Genetic changes in Ebola may impede treatments: Study

Researchers in the US studying the genetic makeup of Ebola in West Africa said Tuesday that they have identified several mutations that could potentially interfere with the effectiveness of new drugs for the deadly virus.

"The (Ebola) virus mutates rapidly," Jeffrey Kugelman of the US Army Medical Research Institute of Infectious Diseases (USAMRIID), the lead author of the study, said in a statement. "And it's an ongoing concern," Xinhua quoted him as saying.

In the US journal mBio, Kugelman and colleagues described the "genomic drift", or natural evolution of the virus, and how it may interrupt the action of potential therapies designed to target the virus's genetic sequence.

According to the study, three types of genetic sequence-based treatments -- monoclonal antibody, small-interfering RNA and phosphorodiamidate morpholino oligomer drugs -- being evaluated during the current outbreak. All were developed using Ebola virus strains from two smaller outbreaks that occurred in 1976 and 1995.

Working with investigators from Harvard University and the Massachusetts Institute of Technology, the USAMRIID team compared the current strain, called EBOV/Mak, with the two previous strains that caused outbreaks in 1976 and 1995 in Zaire, now known as the Democratic Republic of the Congo.

In each comparison, the researchers found more than 600 genetic mutations, which account for about three percent of the genome.

The group also found that 10 new mutations that might interfere with the mechanisms of the sequence-based drugs currently being tested and that three of these mutations appeared during the current West African outbreak.

The researchers urged that drug developers should check whether these mutations affect the efficacy of their therapeutic drugs, which are being used to treat small numbers of patients under a World Health Organisation (WHO) emergency protocol.

"The virus has not only changed since these therapies were designed, but it's continuing to change," Kugelman said. "Ebola researchers need to assess drug efficacy in a timely manner to make sure that valuable resources are not spent developing therapies that no longer work."

So far, there have been more than 21,000 Ebola cases with more than 8,300 deaths since the outbreak began last year in Liberia, Sierra Leone and Guinea, according to the WHO.

One in twelve Indians carries a heart failure causing gene mutation

A new study carried out by Loyola University Chicago’s Stritch School of Medicine and published in Loyola University Chicago Stritch School of Medicine has revealed that as many as 8 per cent of Indians and other South Asians carry a gene mutation that is known to cause heart failure and potentially fatal heart attacks.

According to the research, the mutated gene encodes for a protein dubbed cardiac myosin binding protein-C (cMyBP-C). This protein controls cardiac muscle contractions and is critical for the normal functioning of the heart. In the mutated gene, 25 base pairs (DNA letters) are missing. As a result, the tail end of the protein is altered.

The study details how the gene mutation impairs heart’s ability to pump blood. The mutation causes hypertrophic cardiomyopathy, the most common form of inherited cardiac disease and the leading cause of sudden cardiac death in young people. Carriers have about a 80 per cent chance of developing heart failure after age 45.

The results of the study could enable researchers to formulate treatments and prevention strategies for those suffering from this sort of mutation – an estimated 55 million people of South Asian descent including 200,000 people in the United States.

Dr. Sadayappan first reported the mutation in 2001 at the World Congress of the International Society for Heart Research, and has been studying it ever since. He added that based on a report from one of his collaborators, the mutation likely arose in a single person roughly 33,000 to 55,000 years ago. The mutation then spread throughout South Asia.

The research concluded that determining the disease mechanism will enable researchers to develop therapies and this is the “first priority to prevent the development of heart failure in millions of carriers worldwide.”