Dengue virus is a major health problem in Nepal. The endogenous dengue appeared in 2006 in the country with reported outbreaks in 2010, 2013 and 2016. Eleven years vertical data show there were sporadic cases in all the years and mostly adults between 25 and 40 years of age were infected with dengue virus. Compared with primary infections, secondary infections were observed in relatively larger numbers during the period of 2008-2016. Most of the cases had symptoms of dengue fever; while 7 and 19 cases demonstrated dengue hemorrhagic fever/dengue shock syndrome in 2010 and 2013 respectively. The proportion of dengue hemorrhagic fever amongst all cases of dengue fever was 2.5:4.7% in 2010 and 2013. We found there is shift of serotype from dengue virus serotype-1 (DENV-1) in 2010, DENV-2 in 2013 and DENV-1 in 2016. We feel there is urgent need for better community, hospital and laboratory based surveillance system capable of monitoring the circulating dengue virus (DENV) serotypes in different districts of Nepal. With improvement in surveillance system and efficient management of cases, the case fatality rate due to severe dengue can be reduced.

The aim of this study was to detect the prevalence of hepatitis E virus (HEV) in healthy blood donors so as to decipher the maintenance of (HEV) reservoir if any. Five hundred and eighty-one blood samples along with clinical information were collected from central blood bank, Kathmandu between February and March 2014. Samples were tested for hepatitis B virus surface antigen, anti-hepatitis C virus antibodies, anti-hepatitis A virus IgM, HEV antigen, HEV viral load and anti-HEV antibodies (IgM and IgG) by ELISA. Only those samples positive with anti-HEV IgM were tested for HEV RNA by reverse transcriptase nested PCR. Age adjusted prevalence of IgM anti HEV and IgG anti HEV were 3.6 and 8.3 % respectively. No significant difference in Median ALT levels was noted between HEV RNA positive and negative subjects. Sequence analysis of HEV shows all genotype belongs to genotype 1a. Phylogenetic analysis shows the virus has homology of 95 % with strain from India and Nepal outbreak of April 2014. This study sheds light on how inter epidemic reservoirs can be maintained in healthy population with asymptomatic cases. This raises an important question regarding nature of HEV as well as its tendency to circulate in blind sight and also cause periodic outbreaks in endemic setting like Kathmandu.Keywords HEV Á Nepal Á Blood donors Hepatitis E virus (HEV) infection is endemic in Kathmandu Valley the capital of Nepal. Four epidemics have been documented so far during 1973, 1981-1982, 1987 and 2005-2006 and variable numbers of sporadic acute hepatitis E occurred in between [4]. There have been decline in number of acute hepatitis E cases in recent years and hepatitis A infection has outnumbered HEV as an etiology of acute hepatitis in adults [3]. What maintains the virus in the population during low incidence period of acute hepatitis is a matter of debate. There are some evidences that rodents may serve as animal reservoirs for HEV [2].Occurrence of HEV viremia in healthy blood donors has been increasingly reported across the globe mainly from Europe [5], and China [1] where genotype 3 and 4 predominate. To explore the possibility of HEV viremia in healthy blood donors of Nepal, we collected blood samples along with demographic data from 581 healthy voluntary blood donors from central blood bank, Kathmandu, Nepal during February-March 2014. Study subjects constituted 401 men and 180 women volunteer blood donors. Median age of the subjects was 35 years (range 18-55). Elevated ALT levels ([40 IU/L) were noted in 81(13.9 %) with median ALT value of 23 IU/l (range 5-98 IU/L). IgG anti-HEV was detected in 56 samples (9.5 %) and IgM anti-HEV was detected in 27 samples 4.6 %). When adjusted for the age the prevalence of IgM anti HEV and IgG anti HEV were 3.6 and 8.3 % respectively. No significant difference in Median ALT levels was noted between HEV

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Duchenne muscular dystrophy (DMD) is X-linked recessive neuromuscular disorders caused due to mutation in dystrophin gene, leading to progressive muscle weakness. This study was done to identify mutation in dystrophin gene in Nepalese patients with DMD using Multiplex Ligation Dependent Probe Amplification (MLPA) assay in Nepal. Twenty one patients from different regions of Nepal, who were clinically diagnosed as DMD were enrolled in the study. Peripheral blood samples were collected in EDTA vials, gDNA was extracted, and deletion mutation in the dystrophin gene was analysed using Multiplex Ligation Dependent Probe Amplification (MLPA) assay. Exon deletion mutation in the dystrophin gene was observed in 14 (66.6%) out of 21 DMD cases. The most common exon deletion was observed and confined in exon 7-14 and 45-53 of dystrophin gene. The location of deletion in dystrophin gene is apparently non-random with a preponderance found in the hot spot regions. Use of MLPA is useful in detecting copy number changes in DMD proband and suspected carriers in Nepal.