H1N1 is now a household name. The 4th pandemic flu is making headlines. The flu phobia is visible and mask mania is disturbing.
Obviously this is due to the horrific memory of millions of deaths within months during previous pandemics including the first one in 1918 caused by H1N1. What really are H1 and N1 and why are they important to flu virus and our understanding?
Surface proteins
Like viruses in general, H1N1 depends on its outer surface proteins to infect host cells.
In swine flu virus these are Haemagglutinin (H) and Neuraminidase (N). To survive the virus, the host produces antibodies to these two proteins and inactivates them.
The virus, however, modifies the protein surfaces subtly by genetic mutations and escapes the antibodies. The new strain can therefore cause disease even in survivors of previous attacks.
The numbers denote various forms of these two proteins.
In the case of H1 and N1, the numbers refer to the first type of Haemagglutinin and Neuraminidases identified in the isolates of the virus from the first pandemic.
Since the isolates from different geographical regions or at different times or from animals either did not react with the antibodies to H1 and N1 or reacted only to either one, the new ones were denoted chronologically as H1N2, H2N1, H2N2 (caused Asian flu, 1956-58), H3N2 (caused Hong Kong flu 1968-69), H3N3 etc. There are 16 different H types and 9 different N types known currently.
As the name suggests, Haemagglutinin agglutinates haemoglobin-containing red blood cells by binding to a sugar compound on its surface. The sugar, called Sialic acid, is common and abundant in many cell types, allowing the virus to cause wide-spread damage.
The largest surface area makes respiratory system the most vulnerable. Upon binding to Silaic acid, Haemagglutinin changes shape and mediates viral entry by bringing about fusion of the viral and host surfaces.
Neuraminic acid is another name for Sialic acid. Neuraminidase breaks down Sialic acid, the very compound that Haemagglutinin binds to. Though this appears counter-productive, it actually prevents the newly released viruses binding to dead cells causing non-productive infection.
Though Neuraminidase is not essential for viral infection, its combination with Haemagglutinin is lethal. Since both vary in their structure and effectiveness, the numbers associated with the two letters (H and N) has special significance to virulence. Association of certain combinations with worse epidemics and possibility of new combinations keep us vigilant against flu virus.
Tamiflu and Relenza are neuraminidase inhibitors that prevent viral spread between cells and help reduce the duration and severity of the disease.
Resistance due to structural alteration of Neuraminidase and adverse side effects demand restricted use of these drugs only under prescription.
Vaccination is a viable option, but stockpiling vaccine against a particular type is not possible due to variants (indicated by the notation). Preparations take time even after the viral type is known; Vaccine for H1N1 is expected in a few months. Inflammation (severe host immune response evident from early symptoms) to eliminate germs also destroys body tissues and hence it should be contained promptly with effective anti-inflammatory therapy. The cure rate is almost 100 per cent.
Finally, “Swine virus Flu” appears a misnomer (in Tamil it sounds derogatory).
It could be called Mexican Flu, indicating the origin of the outbreak, as in previous instances.
The peak is expected in the winter months, but can be effectively managed.
Prof. K. SANKARAN Centre for BiotechnologyAnna UniversityChennai
