Salivirus in children with diarrhoea, western IndiaAcute gastroenteritis or infectious diarrhoea is one of the most common diseases affecting children less than 5 years of age and leads to significant morbidity and mortality worldwide, especially in developing countries. 1 Recent studies have revealed that on average up to 40% of diarrhoea cases are of unknown aetiology. 2,3 Salivirus (SalV), also known as klassevirus, a member of the genus Salivirus in the family Picornaviridae, 4 was a relatively recent discovery in stool samples of children with gastroenteritis in the USA in the year 2009. 5 SalV has been found in faecal samples from patients with gastroenteritis in various countries, with a frequency ranging from 0.1% to 8.7%. 6,7 The occurrence of a second type of SalV, A2, was reported after this was detected in sewage samples in Thailand in 2012. 8 Although there are reports suggesting gastroenteritis in infants caused by SalV, 9 as well as its actual prevalence in infants and children, the epidemiology of the virus and its pathogenesis remain unclear.SalV was detected in 16 samples from the community and nine samples from hospitals, in a multicentre study in Vellore, South India during the years 2005-2006, demonstrating klassevirus infection and replication in humans. 10 There appears to have been no further report of SalV detection in India.During an ongoing study by the National Rotavirus Surveillance Network (NRSN) supported by the Indian Council of Medical Research (ICMR), two clinical recruitment sites located in Belagavi (an urban region in Karnataka) and Karad (a rural region in Maharashtra) in western India were investigated to estimate the presence of SalV in children 0-59 months of age hospitalized with diarrhoea as a primary cause of illness. The investigation took place between January and December 2014.A total of 468 faecal samples were collected along with clinical and demographic information, after written informed consent/ assent was obtained and following institutional ethics committee approval at the respective clinical recruitment sites and RMRC, ICMR, Belagavi, Karnataka, India. Faecal samples were suspended to 30% in phosphate-buffered saline (PBS), and viral RNA was extracted using a QIAamp Viral RNA Mini Kit (Qiagen Sciences, Valencia CA, USA). RNA was then converted to complementary DNA (cDNA) using a reverse transcription (RT) kit (Applied Biosystems, Foster City, CA, USA) and random primers (Applied

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Introduction: Type 3 Von Willebrand Disease (VWD) is the least common but the most severe form of a disease, with a prevalence of about 0. 5 to 1 per million in Western countries. The prevalence of type 3 VWD in the developing countries, with a high degree of consanguinity, is about 6 per million. Moreover, due to underdiagnosis of the milder cases, the prevalence of type 3 VWD is about 50% of the cases. Rarely, some patients develop the Von Willebrand Factor (VWF) inhibitors, which may subsequently develop severe anaphylactic reactions on further exposure to the VWF containing factor replacement therapy. The prevalence of inhibitor development in patients with type 3 VWD has been shown to be in the range of 5.8 to 9.5%. In the absence of a gold standard assay for the quantitation of VWF inhibitors, a correct diagnosis and management of these patients are often challenging.Objectives: The objective of this study is to standardize the Bethesda assay for the VWF inhibitors and to estimate the VWD inhibitor titer in two cases of congenital type 3 VWD, which developed the VWF inhibitors.Results and Conclusions: We could successfully standardize the Bethesda assay for the quantitation of VWF inhibitors in two patients with congenital type 3 VWD with inhibitors.