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J E Maynard

Publications and source records attributed to J E Maynard.

At least 91 records · Page 5Linked to original sources
PubMed1981

Pathogenetic aspects of hepatitis A virus infection in enterally inoculated marmosets.

Experimental hepatitis A virus (HAV) infection was studied in marmosets after enteral (intragastric) inoculation with special reference to the primary sites of HAV replication and immunopathology of the disease. The experiment was carried out using 28 Saguinus mystax negative for antibody to HAV (anti-HAV) and with statistically uniform baseline values of serum isocitrate dehydrogenase (SICD) activity. Each animal was infected with 1 ml of a 15% w/v stool suspension that was derived from marmosets infected with the third or fourth passage of the MS-1 strain of HAV. The incubation period measured by the first significant SICD elevation was 32 days in 11 of 13 marmosets. The animals were sacrificed 2, 4, 7, 11, 14, 18, 23, 28, and 32 days after inoculation and 1, 4, 8, 14, 21, 28, and 35 days after SICD elevation. HAV antigen, immunoglobulins, complement, and fibrin were identified in the liver, eight segments of the gastrointestinal tract, lymphoid system, and kidneys. HAV antigen was found only in the cytoplasm of hepatocytes and in gallbladder bile. These findings indicated that the liver was the sole and primary site of virus replication. Combined immunomorphologic and histopathologic observations also revealed that HAV antigen localization was associated with the sites of hepatocellular damage. There was no immunomorphologic evidence for humoral immune clearance of HAV antigen in the liver, lymphoid system, or kidneys.

Animals↗
PubMed1981

Persistent non-A, non-B hepatitis in experimentally infected chimpanzees.

Non-A, non-B (NANB) hepatitis was transmitted to six chimpanzees by intravenous inoculation of antihemophilic (factor VIII) materials, acute-phase chimpanzee liver, and chronic-phase plasma obtained from two NANB hepatitis-infected chimpanzees 10 and 16 months, respectively, after their inoculation. Five of six experimentally infected chimpanzees observed for more than one year demonstrated persistent or intermittent elevations in levels of serum alanine aminotransferase (ALT) indicative of continuing liver dysfunction. Liver biopsy specimens obtained from three chimpanzees with persistent elevations in levels of ALT were positive for hepatocyte cytoplasmic structures associated with NANB hepatitis for as long as 27 months after inoculation. Liver biopsy specimens obtained from four infected animals 13-30 months after inoculation also showed mild but persistent histopathologic lesions of undefined character. The detection of circulating immune complexes in one chimpanzee with persistent elevations in levels of ALT suggests that these complexes may be involved in the pathogenesis of NANB hepatitis.

Animals↗
PubMed1981

Hepatitis B testing in the families and villages of five young eskimos with primary hepatocellular carcinoma.

A 15-year-old female Eskimo and a 22-year-old male Eskimo from a southwestern Alaskan village (population 540) were diagnosed as having primary hepatocellular carcinoma (PHC) in December, 1977. The fathers of both patients also died of PHC. Three additional cases of PHC affecting young Alaskan Eskimos had been diagnosed since 1972, all from neighboring villages. Four of the five young patients were positive for hepatitis B surface antigen (HBsAg), and the family members of three patients were all positive for HBsAg or antibody to this antigen (anti-HBs). The other two families had no members positive for HBsAg. The prevalence of HBsAg in the villages of these patients ranged from 0--5%, and the prevalence of anti-HBs ranged from 3--25%. This part of Alaska has a high rate of infection with hepatitis B virus and an increased incidence of PHC. However, other Alaskan villages of similar ethnic background have considerably higher rates of hepatitis B infection than the four villages described and to date they have no PHC. This suggests that genetic and/or environmental factors in addition to hepatitis B infection may have a role in the etiology of PHC in Alaska.

Adolescent↗
PubMed1981

An outbreak of hepatitis B in a dental practice.

In September 1978, cases of hepatitis B in two patients treated by the same dentist led to investigation of a dental practice in Baltimore, Maryland. The dentist had had acute hepatitis B in June 1978 and had remained positive for hepatitis B surface antigen and hepatitis B e antigen over the ensuing 6 months. He had continued to work while infected, wearing surgical gloves to minimize the risk of transmitting infection. Serologic follow-up of 764 patients showed that a total of six patients, three of whom were symptomatic, had developed hepatitis B infection after dental treatment. All six were among a group of 395 patients treated before the dentist began wearing gloves. In this group, patients having highly traumatic dental work (attack rate 6.9%) were at significantly higher risk than patients having either less traumatic work (attack rate 0.5%) or nontraumatic work (attack rate = 0, p less than 0.02). None of 369 patients treated only when the dentist wore gloves became infected, suggesting that gloves could reduce the risk of virus transmission by the dentist.

Adolescent↗
PubMed1980

Vasculitis in Eskimos living in an area hyperendemic for hepatitis B.

Six cases of hepatitis B-associated vasculitis occurred during a four-year period in Eskimos living in southwest Alaska, an area hyperendemic for hepatitis B. All showed positive results in tests for hepatitis B surface antigen (HBsAg), and all five patients tested for hepatitis B e antigen (HBeAg) showed positive values. Two patients died of the disease. Of three who recovered, two had positive values for HBsAg and HBeAg when tested two years later. In the villages of four patients, the prevalence of hepatitis B virus (HBV) infection ranged from 18.2% to 73.1%. Serological evidence of HBsAg was found in 22% and antibody to HBsAg (anti-HBs) in 30% of close relatives of the patients. Two patients had no previous serological evidence of infection with HBV, indicating that vasculitis followed recent infection. The results provide epidemiologic evidence of the clinical association between HBV infection and vasculitis.

Adolescent↗
PubMed1980

Hepatitis A in day-care centers. A community-wide assessment.

We investigated the spread of viral hepatitis in day-care centers in Maricopa County, Ariz. Over a 10-month period, 398 (40 per cent) of 1008 reported cases of hepatitis Type A or viral hepatitis of unspecified type occurred in persons closely associated with day-care centers. Outbreaks of hepatitis comprising 310 cases were identified in 30 of 308 centers in the county. In 28 outbreaks investigated, the majority of symptomatic cases occurred in household contacts or close relatives of children who attended day-care centers, with 16 per cent of the cases occurring in children who attended the centers and 15 per cent occurring in employees. Hepatitis in both employees and household contacts was strongly related to contact with children one to two years of age who attended the centers (P less than 0.001). Day-care centers appear to be important in the spread of hepatitis A in the United States.

Adolescent↗
PubMed1980

Distribution of hepatitis B e antigen (HBeAg) and anti-HBe in carriers with different levels of HBsAg.

Blood samples from 154 asymptomatic carriers of HBsAg were studied for the presence of HbeAg and anti-HBe using techniques of rheophoresis and a micro solid phase radioimmunoassay (micro-SPRIA). The level of HBsAg in each sample was determined by titration using reverse passive hemagglutination (RPHA) test. The significance of relationship between the titer of HBsAg, HBeAg, anti-HBe, and anti-HBc were statistically analyzed. Micro-SPRIA detected almost twice as many reactives for HBeAg and anti-HBe as were found by rheophoresis; the difference in sensitivity was significant (P less than 0.001). The mean HBsAg titer of 41 samples reactive for HBeAg was 11,181, while it was 3,032 for 92 samples reactive for anti-HBe. The remaining 23 samples with no detectable HBeAg or anti-HBe had a mean HBsAg titer of 1,018. The differences in the distribution of HBsAg among the three categories is statistically significant (P less than 0.005). HBeAg was most likely to be found in samples with higher concentrations of HBsAg.

Antibodies, Viral↗
PubMed1980

Non-A/non-B hepatitis in experimentally infected chimpanzees: cross-challenge and electron microscopic studies.

Inoculation of eight chimpanzees with factor VIII, factor IX, or "H" strain plasma resulted in enzymatic and histopathologic evidence of non-A/non-B hepatitis in all eight animals. Challenge of two chimpanzees convalescent from factor VIII-induced disease with either factor IX or "H" strain plasma resulted in non-A/non-B hepatitis only in the animal inoculated with factor IX materials. Reciprocal cross-challenge of a chimpanzee convalescent from factor IX-induced disease with factor VIII also produced unequivocal enzymatic and histopathologic evidence of non-A/non-B hepatitis. Cross-challenge of a chimpanzee convalescent from "H" strain-induced non-A/non-B hepatitis with factor VII did not cause a second bout of non-A/non-B hepatitis. These findings suggest the factor VIII materials and "H" strain plasma used in these studies share a common etiologic agent (or agents), but that factor VIII and factor IX may contain two distinct agents. Electron microscopic (EM) examination of thin-sectioned, acute-phase liver biopsies from all but one of the chimpanzees receiving the primary inocula revealed the presence of abnormal hepatocyte cytoplasmic structures previously shown to be associated with non-A/non-B hepatitis. Crystalline structure containing 25 to 30 nm particles were visualized by EM in the cytoplasm of endothelial or Kupffer cells in acute-phase liver biopsies obtained from three chimpanzees inoculated with either factor VIII materials or "H" strain plasma.

Animals↗
PubMed1979

Experimental infection of chimpanzees with antihemophilic (factor VIII) materials: recovery of virus-like particles associated with non-A, non-B hepatitis.

Non-A, non-B viral hepatitis was transmitted to four colony-born chimpanzees by infusion of three lots of antihemophilic factor (factor VIII) implicated in the transmission of non-A, non-B hepatitis to two human recipients. All four inoculated animals showed histopathological evidence of viral hepatitis, and all demonstrated significant ALT elevations between seven and one-half weeks after inoculation. Acute-phase plasma from one of the infected chimpanzees (no. 771) was shown to induce non-A, non-B hepatitis in two other chimpanzees approximately three weeks after their inoculation. In addition, an acute-phase open liver wedge biopsy obtained from animal no. 771 was processed and examined by immune electron microscopy (IEM) for virus-like particles with convalescent serum from a serologically confirmed case of non-A, non-B hepatitis. Twenty-five to 30 nm (mean = 27 nm) diameter virus-like particles that were either "full" or "empty" were identified in this liver preparation by IEM. Two additional chimpanzees inoculated with a cesium chloride gradient fraction of an isopycnically banded liver homogenate (animal no. 771) also developed elevated ALT activity two to two and one-half weeks later. Our findings have experimentally verified that commercially produced factor VIII materials can induce non-A, non-B hepatitis in champanzees and that the disease can be subpassaged in these animals by inoculation of either acute-phase plasma or liver. These results also provide evidence for the association of 27 nm-diameter virus-like particles with non-A, non-B viral hepatitis.

Adult↗
PubMed1979

Stability of a reference panel of lyophilized hepatitis B antigens and antibodies.

A lyophilized hepatitis B working/reference panel has been prepared for use in standardization tests. This panel includes HBsAg, anti-HBs, HBeAg/anti-HBe and subtype reagents. Quantitative analysis of the HBsAg reagents indicates that at a storage temperature of -20 degrees C, only 1 log at maximum of RIA counts per minute would be lost in 95 years. After storage at -20 degrees C for 1 year, there has been no loss of reactivity in any of the tests used to detect HBsAg, anti-HBs, HBeAg/anti-HBe or subtypes.

Antibodies, Viral↗