An outbreak of viral encephalitis occurred in Gorakhpur, India, from July through November 2005. The etiologic agent was confirmed to be Japanese encephalitis virus by analyzing 326 acute-phase clinical specimens for virus-specific antibodies and viral RNA and by virus isolation. Phylogenetic analysis showed that these isolates belonged to genogroup 3.

The mechanism of the Golgi-to-ER transport of Golgi glycosyltransferases is not clear. We utilize a cell line expressing the core 2 N-acetylglucosaminyltransferase-M (C2GnT M) tagged with cMyc to explore this mechanism. By immunoprecipitation using anti-c-Myc antibodies coupled with proteomics analysis, we have identified several proteins including non-muscle myosin IIA (NMIIA), heat shock protein (HSP)-70 and ubiquitin activating enzyme E1 in the immunoprecipitate. Employing yeast-two-hybrid analysis and pulldown experiments, we show that the C-terminal region of the NMIIA heavy chain binds to the 1-6 amino acids in the cytoplasmic tail of C2GnT-M. We have found that NMIIA colocalizes with C2GnT-M at the periphery of the Golgi. In addition, inhibition or knockdown of NMIIA prevents the Brefeldin Ainduced collapse of the Golgi as shown by the inhibition of the migration of both Giantin, a Golgi matrix protein, and C2GnT-M, a Golgi non-matrix protein, to the ER. In contrast, knockdown of HSP-70 retains Giantin in the Golgi but moves C2GnT-M to the ER, a process also blocked by inhibition or knockdown of NMIIA. Also, the intracellular distribution of C2GnT-M is not affected by knockdown of β-coatomer protein with or without inhibition of HSPs, suggesting that the Golgi-to-ER trafficking of C2GnT-M does not depend on coat protein complex-I. Further, inhibition of proteasome results in accumulation of ubiquitinated C2GnT-M, suggesting its degradation by proteasome. Therefore, NMIIA and not coat protein complex-I is responsible for transporting the Golgi glycosyltransferase to the ER for proteasomal degradation. The data suggest that NMIIA is involved in the Golgi remodeling.

Chikungunya fever is an important arboviral infection prevalent throughout Africa and Southeast Asia. Recently, in 2006, it has reemerged in many parts of India, affecting more than a million persons. A detail serological, virological, and molecular investigation of this unprecedented outbreak was carried out by collecting and studying 540 samples from all the affected regions of India during this epidemic. An in-depth investigation revealed the presence of anti-Chikungunya antibodies in 68% of the samples and genomic RNA in 49% of them. In addition 32 Chikungunya viruses were isolated from 45 representative polymerase chain reaction-positive samples. The nucleotide sequences of partial E1 gene of 25 representative Chikungunya viruses were deciphered. The sequence analysis indicated that all the isolates of this epidemic belonged to the new Indian Ocean island clade of East Central South (ECS) African genotype. This study conclusively proved the genotype shift from Asian to ECS African as the major factor in the reemergence of Chikungunya in an unprecedented outbreak in India after a gap of 32 years.

Background:The purpose of this study was to test the role of PKN1 in vascular wall remodeling. Results: PKN1 mediates MCP-1-induced HASMC migration/proliferation and balloon injury-induced neointima formation. Conclusion: PKN1 plays a role in vascular wall remodeling following balloon injury. Significance: PKN1 could be a promising target for the next generation of drugs for vascular diseases such as restenosis.

Plague is one of the world’s most lethal human diseases caused by Yersinia pestis, a Gram-negative bacterium. Despite overwhelming studies for many years worldwide, there is no safe and effective vaccine against this fatal disease. Inhalation of Y. pestis bacilli causes pneumonic plague, a fast growing and deadly dangerous disease. F1/LcrV-based vaccines failed to provide adequate protection in African green monkey model in spite of providing protection in mice and cynomolgus macaques. There is still no explanation for this inconsistent efficacy, and scientists leg behind to search reliable correlate assays for immune protection. These paucities are the main barriers to improve the effectiveness of plague vaccine. In the present scenario, one has to pay special attention to elicit strong cellular immune response in developing a next-generation vaccine against plague. Here, we review the scientific contributions and existing progress in developing subunit vaccines, the role of molecular adjuvants; DNA vaccines; live delivery platforms; and attenuated vaccines developed to counteract virulent strains of Y. pestis.