Syed Akbar
Hyderabad, Feb 13: The novel human influenza A virus, which is currently creating problems in north India particularly Delhi, may evolve into a "supervirus" with unique genetic make-up, infecting and replicating in multiple hosts.
This supervirus may develop resistance to all know anti-viral drugs, warn city biologists, adding that "future preparedness is mandatory".
A team of scientists from the city-based Centre for Cellular and Molecular Biology, Vellore Institute of Technology and Florida International University, Miami, USA, found that the novel influenza virus A/H1N1/2009 attaches to the same glycosylation receptor sites as its predecessor influenza A/H1N1/2008 virus.
"But it is antigenically different and may have the potential for initiating a significant pandemic". The study may facilitate the development of better therapeutics and preventive strategies, as well as impart clues for novel H1N1 diagnostic and vaccine development.
The researchers' team comprising Dr Shailendra K Saxena, Dr Niraj Mishra, Dr Rakhi Saxena, Dr ML Arvinda Swamy and Dr Shrish Tiwari noted that the evolution of H1N1 2009 by triple reassortment (from three different hosts and co-infections with other influenza A viral strains) is an alarming concern "because it suggests that the virus is not only assorting in multiple hosts, but also getting more chances to reassort in humans".
Along with antigenic shift and antigenic drift, H1N1 may evolve into a novel influenza A supervirus, which may be antigenenically unique, the study pointed out adding that it may transmit as well as infect and replicate in multiple hosts. "It may have resistance to known antivirals. Therefore, future preparedness is mandatory. Long-term preventive measures should be considered along with short-term prevention".
According to the scientists, the antigenic analysis showed H1N1 strains of 2009 and 2008 have large differences in antigenicity. This finding might be correlated with the large penetrance of H1N1/2009 because this strain has novel antigenicity. Therefore, the human population lacks herd immunity.
Co-infections during bouts of influenza might play a crucial role in the evolution of H1N1 and may cause the development of resistance to known antivirals. "This virus, therefore, can be used to study the involvement of new determinants, which may help us to develop effective vaccines against lethal H1N1 strains," the scientists observed.
The team members emphasised the need for studies on the evolution of H1N1 immunity, as for the first time, they provided evidence that H1N1/2009 uses the same glycosylation sites as its predecessor H1N1/2008 and may have a potential to initiate a more seriously mortal pandemic, owing to its antigenic difference with H1N1/2008.
"Our study may facilitate the development of better therapeutics and preventive strategies," they said.
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