Standard treatment for common STD doesn't eliminate parasite in some women

A new study led by an infectious disease epidemiologist at Tulane University School of Public Health and Tropical Medicine could change the way doctors treat a common sexually transmitted disease.

Professor Patricia Kissinger and a team of researchers found the recommended single dose of medication isn't enough to eliminate trichomoniasis, the most common curable STD, which can cause serious birth complications and make people more susceptible to HIV. Results of the research are published in Lancet Infectious Diseases.

Globally, an estimated 143 million new cases of trichomoniasis among women occur each year and most do not have symptoms, yet the infection is causing unseen problems. The recommended treatment for more than three decades has been a single dose of the antibiotics metronidazole or tinidazole.

The researchers recruited more than 600 women for the randomized trial in New Orleans; Jackson, Mississippi; and Birmingham, Alabama. Half the women took a single dose of metronidazole and the other half received treatment over seven days.

Kissinger and her team found the women who received multiple doses of the treatment were half as likely to still have the infection after taking all the medication compared to women who only took a single dose.

"There about 3.7 million new cases of trichomoniasis each year in the United States," Kissinger said. "That means a lot of women have not been getting inadequate treatment for many decades."

Trichomoniasis can cause preterm delivery in pregnant women and babies born to infected mothers are more likely to have low birth weight. The parasite can also increase the risk of getting or spreading HIV.

Kissinger believes the CDC will change its treatment recommendations because of the results of this study.

"We need evidence-based interventions to improve health," Kissinger says. "We can no longer do something because it's what we've always done. I hope that this study will help to change the recommendations so that women can get the proper treatment for this common curable STD."

Source: https://www.sciencedaily.com/releases/2018/10/181007084044.htm

HIV RNA expression inhibitors may restore immune function in HIV-infected individuals

Immune activation and inflammation persist in most treated HIV-infected individuals and is associated with excess risk of mortality and morbidity. A new study by Boston University School of Medicine (BUSM) researchers suggests that use of HIV RNA expression inhibitors as adjunct therapy might diminish atypical inflammation and restore immune function in HIV-infected individuals on combination antiretroviral therapy (cART).

HIV-1-infected individuals have excess risk of developing non-AIDS complications such as cardiovascular atherosclerosis, neurocognitive dysfunctions, non-AIDS cancers, osteoporosis, and renal disorders. Systemic chronic immune activation has been postulated to lead to these non-AIDS complications.

Despite long-term viral suppression by cART, it has remained unclear how chronic inflammation is induced in HIV-infected individuals. In this study, BUSM researchers identified a mechanism of HIV-1-induced chronic immune activation and T cell dysfunction. In studies performed with primary human macrophages and T cells, they found that persistent infection of macrophages with HIV-1 and expression of intron-containing HIV-1 RNA alone even in the absence of infectious virus production lead to induction of type I interferon (IFN-I)-dependent pro-inflammatory responses and immune exhaustion of co-cultured T cells. They believe that these findings might provide an explanation for the observed chronic inflammation-associated morbidities in HIV-infected individuals who are on cART.

"We hope our study will broaden knowledge of host-HIV interactions and might help to reduce inflammation-associated disorders caused by chronic viral infections," said Rahm Gummuluru, PhD, corresponding author and associate professor of microbiology.

Source: https://www.sciencedaily.com/releases/2018/08/180827102648.htm

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Amyloid beta protein protects brain from herpes infection by entrapping viral particles

A Massachusetts General Hospital (MGH) study has found the mechanism by which amyloid beta (A-beta) -- the protein deposited into plaques in the brains of patients with Alzheimer's disease -- protects from the effects of herpes viruses commonly found in the brain. Along with another study appearing in the same July 11 issue of Neuron, which found elevated levels of three types of herpes viruses in the brains of patients with Alzheimer's disease, the MGH team's results support a potential role for viral infection in accelerating A-beta deposition and Alzheimer's progression.

"There have been multiple epidemiological studies suggesting people with herpes infections are at higher risk for Alzheimer's disease, along with the most recent findings from Icahn School of Medicine at Mt. Sinai that are being published with our study," says Rudolph Tanzi, PhD, director of the Genetics and Aging Research Unit in the MassGeneral Institute for Neurodegenerative Disease (MIND) and co-corresponding author of the Neuron paper. "Our findings reveal a simple and direct mechanism by which herpes infections trigger the deposition of brain amyloid as a defense response in the brain. In this way, we have merged the infection hypothesis and amyloid hypothesis into one 'Antimicrobial Response Hypothesis' of Alzheimer's disease."

Previous studies led by Tanzi and co-corresponding author Robert Moir, PhD, also of the MIND Genetics and Aging Research Unit, found evidence indicating that A-beta -- long thought to be useless "metabolic garbage" -- was an antimicrobial protein of the body's innate immune system, capable of protecting animal models and cultured human brain cells from dangerous infections. Given that brain infection with herpes simplex -- the virus that causes cold sores -- is known to increase with aging, leading to almost universal presence of that and other herpes strains in the brain by adulthood, the MGH team set out to find whether A-beta could protect against herpes infection and, if so, the mechanism by which such protection takes place.

After first finding that transgenic mice engineered to express human A-beta survive significantly longer after injections of herpes simplex into their brains than do nontransgenic mice, the researchers found that A-beta inhibited infection of cultured human brain cells with herpes simplex and two other herpes strains by binding to proteins on the viral membranes and clumping into fibrils that entrap the virus and prevent it from entering cells. Further experiments with the transgenic mice revealed that introduction of herpes simplex into the brains of 5- to 6-week-old animals induced rapid development of A-beta plaques, which usually appear only when the animals are 10 to 12 weeks old.

"Our findings show that amyloid entrapment of herpes viruses provides immediate, effective protection from infection," says Moir. "But it's possible that chronic infection with pathogens like herpes that remain present throughout life could lead to sustained and damaging activation of the amyloid-based immune response, triggering the brain inflammation that drives a cascade of pathologies leading to the onset of Alzheimer's disease. A key insight is that it's not direct killing of brain cells by herpes that causes Alzheimer's, rather it's the immune response to the virus that leads to brain-damaging neuroinflammation."

He continues, "Our data and the Mt. Sinai findings suggest that an antimicrobial protection model utilizing both anti-herpes and anti-amyloid drugs, could be effective against early Alzheimer's disease. Later on when neuroinflammation has begun, greater benefit may come from targeting inflammatory molecules. However, it remains unclear whether infection is the disease's root cause. After all, Alzheimer's is a highly heterogeneous disease, so multiple factors may be involved in its development.

Tanzi says, "We are currently conducting what we call the 'Brain Microbiome Project,' to characterize the population of microbes normally found in the brain. The brain used to be considered sterile but it turns out to have a resident population of microbes, some of which may be needed for normal brain health. Our preliminary findings suggest that the brain microbiome is severely disturbed in Alzheimer's disease and that bad players -- including herpes viruses -- seem to take advantage of the situation, leading to trouble for the patient. We are exploring whether Alzheimer's pathogenesis parallels the disrupted microbiome models seen in conditions like inflammatory bowel disease, and the data generated to date are both surprising and fascinating."

Source: https://www.sciencedaily.com/releases/2018/07/180705143920.htm

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Largest oral HPV study in England shows infection rates lower than expected

Infection rates of high risk human papillomavirus (HR-HPV) oral infection in England are lower than expected, compared to previous US studies.

The research, conducted by the University of Sheffield, also strengthens evidence that smoking and sexual behaviour were shown to be risk factors for oral HPV infection, which can lead to oropharyngeal (throat) cancer.

This timely study published in the British Medical Journal Open, led by Professor Hilary Powers, Dr Vanessa Hearnden and Dr Craig Murdoch and funded by the World Cancer Research Fund UK, coincides with the announcement of a new UK HPV vaccine programme for boys which will reduce the risk of HR-HPV related cancers.

Rates of oropharyngeal cancers are increasing worldwide, attributable to an increase in the rate of oral infection with HR-HPV.

This new study of 700 men and women in Sheffield, which is the largest of its kind in England, looked for HR-HPV infection and also asked participants lifestyle questions relating to their sexual history and tobacco use.

A total of 2.2 per cent of people were infected with oral HR-HPV infection with 0.7 per cent positive for HPV16 or HPV18. There are large variations in oral HR-HPV prevalence globally however this study showed lower rates compared to previous Scottish and US studies which both found 3.7 per cent of individuals positive for oral HR-HPV.

Former smokers were significantly more likely to be HR-HPV positive compared with those that had never smoked. The study also found that participants with a greater number of sexual or oral sexual partners were more likely to be HR-HPV positive.

Dr Vanessa Hearnden, from the Department of Materials Science and Engineering at the University of Sheffield, said: "Previous studies have been US-focused or in smaller UK studies in London or Scotland. This is the first study in the North of England and found lower rates of oral high-risk human papillomavirus infection.

"We fully support the newly announced HPV vaccination programme for boys which will reduce the risk of HPV related cancers including throat cancer in men and will also provide further prevention of cervical cancers through herd immunity.

"However, we found the majority of individuals testing positive for high risk strains of HPV were actually positive for strains other than those covered by the current vaccine (HPV 16 and HPV 18). This shows the need to consider newer vaccines which protect against more HPV strains in the future and for individuals to be aware of lifestyle risk factors such as number of sexual partners and tobacco use."

Dr Craig Murdoch, from the University of Sheffield's School of Clinical Dentistry, said: "Many people associate the HPV virus with cervical cancer but there is less recognition of the fact that HPV causes oropharyngeal cancer, and unfortunately, the prevalence of this cancer has increased dramatically in the past few years.

"The Sheffield Head and Neck Oncology Research Team are conducting research into HPV-related oral cancer in order to find better ways to treat this disease and improve quality of life."

Dr Kate Allen, Executive Director of Science & Public Affairs for World Cancer Research Fund International, said: "This study confirms the importance of lifestyle risk factors in prevention of the disease and sheds new light on the rates of oral HR-HPV infection in England."

Source: https://www.sciencedaily.com/releases/2018/08/180820094502.htm

Plant compound 'much more effective' than traditional anti-HIV drug

Azidothymidine, the first drug that was approved in the fight against AIDS in the 1980s, is still a main component in the medication mix commonly prescribed to HIV patients today. But new research may have found a plant-derived chemical compound that is much more effective than azidothymidine.

In the United States, the Centers for Disease Control and Prevention (CDC) estimate that around 1.1 million people have HIV, and 1 in 7 of them are not aware that they have it.

Due to awareness campaigns and efforts to prevent HIV, the number of new infections dropped by 19 percent between 2005 and 2014. The number of HIV-related deaths has also been falling since the mid-1990s, largely due to advances in HIV treatment.

Although there is yet no cure for HIV, antiretroviral therapy significantly slows down the progression of the virus. The first drug to have been approved in the fight against AIDS is azidothymidine (AZT).

Since 1987, however - the year in which AZT was approved by the U.S. Food and Drug Administration (FDA) - the virus has adapted to the drug. Today, HIV patients are given a combination of various drugs, of which AZT is often still the main component.

AZT works by inhibiting an enzyme that the HIV virus needs to replicate inside a host cell. This enzyme is called reverse transcriptase.

New research, published in the Journal of Natural Products, has found a plant compound that may be more effective at inhibiting this enzyme than AZT.

The chemical compound is called "patentiflorin A" and is derived from a medicinal plant found in East Asia: Justicia gendarussa.

The discovery is the result of a research effort extending over several years, carried out by an international team of scientists from the University of Illinois at Chicago (UIC), the Hong Kong Baptist University in Kowloon Tong, and the Vietnam Academy of Science and Technology in Hanoi.

The team was led by Lijun Rong, a professor of microbiology and immunology at the UIC College of Medicine, who has special expertise in identifying antiviral agents.

Patentiflorin A inhibits HIV 'much more effectively' than AZT

Prof. Rong and colleagues selected Justicia from a pool of more than 4,500 plants.

After separating the extracts of the stems and roots of this plant using bioassay-guided isolation - which is the most common procedure for separating extracted compounds based on their biological activity - the researchers found the "anti-HIV arylnaphthalene lignan glycoside" that is patentiflorin A.

Then, Prof. Rong and team assessed the effect of the compound against the M-tropic and T-tropic HIV isolates. "Tropism" refers to the type of cells that the virus can invade. M-tropism refers to the virus' ability to invade macrophages, while T-tropism refers to its ability to invade T cells, which are both white blood cells with key roles in immunity.

The tropism tests showed that patentiflorin A had "a significantly higher inhibition effect than the clinically used anti-HIV drug AZT."

"Patentiflorin A was able to inhibit the action of reverse transcriptase much more effectively than AZT and was able to do this both in the earliest stages of HIV infection when the virus enters macrophage cells and alter infection when it is present in T cells of the immune system," Prof. Rong explains.

He also notes that his team managed to synthesize the compound de novo, or "from scratch." He says:

"If we can make the drug in the lab, we don't need to establish farms to grow and harvest the plant, which requires significant financial investment, not to mention it has an environmental impact."

He concludes, "Patentiflorin A represents a novel anti-HIV agent that can be added to the current anti-HIV drug cocktail regimens to increase suppression of the virus and prevention of AIDS."

Source: https://www.medicalnewstoday.com/articles/317966.php