried a new approach of identifying these dormant cells by using the MG1 virus. This virus attacks cancer cells that have defects in their interferon pathway, which makes the cells more vulnerable to viruses. Dr. Angel and his team previously found that latently HIV-infected cells also have defects in this pathway.

Using a number of laboratory models of latently HIV-infected cells, the researchers found that the MG1 virus targeted and eliminated the infected cells, and left healthy cells unharmed.
While most of these cells in patients are in the lymph nodes and other organs, a tiny number are found in the blood. When the researchers added MG1 to relevant blood cells taken from HIV-positive individuals, the levels of HIV DNA in the sample dropped. This indicated that the HIV-infected cells had been eliminated.
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Heplisav-B for prevention of Hepatitis B

U.S. Food and Drug Administration (FDA) has approved Heplisav-B [Hepatitis B Vaccine, Recombinant (Adjuvanted)] for prevention of infection caused by all known subtypes of hepatitis B virus in adults. Hepatitis B is an extremely infectious and potentially deadly virus.

 There is no cure for hepatitis B, and infections are on the rise. Hepatitis B can be prevented through effective vaccination. Current hepatitis B vaccines require three shots over a six-month period, however, almost half of adults fail to complete the series within one year.

Prevention of hepatitis B in adults through vaccination is more important than ever given the increase in the rate of infections. A two-dose schedule with higher rates of protection, along with other strategies, may help us move closer to the goal of eliminating hepatitis B.

Hepatitis B is a viral disease of the liver that can become chronic and lead to cirrhosis, liver cancer and death. The hepatitis B virus is 50 to 100 times more infectious than HIV, transmission is on the rise. There is no cure for hepatitis B, but effective vaccination can prevent the disease. In adults, hepatitis B is spread through contact with infected blood and through unprotected sex with an infected person.

 The CDC recommends vaccination for those at high risk for infection due to their jobs, lifestyle, living situations and travel to certain areas. People with diabetes are particularly vulnerable to infection, the CDC recommends vaccination for adults age 19 to 59 with diabetes as soon as possible after their diagnosis, and for people age 60 and older with diabetes.

Heplisav-B is an adult hepatitis B vaccine that combines hepatitis B surface antigen with Dynavax's proprietary Toll-like Receptor (TLR) 9 agonist to enhance the immune response. Dynavax has worldwide commercial rights to Heplisav-B. Heplisav-B is indicated for active immunization against infection caused by all known subtypes of hepatitis B virus. Heplisav-B is approved for use in adults 18 years of age and older.

Do not administer Heplisav-B to individuals with a history of severe allergic reaction like anaphylaxis after a previous dose of any hepatitis B vaccine or to any component of Heplisav-B, including yeast. Appropriate medical treatment and supervision must be available to manage possible anaphylactic reactions following administration of Heplisav-B.

Immunocompromised persons, including individuals receiving immunosuppressant therapy, may have a diminished immune response to Heplisav-B. Hepatitis B has a long incubation period. Heplisav-B may not prevent hepatitis B infection in individuals who have an unrecognized hepatitis B infection at the time of vaccine administration. The most common patient reported adverse reactions reported within 7 days of vaccination were injection site pain, fatigue and headache.
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Solosec for treating bacterial vaginosis

Solosec is a potent, next-generation, 5-nitroimidazole antibiotic with enhanced pharmacokinetic properties that enable delivery in a single dose that has been shown to be efficacious and well tolerated. Solosec is the first and only single-dose oral therapy for bacteria vaginosis the most common gynecologic infection. Bacteria vaginosis has been shown to increase the cause of chlamydia, gonorrhea, herpes, trichomaniasis and HIV, pre-term birth and low birth weight if left untreated.

A single dose regimen may improve adherence and the likelihood of a successful cure. No serious adverse events were reported during the trial and no patients discontinued treatment due to adverse events. Solosec is contraindicated in patients with a history of hypersensitivity to secnidazole, other ingredients of the formulation, or other nitroimidazole derivatives.

Vulvo-vaginal candidiasis may develop with Solosec and require treatment with an antifungal agent. Potential risk of carcinogenicity in patients taking single-dose of Solosec to treat bacterial vaginosis is unclear. Chronic use should be avoided. Solosec may pass into breast milk. Patients should discontinue breastfeeding for 96 hours after administration of Solosec.

Solosec is a single-dose therapy for oral use. The entire contents of Solosec packet should be sprinkled onto applesauce, yogurt or pudding and consumed once within 30 minutes without chewing or crunching the granules. Solosec is not intended to be dissolved in any liquid. In clinical studies, the most common adverse effects of the drug are headache, nausea, dysgeusia, vomiting, diarrhea, abdominal pain and vulvovaginal pruritus.
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Bacteria under the foreskin increases the risk of HIV in men

Some bacteria underneath the foreskin increases the risk of contracting HIV.
These bacteria cause specific immune cells to accumulate at the penis give HIV easy access  to enter the body.

An imbalance in genital bacteria can increase HIV risk. Circumcision reduces the risk of bacteria, since these anaerobic bacteria can not flourish outside of the moist oxygen-starved foreskin.

Researchers analyzed penile swabs from different uncircumcised men, and
examined the 10 bacteria species that are most commonly reduced after male circumcision.

The men who contracted HIV had higher amounts of certain bacterial strains under their foreskin. A 10-fold increase in the species Prevotella, Dialister, Mobiluncus and Murdochiella roughly equated to a 10 percent increase in the risk of contracting HIV.

The researchers discovered that some species of bacteria increase a man's HIV susceptibility by causing specific immune cells to accumulate under the foreskin and act as a direct entry into the body.
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HIV positive women with cytomegalovirus may infect their babies with the virus

HIV-positive women with cytomegalovirus CMV, in their urine at the time of delivery may pass the virus to their babies.

Women who had gonorrhea when they gave birth may also infect their babies with CMV. Babies infected through their mothers and those with weakened immune systems will experience serious health problems.

CMV can impair fetal growth, cause birth defects and babies born with the virus can have damage to their brain, liver, lung and spleen.

 Researchers examined 260 pairs of mothers and 222 babies from who were enrolled in a perinatal study by the National Institute of Child Health and Human Development.

After testing the mothers' and infants' urine for detectable CMV, the researchers discovered that- 2 percent of the women had detectable CMV and 3.8 percent of babies had the virus.

Eight percent of women with detectable CMV had babies with the virus, as opposed to 2.1 percent of women who did not have CMV.

Two percent of women with detectable CMV transmitted the virus to their babies compared with 8.1 of those who did not have CMV.

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HPV infection can cause cervical pre cancer in HIV positive women

Persistent HPV infection can lead to the development of precancerous lesions and cervical cancer.

Previous research has indicated that HIV-positive women face an increased risk of HPV infection, precancerous lesions, and cervical cancer compared with HIV-negative women.

 Researchers analyzed data from six studies conducted from 1994 to 2010 in Senegal, where HIV is endemic. They followed 1,320 women for an average of two years, testing them for HPV and cervical abnormalities approximately every four months.

At each clinic visit, women were characterized as normal, HPV-positive, or HSIL (HPV-positive with high-grade squamous intraepithelial lesions, a precancerous lesion that may progress to cervical cancer if untreated).

The study showed that HIV-positive women had higher rates of acquiring HPV, and lower rates of clearing HPV infection, than HIV-negative women.

Women whose immune systems were compromised by HIV were also more likely to have HPV infection progress to pre-cancer.


                                       haleplushearty.blogspot.com

Scientists remove HIV virus in animals using gene editing

According to the Centers for Disease Control and Prevention (CDC), more than 36 million people across the world are HIV positive.

Presently there is no cure for HIV, researchers used gene editing technology called "CRISPR/Cas9 to excised the HIV-1 provirus in three animal models.

A provirus is an inactive form of virus. It occurs when the virus has integrated into the genes of a cell. In the case of HIV, these host cells are the so-called CD4 cells - once the virus has been incorporated into the DNA of the CD4 cells, it replicates itself with each generation of CD4 cells.

The three mouse models used in the research are: a "humanized" model, in which the mice were genetically modified to have human immune cells, which were then infected with HIV-1.

The team was co-led by Dr. Wenhui Hu, Ph.D., associate professor in the Center for Metabolic Disease Research and the Department of Pathology at the Lewis Katz School of Medicine (LKSOM) at Temple University in Philadelphia, together with Kamel Khalili, Ph.D., Laura H. Carnell Professor and chair of the Department of Neuroscience at LKSOM, and Won-Bin Young, Ph.D, who just recently joined LKSOM.

Gene editing strategy is 96 percent effective. Dr. Hi and team inactivated HIV-1, significantly reducing the RNA expression of viral genes in the organs and tissues of genetically modified mice.

Specifically, the RNA expression was reduced by approximately 60 to 95 percent. Researchers tested their result
 by acutely infecting mice with EcoHIV - the equivalent of the HIV-1 in humans.

The third model, mice received a transplant of human immune cells, including T cells, which were then infected with HIV-1.
One of the main reasons that a cure for HIV has yet to be discovered is the virus's ability to "hide" in the genomes of T cells, where it lives latently. This is why researchers applied the CRISPR/Cas9 technology to these mice with infected T cells.

Defective HIV proviruses prevent cure

Proteins created by defective forms of HIV associate with immune systems are monitored by cytotoxic T cells.

HIV proviruses are many in HIV patients, the faulty proteins they produce can hinder measurement of viral load, exhaust immune systems and prevent suppression of the virus.

Researchers are trying to hypermutate the proviruses and destroy defective HIV proviruses and develop cure for HIV infection.

Scientists collected defective HIV proviruses from 9 HIV patients and transfected cultures of human immune cells in laboratory.

It was discovered that the transfected human immune cells were capable of making HIV protein despite mutations.

Defective proviruses contribute to viral RNA and protein production and increase the viral load of HIV patients.

New HIV reservoir discovered by scientists

Scientists have discovered a new cell in human body where HIV persists in spite of treatment.

Researchers have tried to clear HIV virus from the white blood cells that is part of immune system.

The virus persists in macrophages of infected person, this shows that T cells and some other cells in the body can serve as reservoir for HIV.

Macrophages are large white blood cell in tissue and bloodstream, the discovery shows that macrophages can be infected and they respond to antiretroviral therapy.

Scientists discovered that macrophages can survive in the body and continue to attack the HIV positive patients when their is therapy interruption.

Victor Garcia, a professor of medicine, microbiology and immunology and his team are trying to find out how HIV continues in tissue macrophages during HIV treatment and how it respond to treatment.

HIV lesions treatments

HIV alters the body's immune system and this can leads to development of many health problem like skin infections.

Lesions are abnormal growths on the skin, it can grow on the skin of people who are not suffering from HIV, but it is common in people who are HIV positive.

It may develop as side effect of HIV medication, CD4 count is a blood test that measure the level of white blood cells in the body, if CD4 count is very low, the rate of developing skin lesions will be very high.

Common HIV skin lesions:
• Bullous impetigo
• Human papillomavirus (HPV) warts
• Prurigo nodularis
• Molluscum contagiosum
• Herpes simplex lesions
• Kaposi's sarcoma

Treatments
1. Taking antiviral medication according to Doctor's prescription may increase CD4 cells.
2. Eating balanced diet
3. Getting enough rest
4. Regular exercise

HIV reservoir marker makes it possible to kill the virus

Discovery of HIV marker makes it possible to differentiate between dominant HIV infected cells and healthy cells.

Researchers have discovered a way of isolating and analyzing reservoir cells that are responsible for hosting HIV virus.

HIV virus can hide in these reservoir cells for a long period of time, taking antiviral drugs does not stop the activities of the virus.

The discovery will make it possible to study viral reservoirs and therapeutic plan to kill the hidden HIV virus.

How HIV affects the immune system

Human Immunodeficiency virus (HIV) is a lentivirus that causes HIV and later AIDS. Early signs of HIV are: fever, joint pain, sore throat and skin rashes.

A T-cell is a type of lymphocyte - white blood cell that defend the body against disease, HIV infects a cell by attaching itself to T-cell, multiplies its virus and destroy the T-cell.

CD4 count shows the strength of one's immune system which is between 500 1500 for healthy people, being infected with HIV without treatment will reduce the count below 200.

 HIV  exposes the infected person to opportunistic  infections like: pneumonia, toxoplasmosis, thrush, and tuberculosis.

Presently, there is no cure for HIV. Antiretroviral therapy is recommended for people living with HIV virus.

Common side effects of Antiretroviral drugs are: glucose intolerance, kidney failure, hepatitis of the liver, insulin resistance, osteoporosis, anemia and inflamed pancreas.

MRI scans can detect HIV in the brain

Scientists have discovered a way of using Magnetic Resonance Imaging MRI scans to detect when Human Immunodeficiency Virus HIV is persistent in the brain after several treatment.

Presence of diffuse white matter in the brain shows sign of abnormalities that is linked to cognitive problems can be increased by inflammation in the brain caused by HIV infection.

To confirm HIV infection in the brain, lumbar puncture is perform by inserting a needle into the back of the head to draw spinal fluid and test it for HIV.

MRI scans can diagnose patients with elevated risk of HIV related problem, drugs that cross the blood-brain barrier effectively can be used to control the infection.