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In 1946, Merle Curti's The Roots of American Loyalty offered a narrative history of American patriotism, tracing a "pattern of emotions and ideas" from the eighteenth century up to World War II (p. ix). Curti sought to promote a "more intelligent and understanding patriotism" in contrast to the "blind unthinking love of country" that he saw embodied in veterans groups and hereditary societies' identification of loyalty to America with militarism, nativism, and free-market capitalism (p. vii). But in the half century since Curti's book appeared, a new round of red scares and foreign wars associated the language of patriotism even more firmly with the political right, so much so that subsequent generations of scholars, especially those who came of age in the 1960s, by and large steered clear of the topic. Historians abandoned the study of American patriotism in the 1960s not only because they found the professional patriots repugnant but because the prevailing paradigm used to study it went out of favor. Curti's pioneering work grew out of an intellectual climate in the late 1930s concerned with defining an American culture, in particular understanding the myths and symbols that held Americans together. This concern continued in the postwar years, paralleling the Cold War and the rise of the American Studies movement and consensus history, and culminated in sociologist Robert Bellah's characterization of an American "civil religion" in 1967.1 Since then, although the civil religion paradigm continued to inform important studies such as Sacvan Bercovich's The American Jeremiad (1978), its influence paled beside historians' efforts to characterize the distinctive beliefs of smaller groups, especially the working class, immigrants, African Americans, and women. His

Two hundred four volunteer blood donors with hepatitis B surface antigen found in their blood were followed for 3 to 44 months. The annual clearance rate of this antigen was 1.7%. Liver enzyme levels (aminotransferase) were elevated in 45 (22.1%) on at least one occasion, in 26 (12.7%) for one month or more, and in 13 for more than six months. Liver biopsies were performed on 17 chronic carriers with normal enzymes and nonspecific histologic abnormalities were found in 14 and mild diffuse hepatitis in three. Seventeen carriers with abnormal enzymes were biopsied, and specimens revealed chronic active hepatitis (CAH) in seven, including two with bridging necrosis and three with cirrhosis. CAH was found in 7 of 26 (26.9%) carriers with abnormal liver enzymes persisting for at least one month and 4 of 13 (30.8%) with abnormal liver enzymes for more than six months.

Although hepatitis B virus (HBV) has been closely associated with the development of hepatocellular carcinoma (HCC), no serologic markers of HBV can be found in up to 11% of HCC patients in developing countries and up to 68% of HCC patients in industrialized countries. Despite the absence of HBV serologic markers in these HCC patients, HBV DNA sequences have been found to be integrated into HCC DNA in 13-100% of these patients, indicating a possible role of HBV in the etiology of their HCC. Although six patients with chronic non-A, non-B hepatitis virus infection who were followed have been documented to develop HCC, it is not known whether the non-A, non-B hepatitis viruses cause or contribute to the development of HCC in some HCC patients without HBV serologic markers. Ethanol, cigarette smoking, oral contraceptives, and aflatoxin also have been suggested as possible etiologies and should be studied further. Suggested etiologies that are not supported by the published data include alpha-1-antitrypsin deficiency and schistosomiasis.

Two study chimpanzees were inoculated intravenously with approximately 1,000 chimpanzee infectious doses of hepatitis B virus (HBV), one with subtype adr and one with subtype ayw, each previously incubated with 0.1 ml of a murine monoclonal antibody (IgG 1(K) class) directed against a single epitope on hepatitis B surface antigen common to most or all HBV. Two control chimpanzees received identical doses of HBV not incubated with the murine anti-HBs. Neither study chimpanzee developed HBV infection during 12 months of follow-up as judged by normal serum aminotransferase activity, normal liver biopsies, and negative serological tests for HBV-associated antigens and antibodies. In contrast, both control chimpanzees became infected by HBV as evidenced by elevated serum aminotransferase activity, liver biopsy changes characteristic of viral hepatitis, and the appearance of hepatitis B surface antigen (HBsAg) in their sera. Both study chimpanzees were shown to be fully susceptible to infection with these same HBV inocula when challenged 15 months after the initial inoculations at a time when passively administered anti-HBs was no longer detectable. Prior to challenge with HBV, one of the two study chimpanzees received a second injection of the same volume of the murine monoclonal anti-HBs. The survival of this anti-HBs in serum was reduced from six weeks (after the initial injection) to approximately two weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Non-A, non-B hepatitis, previously transmitted to chimpanzees by inoculation of human serum, was serially transmitted through a second and third passage to additional chimpanzees using serum drawn during acute non-A, non-B hepatitis. Sera obtained at weeks 4 and 5 after inoculation from two different chimpanzees, and from one chimpanzee at week 13 after inoculation, were shown to cause elevation of serum aminotransferase levels and abnormal liver biopsies in recipient chimpanzees, with no serologic evidence of hepatitis A or B, cytomegalovirus, or Epstein-Barr virus infection. Serum obtained 3 wk after inoculation did not cause elevation of aminotransferase levels in the recipient chimpanzee, although a single abnormal biopsy was obtained. Thus, the non-A, non-B hepatitis agent was present in serum during acute disease near the time of the first aminotransferase elevation (week 4; perhaps also week 3), and persisted at least until 1 week after the peak aminotransferase level (week 13).

Chimpanzees that had recovered from non-A, non-B hepatitis transmitted by inoculation of serum from each of three chronically infected humans were challenged by inoculation with a second of the three infectious sera to determine whether recovery from infection caused by one serum afforded protection against later infection by another. None of the challenge inoculations caused recognizable non-A, non-B hepatitis in any of the chimpanzees, a finding suggesting that either one agent or several agents sharing a common or similar antigen were responsible for the original non-A, non-B hepatitis in fections in these chimpanzees. Although circumstantial evidence in the literature suggests the existence of more than one agent of non-A, non-B hepatitis, the fact that the three inocula were obtained from humans residing in different geographic areas of the eastern United States suggests that one agent or a group of related agents may be the cause of many cases of non-A, non-B hepatitis in the United States.

Sera and questionnaires were evaluated retrospectively from 128 volunteer blood donors whose blood had been implicated in cases of clinically recognized post-transfusion hepatitis in recipients of one- or two-unit blood transfusion between 1971 and 1977. Serologic markers of hepatitis B virus (HBV) infection were found in 23 percent, compared to 9.7 percent of 3,230 prospective blood donors. The prevalence of antibody to hepatitis A virus was similar among implicated donors (44%), prospective donors (58%), and among those implicated donors with (41%) and without (44%) HBV markers. Among implicated donors, none had a history at the time of donation of having had clinically recognizable hepatitis, 93 percent had no history of prior blood transfusion, and 80 percent had normal hepatic enzymes. Data from this study confirm that non-A, non-B hepatitis has been a common form of posttransfusion hepatitis in recent years, since 77 percent of these implicated donors had no HBV serologic markers. In addition, these donors could not be distinguished by age, race, sex, history of clinical hepatitis or of prior blood transfusion, or in most cases by hepatic enzyme levels.

Ninety-three patients with biopsy-proven primary hepatocellular carcinoma (PHC) from Uganda, Zambia, and the United States were examined for serologic evidence of hepatitis B virus (HBV) infection. Patients were tested for hepatitis B surface antigen (HBsAg) and its antibody (anti-HBs), antibody to the hepatitis B core antigen (anti-HBc), hepatitis B e antigen (HBeAg), and its antibody (anti-HBe). Active HBV infection, as indicated by positive tests for HBsAg (with or without anti-HBs) and anti-HBc (without anti-HBs), was present in 62% of PHC patients (58 of 93), in contrast with 10% of African controls (9 of 90), and less than 1% of most United States adult populations reported in the literature. The presence of HBeAg or anti-HBe was rare among PHC patients and controls.

Hepatitis B e antigen (HBeAg) and its antibody (anti-HBe) were evaluated using a sensitive radioimmunoassay (RIA) in weekly serum samples obtained from nine chimpanzees experimentally infected with hepatitis B virus (HBV). In two chimpanzees with HBV infection with detectable hepatitis B surface antigen (HBsAG) for less than five weeks, and in one chimpanzee with documented HBV infection with no detectable HBsAg, HBeAg was not detected; in all three, anti-HBe became detectable early in the infection. In six chimpanzees in which HGsAg was detected for 16 weeks or longer, HBeAg was detected early in the infection; in five, anti-HBe became detectable and HBeAg undetectable prior to the clearance of HBsAg. The sixth remained HGsAg-positive and HBeAg-positive for more than two years and never developed anti-HBe. These results confirmed the sensitivity of this RIA and its value in predicting the course of HBV infections.

To determine whether horizontal transmission of the hepatitis B virus contributes to the high prevalence of infection with this virus in an endemic region, residents of five villages in Zambia were tested for hepatitis B serologic markers. The prevalence of hepatitis B was determined by testing samples from 620 residents. By examining paired serum samples from 79 children and 80 adults, it was determined that new infections occurred during the five years of this study in at least 14 children (18%) (aged 4-17 years) and ten adults (12%) (aged 23-65 years). These 24 new infections were distributed among 20 households and were not associated with active HBV infections in the mother or, in most cases, other family members. Intervention to prevent hepatitis B in regions such as rural Zambia will require vaccination of susceptible children and adults as well as newborn infants.

Ten chimpanzees were infected with non-A, non-B hepatitis by inoculation of patient serum or serum from a chimpanzee previously inoculated with patient serum. Convalescent serum from one of them reacted, in indirect immunofluorescent tests, with some of the hepatocyte nuclei in sections of autologous liver biopsy specimens and specimens from eight of the other chimpanzees. Serum from a convalescent patient reacted in the same way. These positive sera did not react with liver sections from uninfected chimpanzees. No reaction with positive liver sections was given by serum from chimpanzees which were uninfected or had antibodies to hepatitis A or B antigens. These control results suggest that the antigen-antibody system detected has specificity for non-A, non-B hepatitis.

Sera from 95 adolescents were examined for markers of hepatitis B virus (HBV) infection and hepatitis A virus (HAV) infection. HBV markers were found in eight adolescents (8%) and evidence of previous HAV infection was found in 18 adolescetits (19%); none had a history of clinically recognizable hepatitis. These findings support the growing evidence that HBV and HAV infections are diseases of the pediatric age group, amid that testing of HBV vaccines when they become available for patient use will have to include a pediatric population.

(1984). NUCLEAR WAR: A Teaching Guide. Bulletin of the Atomic Scientists: Vol. 40, Nuclear War: A Teaching Guide, pp. 1s-32s.

The unexpected occurrence of a hepatitis B virus (HBV) infection in a chimpanzee experimentally inoculated with hepatitis A virus (HAV) provided an opportunity to examine the course of simultaneous acute infections with both agents. A chimpanzee inoculated intravenously with HAV developed elevated levels of aminotransferases in serum, detectable excretion of hepatitis A antigen in feces, and a marked antibody response to HAV. During the acute phase of this experimentally induced infection with HAV, the chimpanzee simultaneously developed an HBV infection. The latter was characterized by jaundice, a second increase in levels of aminotransferases in serum, and the appearance in serum of hepatitis B surface antigen (HBsAg), hepatitis B e antigen, antibody to hepatitis B core antigen, and, later, antibody to HBsAg. During the acute phase of both HAV and HBV infections, marked histopathologic inflammatory changes were observed in serial liver biopsy specimens. In this chimpanzee, the concurrent acute infection with both HAV and HBV occurred in association with marked liver damage.

Guillain-Barré syndrome and other neurologic syndromes occur rarely as complications of viral hepatitis, although a causal association has not been established. Seven cases of serologically documented hepatitis A have been reported with Guillain-Barré syndrome; all recovered, with mild neurologic residua in four. Eight cases of serologically documented acute hepatitis B have been reported with Guillain-Barré syndrome; all recovered, with mild neurologic residua in two. In one case, immune complexes of hepatitis B surface antigen and its antibody were present in the cerebrospinal fluid. Other neurologic syndromes have also been reported in patients with serologically defined viral hepatitis, including mononeuritis, auditory neuritis, and seizures. Chronic hepatitis B and mononeuritis multiplex are found together in 31-54% of patients with periarteritis nodosa. The mechanisms for these associations are unknown, but may include direct cytotoxicity of the virus or immune-mediated damage. Vasculitis of the vasa nervorum plays an intermediate role in at least some cases.

Serial serum samples from the time of exposure until fatal outcome in 3 patients with fulminant viral hepatitis, type B, were examined for the presence of the antigens associated with hepatitis, type B, and their corresponding antibodies. The titers of hepatitis B surface antigen (HB s Ag) were found to decrease by greater than 50% before death. Antibody to surface antigen (anti-HB s ) was not detectable in any sample. Patterns of antibody to core antigen (anti-HB c ), HB c Ag subtype, "e" antigen, and anti-"e" were unremarkable, and could not be distinguished from those that might occur in many selflimited cases of hepatitis, type B. A rise in α-fetoprotein before demise suggests that late but inadequate liver regeneration occurred in these patients

n 1926, over fifty thousand people gathered at the Custer Battlefield National Monument to celebrate the semi-centennial of Custer's Last Stand, and to reaffirm several key elements of America's public faith. These pilgrims came to hear martial liturgists declare again that Custer and his men sacrificed themselves to open the West, that the battle was a moral victory for the nation, and that the progress of civilization since Custer's time was undoubtedly a providential sign that God was well pleased with the American experiment. Pilgrims also heard that Americans die in battle heroically, and that cherished values, ritually revivified at commemorations like this one, must often be won through conflict.

Hepatitis B e antigen (HBeAg) was detected by agar gel diffusion in the serum of four Ugandan adults (three patients with tropical splenomegaly syndrome and one healthy adult) who did not have detectable hepatitis B surface antigen (HBsAg) by radioimmunoassay. Two of them had antibody to hepatitis B core antigen, and the other two had antibody to HBsAg. Detection of HBeAg by a relatively insensitive immunodiffusion test in the absence of HBsAg detectable by a sensitive radioimmunoassay suggested that production or removal of these two antigens may occur independently.

Samples of serum (0.1 ml each) containing an agent of human non-A, non-B hepatitis of documented infectivity were incubated with formalin in a concentration of 1:1,000 at 37 C for 96 hr. Three colony-born infant chimpanzees were then inoculated with this formalin-treated serum; one received a single intravenous inoculation, and two received two subcutaneous inoculations one month apart. A fourth uninoculated chimpanzee served as a control. None developed recognizable non-A, non-B hepatitis during seven months of observation, as judged by normal aminotransferase levels in weekly serum samples, normal liver histology in liver biopsy specimens, and the absence of non-A, non-B hepatitis-associated antigen and antibody in their sera. All four chimpanzees were subsequently shown to be susceptible to non-A, non-B hepatitis when challenged with 0.1 ml of the untreated infectious serum 31 weeks after the initial inoculations.

Sera from 200 volunteer blood donors and 200 paid blood donors, all positive for hepatitis B surface antigen (HBsAg), were tested for the presence of hepatitis B e antigen (HBeAg). HBeAg was detected in 31 HBsAg-positive paid donors (15%), and in 11 HBsAg-positive volunteer donors (5%) by agar gel diffusion. The presence of HBeAg was associated with higher titers of HBsAg. No significant difference was found in the prevalence of antibody to HBeAg (anti-HBe) in the two donor groups. Rheumatoid factor was not associated with the presence or absence of HBeAg or anti-HBe, indicating that HBeAg is probably not an anti-IgG. These data support the epidemiological evidence that paid blood donors appear to be more likely than volunteer donors to transmit hepatitis B virus infection to recipients of their blood.

Hepatitis B surface antigen (HBsAg) was detected in the cerebrospinal fluid (CSF) of five of nine leukemia patients with HBsAg-positive sera. These five CSF samples were shown to be free of occult blood using a sensitive hemoglobin extraction technique. The presence of HBsAg in CSF was unrelated to cranial irradiation, prior lumbar punctures, or current chemotherapy. The findings indicate that many blood-free CSF specimens from HBsAg-positive patients, as well as all blood-contaminated specimens, contain detectable HBsAg. This suggests that CSF from patients who are HBsAg-positive should be handled with care, as it may be capable of transmitting hepatitis B to health care personnel caring for these patients and laboratory personnel handling their specimens.

Evidence supporting the existence of two agents of human non-A, non-B hepatitis was obtained by the inoculation of chimpanzees sequentially with serum from a chronically infected human (Inoculum I) and with fibrinogen prepared from pooled plasma (Inoculum IV), each of which had transmitted non-A, non-B hepatitis to humans. Passage inoculations of serum samples obtained during the acute stages of chimpanzee infections transmitted by either the agent in Inoculum I or IV also transmitted non-A, non-B hepatitis to additional chimpanzees. Transmission and passage of the agent in Inoculum IV were conducted in chimpanzees which previously had recovered from infection by the agent in Inoculum I. Cytoplasmic tubules in hepatocytes, which have been described during non-A, non-B hepatitis, were observed by electron microscopy in liver biopsies obtained during all infections transmitted by the agent in Inoculum I. These cytoplasmic tubules were not detected in liver biopsies from chimpanzees infected by Inoculum IV, except in one chimpanzee inoculated by Inoculum IV without prior exposure to the agent in Inoculum I. The cytoplasmic tubules observed in this study were found to be composed of transverse bands arranged with a periodicity of approximately 17 nm. These studies suggest that two different agents or distinct serotypes of human non-A, non-B hepatitis may have been present in these inocula, although reactivation of latent infection or reinfection could not be ruled out completely.

The recent report that antithrombin III (AT-III) prepared in solution with 0.5 M sodium citrate can withstand heating at 60°C for 10 hours suggested that this method of preparation could permit the heat-inactivation of hepatitis B virus (HBV) which might be present. Although heating at 60°C for 10 hours will inactivate HBV in albumin, this will not inactivate HBV in whole plasma or in some purified hepatitis B surface antigen (HBsAg) preparations. HBV, subtype ayw, hepatitis B e antigen positive, containing 103.5 chimpanzee infectious doses per ml, was added to each of two vials containing 690 plasma units each of AT- III. One was kept at 4°C for 10 hours (unheated AT-III), the second was heated at 60°C for 10 hours. The contents of both vials were separately dialyzed and inoculated intravenously into chimpanzees with no prior exposure to hepatitis B virus and with no serologic evidence of prior hepatitis B infection. No evidence of hepatitis B was detected in the chimpanzee inoculated with the heated AT-III during six months of evaluation. Aspartate and alanine aminotransferase levels (AST, ALT) remained within or near the normal range. Neither HBsAg, antibody to hepatitis B core antigen (anti-HBc), nor antibody to HBsAg (anti-HBs) was detected in any of the weekly serum samples. The chimpanzee inoculated with the unheated AT-III developed hepatitis B. AST and ALT became elevated 13 weeks after inoculation; HBsAg (subtype ayw) was detected six weeks after inoculation and remained detectable; anti-HBc became detectable 12 weeks after inoculation. Liver biopsies obtained 20 and 23 weeks after inoculation showed histologic changes of acute hepatitis. This study shows that the application of heat at 60°C for 10 hours to AT-III stabilized with 0.5 M sodium citrate can inactivate > 1,000 chimpanzee infectious doses of HBV.

An antigen was detected by counterelectrophoresis in serum samples from six of seven chimpanzees during the acute phase of experimentally induced non-A, non-B hepatitis using antiserum from a chimpanzee convalescent from human non-A, non-B hepatitis. This antigen could not be detected in 35 preinoculation serum samples from these chimpanzees, or in 94 weekly bleedings from three chimpanzees with hepatitis A and three chimpanzees with hepatitis B. The antigen was detected in serum samples obtained from three humans with chronic non-A, non-B hepatitis whose blood had transmitted non-A, non-B hepatitis to other humans (including a nurse by accidental needlestick) and to chimpanzees by experimental inoculation. In addition, the antigen was detected in serum obtained retrospectively from 11 to 31 former blood donors whose blood had transmitted posttransfusion non-A, non-B hepatitis several years previously to recipients of a single unit of their blood. Antibody to this antigen was detected in convalescent serum samples from all seven chimpanzees studied, in convalescent serum from the nurse infected by accidental needlestick, and in serum from a hemodialysis patient convalescent from non-A, non-B hepatitis.

Dilutions of human sera containing between 10(3) and 10(5) chimpanzee infectious doses of hepatitis B virus per ml, subtype adr or ayw, were treated with either 1 microgram/ml pepsin at pH 2.0 for 18 hours, 8 M urea for four hours, or 1:4,000 formalin for 72 hours. One ml of the serum containing hepatitis B virus subjected to each of the procedures was inoculated intravenously into one or two susceptible chimpanzees (total of eight chimpanzees). No evidence of hepatitis B infection was detected in weekly serum samples from the chimpanzees during six months of observation. These three procedures are currently applied during manufacture to inactivate HBV which might be present in the hepatitis B vaccine licensed in the United States. The data from this study combined with data documenting that the physical purification of the vaccine is capable of removing hepatitis B virus provide assurance that there is no residual live hepatitis B virus in the vaccine.

The infectivity of three inocula (subtypes ayw, adr, and adw) of hepatitis B virus was evaluated by intravenous inoculation of 54 chimpanzees. End-point infectivity titers were 10(-7.5) (ayw), 10(-8.0) (adr), and 10(-7.0) (adw). In contrast, the end-point titers for detection of hepatitis B surface antigen by radioimmunoassay were 10(-4) (ayw), 10(-4) (adr), and 10(-5) (adw). The mean incubation period for infections transmitted by each dilution of each of the inocula was inversely proportional to the amount of infectious virus in the dilution, but substantial overlap was observed among proximate dilutions. The severity of hepatitis in the chimpanzees differed among the inocula, but it was unrelated to the amount of virus inoculated. Thus, conclusions about the infectivity of hepatitis B virus after inactivation based on titers of hepatitis B surface antigen or on the inverse relationship between the incubation period and the end-point infectivity titer must be made with caution.

Non-A, non-B hepatitis was transmitted to four colony-born chimpanzees by intravenous inoculation of human sera. Two chimpanzees were inoculated with serum from a patient with a clinical and serological diagnosis of chronic non-A, non-B hepatitis whose blood appeared to transmit this disease to a nurse following accidental needle-stick, and the other two chimpanzees were inoculated with serum from either of two former blood-donors whose HBsAg-negative blood appeared to transmit clinically recognisable hepatitis, and who were found to have raised serum-aminotransferase levels 1 1/2 and 5 years later. Serum-aminotransferase levels rose in all four chimpanzees, beginning 2--4 weeks after inoculation: peak alanine-aminotransferase values were 210 to 328 I.U./l. Evidence of hepatitis was present in liver biopsy specimens from all four chimpanzees, beginning 8--10 weeks after inoculation. None showed serological evidence of infection with hepatitis A virus, hepatitis B virus, cytomegalovirus, or Epstein-Barr virus.

Seventy-eight persons in an Italian-American family were tested for hepatitis B serologic markers. Fifty-one (65%) had serologic evidence of active or prior hepatitis B infection. Twenty-eight (36%) had evidence of active infection, including twenty-six with hepatitis B surface antigen (HBsAg), and two with antibody to the hepatitis B core antigen only. Severe chronic liver disease was documented in four family members, three of whom had serologic evidence of active hepatitis B infection and the fourth died before the availability of hepatitis B testing. Thirteen of 18 (72%) offspring of six HBsAg positive mothers were HBsAg positive. No epidemiologic explanation of the high prevalence of hepatitis B infection in this family was found, although mother-to-child transmission in years past is a possible explanation.