Decoding the cold bug: why most drugs don’t work

Decoding the cold bug: why most drugs don’t work
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First Published: Fri, Feb 13 2009. 12 45 AM IST

Updated: Fri, Feb 13 2009. 12 45 AM IST
Bangalore: Scientists may be a step closer to solving one of mankind’s enduring mysteries, and one most men and women have to endure—the common cold, an infection that causes sneezes and sniffles, yet remains unaffected by drugs.
Decoding the genetic make-up of more than 100 strains of the common cold bug—rhinovirus—collected from all over the world, a team of US scientists has created a family tree of the viruses and is using this to demonstrate how distantly related viruses can recombine and produce new strains.
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In Friday’s issue of the journal Science, scientists report that human rhinoviruses (HRV) are organized into about 15 small groups that come from two broad species categories— types A and B. A new species, type C, is also being reported for the first time and researchers suspect another new type D is also lurking somewhere.
“The discovery of these multiple groups explains why a one-drug-fits-all approach for antiviral agents does not work,” says Stephen B. Liggett, a co-author of the study who is at the University of Maryland School of Medicine in Baltimore.
The new data provides scope for development of several antiviral drugs, which would target specific genetic regions of certain groups; and the choice of drug would depend on the genetic nature of a patient’s rhinovirus, Liggett suggests.
The genomes of 99 strains, from the repository of frozen HRV strains taken from patients over a period of two decades, were completed and analysed. Additionally, 10 new strains were taken from the field.
“It is a very good piece of work where the genetic information is nicely curated through bioinformatics to present details of the genome architecture that are common across HRV — A, B, and C, as also the differences between the A, B, and C species,” says Shahid Jameel, senior virologist at the International Centre for Genetic Engineering and Biotechnology, New Delhi.
Understandably, this is leading to new insights. For instance, it can now be explained why no effective treatment exists or why a person feels sick soon after the infection, the latter being due to the fact the virus skips a step when it makes its protein product. It is also becoming clear that new strains, with “dramatic” properties, may develop as viruses swap their genetic material.
The new type C is seen to have many more mutations (800) compared with the older frozen strains, which, some argue, could make it more virulent and hence capable of infecting cells deep in the lungs.
But, Jameel says, the viruses of HRV-C analysed thus far are too few (only seven) to conclusively say that HRV-C is more virulent. “It just happens that all uncharacterized and uncultured viruses obtained from severe flu-like illnesses turned out to be HRV-C. Disease symptoms depend not just on the virus, but also on how the host (patient) responds to the infection.”
Common cold is often dismissed as a nuisance, but doctors say it can be debilitating, particularly in the very young and in older individuals. Besides being a factor in bronchitis, sinusitis, middle-ear infections and pneumonia, HRV is also responsible for half of all asthma attacks. “This (asthma correlation) could be even higher in India, as people from lower income groups catch more infection than the middle and higher income groups,” says Naval K. Vikram, professor of internal medicine at the All India Institute of Medical Sciences, New Delhi.
In the US, the direct and indirect cost of common cold and asthma-related complications amounts to about $60 billion (Rs2.9 trillion) per year. No such analysis has been done in India, Dr Vikram says, but the problem is serious, with people, on average, catching three-five infections in a year. According to the latest Report of the National Commission on Macroeconomics and Health, the annual economic burden of asthma in India is estimated to reach Rs10,641 crore in 2011, up from Rs7,641 crore in 2006.
Since the HRVs—also called the “nose viruses” after the Greek word “rhino” meaning nose—are usually not life-threatening, serious investment has not gone into them. But the new data will be helpful in finding the conserved regions in the viral genome, says Sunit K. Singh, scientist at the Centre for Cellular and Molecular Biology, Hyderabad, who works on infectious diseases and immunobiology. “These regions (which do not undergo mutation) could serve as targets for antiviral drugs and vaccine.”
In fact, vaccines for the cold, which were unthinkable so far, are already a subject of study at Liggett’s lab as his team gathers multiple-patient samples to see how frequently HRVs mutate during a cold season. In terms of evolutionary knowledge, says Singh, the family tree will help understand the relationship among the different strains of HRV.
In the Indian context, says Jameel, we need to generate data on HRV infections in children, adolescents and adults from different parts of the country, and in a seasonal manner. “We should screen severe flu-like cases for HRV to see if we also find HRV-C associations.”
Chart by ‘Science’ and image by University of Wisconsin, Madison
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First Published: Fri, Feb 13 2009. 12 45 AM IST