Trend of Japanese encephalitis in North India: evidence from thirty-eight acute encephalitis cases and appraisal of niceties.

BACKGROUND: In the year 2005, an epidemic of Japanese encephalitis (JE) occurred in the northern states of India. The present study was planned to reconfirm the circulation of JE in the area and to assess the trend of the disease to slow down the burden of JE. METHODOLOGY: Surveillance was conducted to identify patients with acute encephalitis. Blood and cerebrospinal fluid specimens from suspected cases underwent pathological, serological, and demographic investigations. Viral testing for evidence of Japanese encephalitis virus (JEV) infection was also performed, either by IgM capture ELISA/RT-PCR or both. To identify circulating JEV strains, RT-PCR, sequencing and phylogenetic analysis was performed. Based on clinical cases reported between 1992 and 2008, the trend of JE infection in the state was analyzed to examine the dynamics of infection. RESULTS: Our investigations (n = 38) revealed that only 55.3% cases were positive for JE. Pathological examination revealed marked pleocytosis in CSF (90+/-76.9 cells/mm(3)), and peripheral leucocytosis (64.7+/-8.86% neutrophils) with mild anemia. Males were more susceptible than females with a ratio of 1.63:1 and significant gender difference (P<0.05) was observed in patients below six years. In the patient group younger than six years, the rate of infection per million was six-fold higher (P<0.005) in males as compared to females. Our phylogenetic study suggests that the circulating strain during the 2005 JE epidemic was close to GP78, and in the future a larger epidemic may occur. CONCLUSIONS: The 2005 JE epidemic was possibly caused by JEV GP78 and it is spreading into newer areas. The trend of JE suggests that the problem in North India is escalating and larger epidemics may occur in the future; therefore, serious steps are necessary to combat JE, including the development of more efficient surveillance methods and differential diagnosis.

Structural and antigenic variance between novel influenza A/H1N1/2009 and influenza A/H1N1/2008 viruses.

BACKGROUND: The emergence of influenza A/H1N1/2009 is alarming. The severity of previous epidemics suggests that the susceptibility of the human population to H1N1 is directly proportional to the degree of changes in hemagglutinin/HA and neuraminidase/NA; therefore, H1N1/2009 and H1N1/2008 were analyzed for their sequence as well as structural divergence. METHODOLOGY: The structural and sequence divergence of H1N1/2009 and H1N1/2008 strains were analyzed by aligning HA and NA amino acid sequences by using ClustalW and ESyPred3D software. To determine the variations in sites of viral attachment to host cells, a comparison between amino acid sequences of HA and NA glycosylation sites was performed with NetNGlyc software. The antigenic divergence was executed by CTL epitope prediction method. RESULTS: The amino acid homology levels of H1N1/2009 were 20.32% and 18.73% compared to H1N1/2008 for HA and NA genes, respectively. In spite of the high variation in HA and NA amino acid composition, there was no significant difference in their structures. Antigenic analysis proposes that great antigenic differences exist between both the viral strains, but no addition of a new site of glycosylation was observed. CONCLUSIONS: To our knowledge, this is the first report suggesting that the circulating novel influenza virus A/H1N1/2009 attaches to the same glycosylation receptor sites as its predecessor influenza A/H1N1/2008 virus, but is antigenically different and may have the potential for initiating a significant pandemic. Our study may facilitate the development of better therapeutics and preventive strategies, as well as impart clues for novel H1N1 diagnostic and vaccine development.