Human herpesvirus-8 K8.1 gene encodes for two immunogenic class I glycoproteins, K8.1A and B, originating from spliced messages [(1998) Virology 243, 208-217]. The 228-amino-acid-long K8.1A open reading frame (ORF) contains four N-glycosylation sites and the 167-amino-acid-long K8.1B ORF contains three N-glycosylation sites, sharing similar amino- and carboxyl-termini with ORF K8.1A but with an in-frame deletion [(1998) Virology 249, 140-149]. To characterize the K8.1A and B glycoproteins in the infected body cavity-based B cell lymphoma (BCBL-1) cells and in the virion envelopes, monoclonal antibodies (MAbs) recognizing only K8.1A protein or both K8.1A and B proteins were generated. These antibodies reacted with the infected cell membranes and virion envelopes. Stable COS-1 transformant cells expressed the K8.1A and B proteins independently on the plasma membranes. MAbs recognized multiple proteins with molecular weights ranging from 23 to 72 kDa from the BCBL-1 cells and COS-1 cells and the 72 to 68 kDa molecular-weight proteins from the virion particles. The K8.1A is the predominant protein affinity purified from the infected BCBL-1 cells. Digestion with glycosidases show that these proteins contain both N- and O-linked sugars, suggesting that the multiple proteins recognized by the MAbs represent the precursor and product forms of K8.1A and B proteins, and the 72 to 68 kDa molecular-weight proteins represent the virion particle-associated mature forms of these glycoproteins.

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The Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) represent family of structurally-related eukaryotic transcription factors which regulate diverse array of cellular processes including immunological responses, inflammation, apoptosis, growth & development. Increased expression of NF-kB has often been seen in many diverse diseases, suggesting the importance of genomic deregulation to disease pathophysiology. In the present study we focused on acute kidney injury (AKI), which remains one of the major risk factor showing a high rate of mortality and morbidity. The pathology associated with it, however, remains incompletely known though inflammation has been reported to be one of the major risk factor in the disease pathophysiology. The role of NF-kB thus seemed pertinent. In the present study we show that high dose of folic acid (FA) induced acute kidney injury (AKI) characterized by elevation in levels of blood urea nitrogen & serum creatinine together with extensive tubular necrosis, loss of brush border and marked reduction in mitochondria. One of the salient observations of this study was a coupled increase in the expression of renal, relA, NF-kB2, and p53 genes and proteins during folic acid induced AKI (FA AKI). Treatment of mice with NF-kB inhibitor, pyrrolidine dithio-carbamate ammonium (PDTC) lowered the expression of these transcription factors and ameliorated the aberrant renal function by decreasing serum creatinine levels. In conclusion, our results suggested that NF-kB plays a pivotal role in maintaining renal function that also involved regulating p53 levels during FA AKI.

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