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“Survival of the fittest” is an old axiom laid down by the great evolutionist Charles Darwin and microorganisms seem to have exploited this statement to a great extent. The ability of viruses to adapt themselves to the changing environment has made it possible to inhabit itself in this vast world for the past millions of years. Experts are well versed with the fact that influenza viruses have the capability to trade genetic components from one to the other within animal and human population. In mid April 2009, the Centers for Disease Control and Prevention and the World Health Organization had recognized a dramatic increase in number of influenza cases. These current 2009 infections were found to be caused by a new strain of influenza type A H1N1 virus which is a re-assortment of several strains of influenza viruses commonly infecting human, avian, and swine population. This evolution is quite dependent on swine population which acts as a main reservoir for the reassortment event in virus. With the current rate of progress and the efforts of heath authorities worldwide, we have still not lost the race against fighting this virus. This article gives an insight to the probable source of origin and the evolutionary progress it has gone through that makes it a potential threat in the future, the current scenario and the possible measures that may be explored to further strengthen the war against pandemic.

Acute tropical pulmonary eosinophilia (TPE) is characterized by wheezing, pulmonary infiltrates, marked peripheral blood eosinophilia, and very high serum levels of filaria-specific antibodies. To evaluate the amount and character of the filaria-specific antibodies in the lungs in this disorder, bronchoalveolar lavage was carried out in individuals with acute TPE, in normal subjects, and in patients with elephantiasis or asthma. Striking elevations of total IgE were found in the lower respiratory tract epithelial lining fluid (ELF) of patients with TPE along with high levels of filarial-specific IgG, IgM, and IgE. When patients with acute TPE weretreated with diethylcarbamazine and evaluated again 6–14 d later, there was marked reduction in ELF parasite-specific IgG and IgE, which paralleled a rapid clinical response. Immunoblot comparison of the antigen recognition patterns of ELF and serum antibodies demonstrated a general similarity in parasite antigens recognized, but the lung IgE and IgG antibodies appeared to recognize only a certain subset of the parasite antigens recognized by serum antibodies. Thus, a profound antibody response to filarial infection is found in the lungs of patients with TPE, suggesting that these filaria-specific antibodies play an important role in the pathogenesis of this disorder.