Vaccination with experimental feline immunodeficiency virus vaccines, based on autologous infected cells, elicits enhancement of homologous challenge infection.
(33/8916)
Cats were vaccinated with fixed autologous feline immunodeficiency virus (FIV)-infected cells in order to present viral proteins to the immune system of individual cats in an MHC-matched fashion. Upon vaccination, a humoral response against Gag was induced. Furthermore, virus-neutralizing antibodies were detected in a Crandell feline kidney cell-based neutralization assay, but not in a neutralization assay based on primary peripheral blood mononuclear cells. Despite the induction of these FIV-specific responses, vaccinated cats were not protected. Instead, accelerated virus replication was found, an observation similar to what previous experiments using other vaccine candidates have shown. Here, the results of the present study are discussed in the light of enhancement of lentivirus infections as a complicating factor in lentivirus vaccine development. (+info)
Encephalitis induced by bovine herpesvirus 5 and protection by prior vaccination or infection with bovine herpesvirus 1.
(34/8916)
Calves were intranasally challenged with bovine herpesvirus 5 (BHV5) and followed for the development of viral infection, clinical encephalitis, histologic lesions in the brain, and viral sequences in the trigeminal ganglia. Calves that were previously vaccinated with bovine herepesvirus 1 (BHV1, n = 4) or previously infected with BHV1 (n = 5) or that had not been exposed to either virus (n = 4) were compared. No calf developed signs of encephalitis, although all calves developed an infection as indicated by nasal secretion of BHV5 and seroconversion to the virus. Histologic lesions of encephalitis consisting of multifocal gliosis and perivascular cuffs of lymphocytes were observed in calves not previously exposed to BHV1. BHV5 sequences were amplified from the trigeminal ganglia of calves previously vaccinated and from calves not previously exposed to BHV1; calves sequentially challenged with BHV1 and later BHV5 had exclusively BHV1 sequences in their trigeminal ganglia. Administration of dexamethasone 28 days after BHV5 challenge did not influence clinical disease or histologic lesions in either previously unexposed calves (n = 2) or previously immunized calves (n = 2), although it did cause recrudescence of BHV5, as detected by nasal virus secretion. (+info)
Complementary randomly amplified polymorphic DNA (RAPD) analysis patterns and primer sets to differentiate Mycoplasma gallisepticum strains.
(35/8916)
Randomly amplified polymorphic DNA (RAPD) analysis was used to differentiate 7 strains of Mycoplasma gallisepticum. Six commercially available primers or primer combinations were screened for their ability to differentiate vaccine and type strains. Although major and minor bands were produced with each primer, many of the primers were unsuitable for strain differentiation. The use of primer 6 and combined primers 3 and 4 resulted in complementary RAPD banding patterns for each M. gallisepticum strain. Eleven different isolates representing 7 different strains were segregated into 7 different patterns, corresponding to the 7 strains. (+info)
Seroprevalence of hepatitis B virus, hepatitis C virus and GB virus-C infections in Siberia.
(36/8916)
We studied the seroprevalence of hepatitis B virus (HBV), hepatitis C virus (HCV) and GB virus-C (GBV-C) infections in 348 Siberian natives who lived in the Kamchatka Peninsula of Russia. Of 348 samples studied, the seroprevalence of HBsAg and anti-HBs were 11.8% (41 of 348 samples) and 35.9% (125 of 348 samples), respectively. The prevalence of HCV infection was 1.4% (5 of 348 samples), and that of GBV-C RNA, using RT-PCR methods, was 7.5% (26 of 348 samples). In Siberia, the prevalences of HBV and GBV-C infections were about tenfold higher than those in Japan. The prevalence of HBsAg in subjects under 50 years of age was significantly higher than that in those over 50 years old (P < 0.05). Because HBV infection is highly endemic in Siberia, we propose that the community-based mass immunization must be conducted as soon as possible in this area. (+info)
Oral transmission of primate lentiviruses.
(37/8916)
Oral transmission of human immunodeficiency virus type 1 (HIV-1) is well documented in children who become infected postnatally through breast milk. In contrast, epidemiologic surveys have yielded conflicting data regarding oral HIV-1 transmission among adults, even though case reports have described seroconversion and the development of AIDS in adults whose only risk was oral-genital contact. To study oral virus transmission in primate models, we exposed rhesus macaques of various ages to cell-free simian immunodeficiency virus (SIV), including uncloned and molecularly cloned viruses. In neonates, viremia and AIDS developed after nontraumatic oral exposure to several SIV strains. Furthermore, chimeric simian human immunodeficiency viruses containing the HIV-1 envelope can also cross intact upper gastrointestinal mucosal surfaces in neonates. In adult macaques, infection and AIDS have resulted from well-controlled, nontraumatic, experimental oral exposure to different strains of SIV. These findings have implications for the risks of HIV-1 transmission during oral-genital contact. (+info)
Mucosal vaccination strategies for women.
(38/8916)
Women were immunized orally, rectally, or vaginally with a recombinant cholera toxin B-containing vaccine to determine which of these mucosal immunization routes generate the greatest levels of antibody in the female genital tract and rectum. ELISA was used to measure concentrations of cholera toxin B-specific IgA and IgG antibody in serum and secretions before and after three immunizations. Each immunization route similarly increased specific IgG in serum and specific IgA in saliva. Only the vaginal route increased IgA antibodies in genital tract secretions and could be shown to induce a local IgG response. However, vaginal immunization failed to produce antibody in the rectum. In a similar fashion, rectal immunization elicited highest concentrations of locally derived IgA and IgG antibody in the rectum but was ineffective for generating antibody in the genital tract. The data suggest that local immunization may induce the greatest immune responses in the female genital tract and rectum of humans. (+info)
Surface display of functional fibronectin-binding domains on Staphylococcus carnosus.
(39/8916)
The surface expression in Staphylococcus carnosus of three different fibronectin binding domains (FNBDs), derived from fibronectin binding proteins of Streptococcus dysgalactiae and Staphylococcus aureus, has been investigated. Surface localization of the chimeric proteins containing the FNBDs was demonstrated. All three surface-displayed FNBDs were demonstrated to bind fibronectin in whole-cell enzyme-linked binding assays. Furthermore, for one of the constructs, intranasal immunizations with the recombinant bacteria resulted in improved antibody responses to a model immunogen present within the chimeric surface proteins. The implications of the results for the design of live bacterial vaccine delivery systems are discussed. (+info)
Immunity to Brucella in mice vaccinated with a fraction (F8) or a killed vaccine (H38) with or without adjuvant. Level and duration of immunity in relation to dose of vaccine, recall injection and age of mice.
(40/8916)
Immunity to Brucella in the mouse, assessed by bacterial spleen counts 15 days after intraperitoneal inoculation of a standard challenge of B. abortus 544, has been studied with two vaccines, one experimental, composed of a fraction of the bacterial cell-wall (F8) extracted from B. abortus 99, the other of killed whole bacteria, B. melitensis 53 H38, taken as reference (H38). The level of primary immunity depended on the dose of vaccine, the presence of oil adjuvant and the age of the mouse. The presence of adjuvant enabled the immunization to F8 to continue beyond the first month, to reach its maximum around the fourth month, and to remain stable for at least 7 months. A booster injection 3 or 6 months after the primary vaccination reinforced existing immunity but did not increase it beyond a certain level. The effect of the recall injection was clearly demonstrated with low doses which gave a lower level of primary immunity. (+info)