Commonly used disinfectants do not kill human papillomavirus (HPV) that makes possible non-sexual transmission of the virus, thus creating a need for hospital policy changes, according to researchers from Penn State College of Medicine and Brigham Young University.

‘Because it is difficult to produce infectious HPV particles for research, little has been known about HPV susceptibility to disinfection,’ said Craig Meyers, Distinguished Professor of Microbiology and Immunology, Penn State College of Medicine.

Use of disinfectants on HPV in health care settings has been based on what works on other viruses or what is thought should be effective.

Meyers collaborated with Richard Robison, an expert in microbial disinfectants at Brigham Young University.

HPV is estimated to be among the most common sexually transmitted diseases and is linked to cervical cancers. For this study, researchers grew HPV16, a specific strain that is responsible for up to 60 percent of all HPV-associated cancers. They then used 11 common disinfectants on the virus.

These disinfectants included ones made of ethanol and isopropanol because these are common ingredients in surface disinfectants and hand sanitises used in both public and health care settings. Study of these hand sanitises is important because other research has shown high levels of HPV DNA on fingers of patients with current genital infections. While HPV is susceptible to certain disinfectants, including hypochlorite and peracetic acid, it is resistant to alcohol-based disinfectants.

‘Chemical disinfectants in hand sanitiser are commonly used in the general population to prevent the spread of infectious diseases,’ Meyers said. ‘For flu or cold viruses they are very effective. But the data shows that they do nothing for preventing the spread of human papillomavirus.’

They also tested other common disinfectants, including glutaraldehyde, which is used for sterilisation in medical and dental facilities. Results show that glutaraldehyde is not effective at inactivating the HPV virus.

Other research has suggested that HPV could be transmitted non-sexually. The current study shows that medical instruments considered sterile could pose a risk for transmission.

‘Chemical disinfectants used in the hospitals and other healthcare settings have absolutely no effect on killing human papillomavirus,’ Meyers said. ‘So unless bleach or autoclaving is used in the hospital setting, human papillomavirus is not being killed and there is a potential spread of HPV through hospital acquired or instrument or tool infection.’

Meyers said the results suggest a need for a change in disinfectant use policies. Penn State University

Men who show signs of chronic inflammation in non-cancerous prostate tissue may have nearly twice the risk of actually having prostate cancer than those with no inflammation, according to results of a new study led by researchers from the Johns Hopkins Kimmel Cancer Center. The link between persistent inflammation and cancer was even stronger for men with so-called high-grade prostate cancer

Your smartphone now can see what the naked eye cannot: A single virus and bits of material less than one-thousandth of the width of a human hair.
Aydogan Ozcan, a professor of electrical engineering and bioengineering at the UCLA Henry Samueli School of Engineering and Applied Science, and his team have created a portable smartphone attachment that can be used to perform sophisticated field testing to detect viruses and bacteria without the need for bulky and expensive microscopes and lab equipment. The device weighs less than half a pound.

Researchers from Massachusetts Eye and Ear, Harvard Medical School, and Massachusetts Institute of Technology (MIT) have designed a protype system-on-chip (SoC) that could make possible a fully implanted cochlear implant.
A cochlear implant is a device that electronically stimulates the auditory nerve to restore hearing in people with profound hearing loss. Conventional cochlear implants are made up of an external unit with a microphone and sound processor to pick up and encode sound, and an internal unit that is seated in the skull and connected to an electrode array inserted into the cochlea. The external unit raises concerns in some individuals with social stigma and has limited use in the shower or during water sports.

Inhibiting enzymes that cause changes in gene expression could decrease chemotherapy resistance in ovarian cancer patients, researchers at Georgia State University and the University of Georgia say.
Dr. Susanna Greer, associate professor of biology, and research partners at the University of Georgia have identified two enzymes that suppress proteins that are important for regulating cell survival and chemoresistance in ovarian cancer.
Ovarian cancer is one of the deadliest gynaecological cancers, with a 60 percent mortality rate and a five-year survival rate for less than 30 percent of women in the advanced stage of the disease. The high mortality rate is largely due to the development of resistance to chemotherapeutic drugs. Understanding the molecular and genetic mechanisms that drive the development of acquired chemoresistance can help improve therapeutic agents for ovarian cancer treatment.
‘Ovarian cancer is usually treated by surgery followed by chemotherapy,’ Greer said, ‘but because it’s typically found fairly late, ovarian cancer is often refractory to chemotherapy. You have tumours that initially respond to chemotherapy and then don’t. Ovarian cancer is the 8th most commonly diagnosed cancer in U.S. women, but due to its late diagnosis, causes more deaths than any other cancer of the female reproductive system.’
In a previous study, Greer found the expression of the protein RGS10, which regulates ovarian cancer cell growth and survival, is suppressed in ovarian cancer cells that are chemoresistant. The suppression was caused by two important mechanisms that silence genes and contribute to the progression of many cancers – DNA methylation, a biochemical process in which a methyl group is added to specific building blocks of DNA, and histone deacetylation, a process in which enzymes remove functional groups of atoms from proteins associated with DNA.
In their study, the researchers investigate the silencing of RGS10 expression in ovarian cancer cells by epigenetics, which is heritable changes in genes and gene expression that are not caused by changes in the DNA sequence, but rather by reversible and self-perpetuating mechanisms of DNA programming.
They identified two epigenetic regulators, HDAC1, a histone deacetylase, and DNMT1, a DNA methyl transferase. Decreasing the expression of HDAC1 and DNMT1 and blocking their activity significantly increased RGS10 expression and cell death. This also decreased the binding of HDAC1 to RGS10 in chemoresistant cells.
The research suggests that inhibiting HDAC1 and DNMT1 could be a novel therapeutic approach to overcoming chemoresistance in ovarian cancer. EurekAlert