Hema Gupta

Transmission of enteric non-A, non-B hepatitis virus in Macaca mulatta monkeys by intraportal route: subsequent passages of HEV virus.

Abstract Macaca mulatta monkeys have been used for the transmission of enteric non‐A, non‐B hepatitis (HEV) virus by intraportal route. Subsequent passages of HEV virus have been completed in these monkeys. In the first passage, 2 monkeys were inoculated by intra‐portal route with 27–34 nm virus‐like particles (VLP) obtained from known epidemics of HEV hepatitis in India, and biochemical and serological changes in the blood, histological changes in the liver and excretion of 27–34 nm VLP in the stool were studied. Results were compared with those of 4 negative control monkeys inoculated with stool extracts from healthy individuals. The second passage of 27–34 nm VLP was carried out on 2 monkeys using pools of stool suspension positive for 27–34 nm VLP from first passaged animals. Similarly, the third passage of 27–34 nm VLP was completed intraportally in another monkey. All monkeys developed acute hepatitis, as evidenced by transient elevation of aminotransferases, histopathological changes in the liver, development of antibodies aggregating 27–34 nm VLP and excretion of 27–34 nm VLP in stools. No control monkeys developed these features.

Epidemiology of HBsAg carriers in India. A holistic approach to control of hepatitis-B reservoir

Abstract Morbidity and mortality due to hepatitis B virus (HBV) infection is a matter of concern all over the world. The incidence of HBV infection depends upon the human reservoir particularly located in Asian Pacific and some of the African countries. Knowledge of the epidemiology of HBV infection is essential to formulate a strategy for its control. Six thousand and twenty‐four persons of different categories which included urban, rural, pregnant, non‐pregnant, diabetic, alcoholic and occupational high‐risk groups were tested for HBsAg. Personal and environmental factors contributing to the development of the HBsAg carrier state were studied. It was found that hospital environment, blood transfusion, perinatal transmission and urbanization were the major factors responsible for the spread of the HBV infection. A holistic approach for the control of HBV infection, which should include an improvement of the hospital and urban environment, complete exclusion of commercial blood donors and HBsAg screening of the voluntary blood donors is recommended, while immunoprophylaxis should be reserved for the protection of high‐risk groups and to prevent perinatal transmission.

Entamoeba histolytica: elevated nitroblue tetrazolium reduction activity in polymorphs during amoebic liver abscess

Peripheral blood polymorphonuclear leucocytes (PMN) from patients with invasive amoebiasis, i.e. amoebic liver abscess (ALA) and acute amoebic dysentery, showed marked elevation of nitroblue tetrazolium dye (NBT) reduction. This dramatic change was not observed in PMN from patients with non-invasive amoebiasis, i.e. non-suppurative hepatic amoebiasis, or in asymptomatic Entamoeba histolytica cyst passers. A small number (12%) of patients with viral hepatitis displayed increased NBT reduction. 10 to 12 days after recovery following treatment, the majority (75%) of ALA patients failed to show increased NBT reduction. Our results suggest that the PMN-NBT reduction test could be useful as an aid to the diagnosis of ALA.

Localization of a new enteric non-A, non-B [HEV] virus in target organ liver.

SummaryThirteenMacaca mulatta monkeys were used for transmission of enteric non-A, non-B hepatitis virus (HEV) by the portal vein (PV) route. All these animals developed changes which are found in selflimiting acute viral hepatitis e.g. rise in liver enzymes, the presence of HEV specific viral particles in the stool and histological changes in the liver from 21 to 45 days after HEV inoculation. All the animals recovered completely as reflected by normalization of liver enzymes, and regenerative changes in the liver. The present report highlights the ultrastructural changes in the livers of these experimental monkeys. The histopathological changes included infiltration of lymphocytes and polymorphonucleocytes around the necrotic area, swelling of mitochondria, dilation of smooth endoplasmic reticulum (ER), and presence of 27–34 nm virus particles during the acute phase of the disease. In comparison, 9 control monkeys did not show any such histological changes.

Hepatitis C virus antibody in acute and chronic liver diseases in India

Non-A, non-B hepatitis (NANBH) is the major cause of acute and chronic active hepatitis in India (1). This infection leads to severe liver damage when associated with hepatitis B virus (HBV) infection (2). The etiological agents responsible for NANBH are 2 recently characterised major groups of viruses, i.e. hepatitis-E virus, HEV (3) and hepatitis-C virus, HCV (4). HEV is associated with waterborne hepatitis, HCV is the causative agent of bloodborne hepatitis. It is already established that HEV is the foremost cause of waterborne epidemics of viral hepatitis in different parts of the world. However, the relative roles of HEV and HCV in the causation of acute sporadic hepatitis is not known. The present study was designed to evaluate the prevalence of anti-HCV in sporadic acute and chronic viral hepatitis patients in India. Using Ortho-ELISA kits for anti-HCV, the antibody was tested by the courtesy of Dr T. Uchida (Nihon University, School of Medicine, Tokyo, Japan) in serum samples collected from patients of fulminant hepatitis (n=28), subacute hepatic failure (a= 12) and chronic active hepatitis (n=7). All these patients were positive for HBsAg but negative for IgM anti-HBc and IgM anti-HAV, thus forming a group of HBV carriers without active HBV or hepatitis A virus (HAV) infections. The results of this study demonstrated that antiHCV was present in 45% of fulminant hepatitis, 58% of subacute hepatitis and 43% of chronic active hepatitis patients. These data indicate that HCV infection is quite frequent in India. However, at present, it appears difficult to explain such a high prevalence of anti-HCV in fulminant and subacute hepatitis patients, which is in contrast to the earlier reports that anti-HCV is present only in 15-25 Yo (5) of cases with acute infection. Presumably presence of HBsAg helps in aggravating the situation by enhancing host immune response vs. HCV leading to high anti-HCV positivity in acute infections. These antibodies may be involved in the pathogenesis of liver causing a massive liver damage. This is also supported by our earlier findings of high morbidity and mortality in the patients with superimposed NANB infection in HBV carriers (2).