Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specificity of cytotoxic T-cell function was investigated for a range of different influenza viruses. T cells from mice immunized with A or B strain influenza viruses, or with vaccinia virus, showed reciprocal exclusion of cytotoxicity. Extensive cross-reactivity was, however, found for lymphocyte populations from mice infected with a variety of serologically distinct influenza A viruses, though serum antibodies did not cross-react when tested in a radioimmunoassay using comparable target cells as immunoadsorbents. This apparent lack of T-cell specificity was recognized for immune spleen cells generated after intraperitoneal inoculation of high titers of virus, and for mediastinal lymph node populations from mice with pneumonia due to infection with much less virus. The phenomenon could not be explained on the basis of exposure to the chicken host component, which is common to A and B strain viruses. However, not all of the virus-immune T-cell clones are cross-reactive. Competitive-inhibition experiments indicate that a considerable proportion of the lymphocyte response is restricted to the immunizing virus. Even so, the less specific component is significant. Also, exposure to one type A virus was found to prime for an enhanced cell-mediated immunity response after challenge with a second, serologically different A strain virus.
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PMID:Generation of both cross-reactive and virus-specific T-cell populations after immunization with serologically distinct influenza A viruses. 23 1

Several viruses may cause more or less severe acute respiratory infections in man, some of which are followed by systemic infection. Only for influenza and measles are licensed vaccines available at present. The protection induced by influenza vaccines, which are based on inactivated whole virus or viral subunits, depends largely on the matching of vaccine strain and circulating virus. Measles vaccines, which are based on attenuated live virus, have been quite effective in controlling the disease in vaccinated populations in the industrialized world. In developing countries, severe measles infections occur in infants from six to nine months of age, which necessitates the vaccination of children of less than six months. At that time maternal antibodies, that may interfere with the induction of protection, may still be present. Therefore, instead of using the parenteral route, the possibility to use the mucosal route of primary immunization is also investigated for vaccination with attenuated live measles vaccines. The use of inactivated measles vaccines has resulted in a state of immunity which upon exposure to the virus may induce an atypical measles syndrome including a severe pneumonia. Measles virus proteins presented in an iscom matrix have recently been shown to induce functional B and T cell responses to both the surface glycoproteins of the virus. These responses could also be induced in the presence of virus neutralizing antibodies and they proved to be protective in several animal model systems. Many of the problems that have been encountered in the development of measles vaccines, proved to be similar in the development of vaccines against other paramyxoviruses causing acute respiratory infections in man, including respiratory syncytial virus. Parenteral application of inactivated and attenuated live vaccines against these paramyxoviruses has generally had little success. Topical application of attenuated live vaccines has been more successful, and also the use of vaccinia recombinant viruses expressing foreign paramyxoviral glycoproteins has shown promising results in laboratory animals. Live vaccines based on adenovirus types 4 and 7 in oral enteric-coated vaccines, which lead to virus replication in the intestines but not in the respiratory tract have been included in military vaccination programs. The possibility to replace e.g. the E3 region with foreign DNA makes adenoviruses also suitable as cloning vectors for proteins of other respiratory viruses. Although live attenuated vaccines against some of the serotypes of rhinoviruses have shown promising results, the generation of a multivalent vaccine against this epidemiologically most significant cause of acute respiratory infections will be almost impossible, due to the multiplicity of serotypes involved.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vaccination against acute respiratory virus infections and measles in man. 158 42

Benzalkonium chloride (as Roccal or Zephiran) was found to inactivate influenza, measles, canine distemper, rabies, fowl laryngotracheitis, vaccinia, Semliki Forest, feline pneumonitis, meningopneumonitis, and herpes simplex viruses after 10 min of exposure at 30 C or at room temperature. Poliovirus and encephalomyocarditis virus were not inactivated under the same conditions. It was concluded that all viruses tested were sensitive except members of the picorna group. The literature was reviewed.
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PMID:Inactivation of viruses by benzalkonium chloride. 428 40

A case of progressive vaccinia complicating chronic lymphocytic leukaemia is reported. At necropsy a vaccinial pneumonia, focal pancreatitis, and evidence of disseminated intravascular coagulation were found. Epithelial proliferation was noted in sweat glands, bronchi, and pancreatic ducts associated with lesions in these sites. The significance of these findings is discussed.
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PMID:Necropsy findings in a case of progressive vaccinia. 501 14

An epizootic of mousepox in two colonies of mice was described. Clinical signs, morbidity and mortality rates, and necropsy lesions were substantially influenced by husbandry practices, intercurrent diseases (Sendai pneumonia, mouse hepatitis virus), and total body x-irradiation. In one colony, 54 mice were necropsied; 19 mice had cutaneous or visceral lesions of mousepox although none had combined visceral and cutaneous lesions. In the other colony, 20 mice were necropsied, and 10 mice had cutaneous lesions; none had visceral lesions. Sera from 24 mice with the cutaneous form of the disease had no demonstrable HI antibody titer. Experimental mice injected with spleen/liver homogenates from infected colony mice developed typical visceral lesions with numerous poxvirus profiles on electron micrographs and positive HI titers. Mice immunized with vaccinia virus were not susceptible to the disease.
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PMID:Clinical, pathologic, and serologic features of an epizootic of mousepox in Minnesota. 628 60

The adenovirus (Ad) 14.7-kDa protein, which is called "14.7K," has been shown to function as a general inhibitor of tumor necrosis factor alpha (TNF) cytolysis in tissue culture assays, and the effect of this antagonism on viral pathogenesis in vivo has recently been explored. In infections of immunocompetent BALB/c mice, we have shown previously that Ad type 2 (Ad2) 14.7K, when cloned into a vaccinia virus (VV) vector in combination with the gene for murine TNF, is able to counteract much of the attenuating effect of TNF on VV virulence. In the present study we utilized VV constructs expressing various combinations of Ad 14.7K and TNF in infections of T- and B-cell-deficient C.B-17 severe combined immunodeficient (SCID) mice to determine whether these cells are directly necessary for 14.7K's reversal of TNF-mediated viral attenuation. The mice were infected by the intranasal route, and mortality, morbidity, histopathology, and virus replication in selected organs were evaluated at various times after infection. We found that, in the SCID murine pneumonia model, neither the attenuation by TNF nor its reversal by Ad 14.7K require the participation of T or B lymphocytes or their secreted products. SCID mice infected with VV expressing both 14.7K and TNF [VV 14.7(+)/TNF] were generally well clinically for the first 7-10 days after infection; however, they developed a subacute or chronic illness, succumbing to diseminated VV infection at least 3 weeks earlier than mice infected with VV expressing TNF alone [VV 14.7(-)/TNF]. Animals infected with VV 14.7(+)/TNF were shown to have higher initial titers of virus and delayed clearance from the lungs as well as more rapid spread of virus to internal organs than animals infected with VV 14.7(-)/TNF. SCID mice infected intranasally with VV without TNF showed a dramatic increase in acute disease and succumbed within the first 1-2 weeks after infection, independent of Ad 14.7K expression.
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PMID:Adenovirus E3 14.7-kilodalton protein, an antagonist of tumor necrosis factor cytolysis, increases the virulence of vaccinia virus in severe combined immunodeficient mice. 797 96

The adenovirus type 2 (Ad2) early region 3 (E3) codes for a 19-kDa glycoprotein (gp19) that associates with the class I major histocompatibility (MHC) heavy chain in the endoplasmic reticulum (ER) and prevents the transport of class I MHC protein products to the cell surface. It has been shown previously in tissue culture that this reduction in class I MHC expression allows infected cells to escape detection by class I MHC restricted CD8+ cytotoxic T-lymphocytes (CTL). We now report the results of studies on the effects of Ad2/gp19 expression on virulence in vivo. Since we wanted to isolate the effect of Ad2/gp19 from the effects of other Ad E3 region gene products and human Ads do not replicate in the mouse, we cloned the Ad2/gp19 open reading frame (ORF) into the HindIII C region of WR vaccinia virus (VV). Two VV recombinants were constructed by inserting the Ad2/gp19 ORF in either an expressing (V-e19(+)) or a non-expressing (V-e19(-)) orientation under control of the VV P7.5 promoter. The V-e19(+)recombinant expressed Ad2/gp19 in infected tissue and could be co-precipitated with an antibody to the class I MHC antigen Kd. However, intracerebral or intranasal infections of BALB/c (H-2d), BALB.G (H-2g), or C3H (H-2k) mice showed that Ad2/gp19 expression by V-e19(+) had no significant effect either on viral lethality or on its ability to replicate in vivo when compared to V-e19(-). Furthermore, the nature of the CD8+ CTL response to a V-e19(+)-induced pneumonia in (H-2d) mice was unchanged by Ad2/gp19 expression. Modulating the CD8+ CTL response, by interfering with infected target presentation, may not be important in the control of VV replication or virulence in vivo when other aspects of the immune response to viral infection are not altered. However, the two VV recombinants V-e19(+) and V-e19(-) were both equally attenuated (10-fold) when compared to wild-type VV. This attenuation, which has been reported previously for an intracerebral infection, is believed to be caused by the disruption of a 37-kDa ORF in the VV HindIII C region. Interestingly, our studies showed that the attenuation is not accompanied by a reduction in viral titers in infected tissue.
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PMID:Association of vaccinia virus-expressed adenovirus E3-19K glycoprotein with class I MHC and its effects on virulence in a murine pneumonia model. 817 41

Peste des petits ruminants (PPR) is a viral disease of goats and sheep characterized by necrotizing and erosive stomatitis, enteritis and pneumonia. The causative agent, PPRV, is a member of the family Paramyxoviridae and the genus Morbillivirus. Other members of the genus include rinderpest (RPV), measles, canine distemper and phocid distemper viruses. PPR has a very high rate of morbidity and mortality, and effective control of this disease is of economic importance in Africa, Asia and the Middle East. Currently, there is no safe and effective vaccine available against the disease. The tissue culture rinderpest vaccine (TCRV) protects small ruminants against severe disease; there are, however, clinical problems associated with vaccination. This laboratory has recently developed several effective vaccinia virus recombinant vaccines for rinderpest. These vaccines are easy to administer, inexpensive to produce and heat-stable. Goats were vaccinated with a vaccinia virus double recombinant expressing the haemagglutinin and fusion genes of RPV. Although vaccinated animals developed antibodies (neutralizing and ELISA) to RPV, and not to PPRV, they were completely protected against challenge inoculation with virulent PPRV. This would indicate that protection is most probably due to cell-mediated immunity. Use of the rinderpest double recombinant vaccinia virus in areas of the world where PPRV is endemic would aid in the control and eradication of PPR.
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PMID:Protection of goats against peste des petits ruminants with a vaccinia virus double recombinant expressing the F and H genes of rinderpest virus. 821 44

Respiratory syncytial virus (RSV) is the most common cause of viral bronchiolitis and pneumonia in children. The present study compares the level of attenuation, genetic stability and efficacy of three conditional-lethal temperature-sensitive (ts) mutants of the RSV A2 wild-type virus, designated ts-1, ts-1-NG1, and ts-4, in seronegative chimpanzees and also compares their efficacy with that of vaccinia virus recombinants that express the surface glycoproteins of RSV. Each of the ts mutants was highly attenuated in the lower respiratory tract, but still retained the capacity to induce significant rhinorrhoea. Each of the three ts mutants underwent partial reversion to a non-ts (ts+) phenotype during replication in a minority of the chimpanzees. The ts+ virus present in the upper respiratory tract of the chimpanzees did not spread to the lower respiratory tract and represented only a minority fraction of the virus present in the nasopharyngeal swab specimens. The ts mutants were highly immunogenic and provided resistance that effectively restricted RSV replication following virus challenge. In contrast, the vaccinia-RSV recombinants were less immunogenic. They protected the lungs of two of four chimpanzees challenged with RSV, but failed to protect the upper respiratory tract. The chimpanzee can serve as a model for the rapid evaluation of further attenuated live RSV vaccines.
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PMID:A comparison in chimpanzees of the immunogenicity and efficacy of live attenuated respiratory syncytial virus (RSV) temperature-sensitive mutant vaccines and vaccinia virus recombinants that express the surface glycoproteins of RSV. 831 Jul 60

Elderly humans have increased morbidity and mortality after viral influenza despite immunization. A mouse model of influenza infection was used to search for a more effective way to induce immunity to influenza. Old (18 months) BALB/c mice were more susceptible to influenza pneumonia than young (2 months) BALB/c mice after intranasal challenge with PR/8 influenza virus despite prior immunization with influenza virus. The decreased resistance to live influenza virus challenge was associated with an impaired generation of anti-hemagglutinin antibody and cytotoxic T lymphocytes in old mice. In contrast, immunization of old mice with a recombinant vaccinia virus expressing the PR/8 influenza hemagglutinin gene protected them from intranasal challenge with live influenza virus and generated high levels of anti-PR/8 influenza virus hemagglutinin antibody and PR/8-specific cytotoxic T cells. Recombinant vaccine overcame the age-associated immune defect that follows the administration of conventional viral vaccine.
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PMID:Recombinant vaccinia virus expressing the PR/8 influenza hemagglutinin gene overcomes the impaired immune response and increased susceptibility of old mice to influenza infection. 833 70


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