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In September 2010, an outbreak of acute hepatitis B virus (HBV) infections in a nursing home was notified to public health authorities in Northern Germany. To identify the route of transmission and prevent further cases a retrospective cohort study was conducted. Blood samples of residents were tested for serologic markers of HBV infection and HBV subgenotypes and sequences were analyzed. Outbreak-related cases were defined as residents of the nursing home with detection of hepatitis B surface antigen (HBsAg) and the HBV DNA sequence of the outbreak strain in 2010. Information on possible risk factors as patient care, invasive diagnostic, and therapeutical procedures was collected using a standardized questionnaire. Risk ratios (RR) and 95% confidence intervals (CI) were estimated with exact Poisson regression and binomial regression. Sixty-four residents were included in the study, 5 of them were outbreak-related cases, 12 had a past HBV infection. The outbreak strain belonged to HBV genotype D2 (HBsAg subtype ayw3, Ala118) which is not prevalent in Germany but in Eastern Europe. All cases (median age 81) were female, had diabetes, blood glucose monitoring, and chiropody. In multivariable analysis only blood glucose monitoring was associated with HBV infection (RR = 22, 95%CI 3.0-∞). Blood glucose monitoring was reported to be done by nursing home staff with patient-based reusable lancet devices. In nursing home settings the use of single use lancets for blood glucose monitoring is recommended strongly to prevent transmission. National guidelines on the handling of point-of-care devices and reusable equipment in long-term care facilities should be developed.

The analysis of spatial data by means of Markov random fields usually is based on strict stationarity assumptions. Although these assumptions rarely hold, they are necessary in order to obtain parameter estimates. For Gaussian data the necessary assumptions are mean- and covariance stationarity. While simple techniques are available to deal with violations of mean stationarity, the same is not true for covariance stationarity. In order to handle mean nonstationarity as well as covariance nonstationarity, we propose the modelling by spatially varying coefficients. This aproach not only yields more appropriate models for nonstationary data but also can be used to detect violations of the stationarity assumptions. The method is illustrated by use of the well known wheat yield data.

Polypeptide micelles with relative molecular weights of 25,000 (p25) and 30,000 (gp30) daltons were prepared from native 22-nm hepatitis B surface antigen (HBsAg) particles. This p25/gp30 complex was alum-adsorbed, and three dosage levels (20 micrograms, 4 micrograms, and 0.8 micrograms) were administered at 0, 1, and 6 months to 51 human volunteers. Local and systemic reactions were clinically insignificant, and all vaccinees seroconverted, regardless of dose. As anticipated, antibody responses diminished as the dosage was reduced. Seroconversion rates and geometric mean antibody levels for the 20 micrograms dosage group were significantly better than those observed with a commercial vaccine and were comparable to those achieved after immunization with 40 micrograms of the intact 22-nm particles used to prepare the polypeptides. By 2 weeks, an anti-HBs response was elicited in 80% of the group receiving 20 micrograms of the polypeptide vaccine. This rapid response to immunization may be particularly beneficial for postexposure prophylaxis where the early development of immunity is advantageous.

A common idiotype was defined by a rabbit anti-idiotypic antiserum generated against human antibodies to hepatitis B surface antigen (anti-HBs). This idiotype was detected in anti-HBs from eight different individuals who had been previously infected with hepatitis B virus and is referred to as the CHBs idiotype. The CHBs idiotype was also identified in sera from rabbits, mice, guinea pigs, swine, goats and chimpanzees that had been immunized with hepatitis B surface antigen (HBsAg). Expression of the CHBs idiotype in sera from other species was associated with anti-HBs molecules. These results suggested that variable-region genes responsible for the CHBs idiotype have been conserved through long periods of evolution. It was noteworthy that the CHBs idiotype was not detected in the sera of a nonmammalian species, chickens, that had been successfully immunized with HBsAg.

The receptors for polymerized (P) human (Hu) serum albumin (SA) present on intact hepatitis B surface antigen (HBsAg) have been shown to be associated with the major HBsAg polypeptides, as well as HBsAg produced in vitro by a hepatoma cell line. These observations demonstrate that the albumin receptors are virus-specific.

Virus-like particles have been visualized by electron microscopy in the liver hepatocytes of two out of four chimpanzees inoculated with two different human non-A, non-B hepatitis-implicated plasmas. The first two chimpanzees, which were infected with the same inoculum (inoculum A), developed liver histological features characteristic of mild acute viral hepatitis as well as rises in their serum alanine aminotransferase levels. Clusters of intranuclear particles, 22 ± 2 nm in diameter, were visualized in one of every fifth hepatocytes in one of these two chimpanzees. Intracytoplasmic circular membrane fusions, 100 to 350 nm in diameter, were observed in the hepatocytes of the other chimpanzee receiving inoculum A. The second two animals were infected with a different human plasma containing infectious NANB material (inoculum B). Both animals developed mild increased serum enzyme levels that were variable but generally elevated throughout the course of this study (220 days); minor, equivocal histologic changes were also observed. Intranuclear and intracytoplasmic particles, 20 ± 1 nm and 37 nm in diameter, respectively, were visualized in the liver of one of the two chimpanzees infected with inoculum B; intranuclear particles were observed in one of seventy-five hepatocytes and intracytoplasmic particles were observed less frequently. In this same animal, intracytoplasmic circular membrane fusions, similar, if not identical to those described above, were also noted. The intranuclear particles observed in animals receiving inocula A and B were essentially identical, as were the cytoplasmic membrane fusions. Thus, both inocula produced nuclear and cytoplasmic ultrastructural changes. The intracytoplasmic particle clusters (37 nm) were seen in only one animal and demonstrated a high degree of homogeneity, as evidenced by their presence in highly ordered crystalline arrays. All chimpanzees were screened for and found to be negative for evidence of hepatitis A and B, as well as for Epstein-Barr virus or cytomegalo-virus-induced hepatitis. Previous studies have suggested that nuclear and cytoplasmic ultrastructural changes, similar to those described herein, result from two distinct NANB infectious agents. In contrast, our data suggest that both morphologic changes may be caused by a single agent.

A chemically synthesized peptide corresponding to the amino acid sequence 503-532 of gp160 of human immunodeficiency virus (HIV) was used to generate monoclonal antibodies reactive with the env glycoprotein gp120. One monoclonal antibody, 120-1, was isolated that reacted with the peptide and with HIV antigen(s). Western blot analysis showed reactivity with two bands of 120 kDa and 88 kDa. 120-1 reacted in indirect immunofluorescence with 15-20% of infected human T cell line A3.01 as early as 4 days post in vitro infection, 2-3 days prior to detectable reverse transcriptase activity in supernatant fluids.

One thousand one hundred thirty-four women, enrolled in a prospective study of the development of cervical neoplasia in women exposed to diethylstilbestrol (DES) in utero, were examined at least once a year. Twenty-three women developed cervical intraepithelial neoplasia (CIN) of different degrees during the 7-year follow-up period and were matched with women who did not develop CIN during the study period. Serum samples were obtained at the time of entry into the study and at the time of diagnosis of neoplasia. In the control group, a second serum sample was obtained close to the time when CIN was diagnosed in the other group of women. The sera were studied for antibodies to both types of herpes simplex virus (HSV) by microneutralization assay and by a radioimmunoassay using, as antigens, glycoproteins VP123 for HSV type 1 and VP119 for HSV type 2. Women who developed CIN had, in the enrollment specimen which preceded the neoplasia, a higher rate of antibodies to HSV-1 than did the matched controls (22%), while the two groups did not differ in frequency of antibodies to HSV-2 (9%). Similar differences were observed in the sample drawn at the time of diagnosis of CIN. Women who later developed CIN and had, at the time of entry into the study, cervical epithelial changes associated with DES exposure, were infected with HSV-1 at a higher rate than women who remained free of neoplasia or women with CIN but without DES-associated cervical epithelial changes. Morphologic evidence of associated papillomavirus (HPV) infection was observed in 74% of CIN cases and no such observation was made in biopsy specimens taken prior to development of CIN. Morphologic evidence of HPV infection was found in a women of the control group having squamous metaplasia. HPV structural antigens were found in 3 of 10 CIN I and CIN II cases, and none in the CIN III specimens. The possible role of the HSV and HPV infection in the pathogenesis of cervical neoplasia is discussed.

Following inoculation with plasma from human patients with AIDS, two chimpanzees demonstrated specific antihuman T-cell leukemia virus type 3 (HTLV-III) antibodies. One of the two chimpanzees also developed massive lymphadenopathy that persisted for 32 weeks and demonstrated a concurrent and more frequent depression of total T cells (T3) and T helper cells (T4) with a decrease in the ratios of T4 to T suppressor cells (T8). These results indicate that chimpanzees demonstrate a range of T-cell subpopulations during infection and disease induced by HTLV-III.