PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Retroviridae Infections”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1995

Genetic determinants of feline leukemia virus-induced multicentric lymphomas.

Three discrete forms of feline leukemia virus (FeLV)-associated lymphoma have been described clinically: (1) thymic, (2) alimentary, and (3) multicentric. The most common and best-characterized lymphomas are of T-cell origin, generally occurring in the thymus. These tumors typically contain mature T-cells, involve the activation of a distinctive set of proto-oncogenes, and contain FeLV proviruses whose long terminal repeat (LTR) sequences contain tandemly repeated enhancers. Previous studies of a small group of extrathymic, multicentric lymphomas implicated a different set of genetic determinants. The present study expands those observations by examining the lineage of origin, the involvement of proto-oncogenes, and the structure of LTR and env gene sequences in a set of 11 natural, extrathymic lymphomas of the multicentric type. A pattern of genetic events associated with FeLV-positive multicentric lymphomas emerges from this analysis that is clearly distinct from the pattern associated with thymic lymphomas. The tumors do not contain T-cells or B-cells, as evidenced by the germ line organization of TCR beta and IgH loci. Proto-oncogenes strongly implicated in T-cell lymphomagenesis are not involved in these tumors. Rather, a distinct set of proto-oncogenes may be involved. Most striking is the repeated occurrence of an FeLV isolate whose LTR and env gene bear unique sequence elements.

Amino Acid Sequence↗
PubMed1998

Inhibition of Friend virus replication by a compound that reacts with the nucleocapsid zinc finger: anti-retroviral effect demonstrated in vivo.

The zinc finger structure that is found in the nucleocapsid protein of nearly all retroviruses has been proposed as a target for antiviral therapy. Since compounds that chemically attack the cysteines of the finger have been shown to inactivate both human immunodeficiency virus type 1 (HIV-1) and murine leukemia virus (MuLV) in vitro, 14 of these compounds were tested in an MuLV-induced Friend disease model to assess their ability to inhibit retroviral replication in vivo. Of the 14 compounds tested, only Aldrithiol-2 clearly exhibited anti-retroviral activity as measured indirectly by the delay of Friend disease onset (P < 0.05). These results were confirmed by quantitative competitive polymerase chain reaction studies which monitored viral spread by measuring the level of viral DNA in the peripheral blood mononuclear cells of treated mice. Comparison of treated mice with untreated mice revealed that Aldrithiol-2 produced a greater than 2-log reduction in virus levels. These results functionally demonstrate that a zinc finger-attacking compound can inhibit viral replication in vivo. Since only 1 of the 14 compounds studied was effective, this study also shows the importance of in vivo testing of these types of antiviral compounds in an animal model. Given the strict conservation of the metal-coordinating cysteine structure within HIV-1 and MuLV zinc fingers, our results support the proposal that anti-retroviral drugs which target the nucleocapsid zinc finger may be clinically useful against HIV-1.

Animals↗
PubMed1999

Complete sequence of enzootic nasal tumor virus, a retrovirus associated with transmissible intranasal tumors of sheep.

The sequence of the complete genome of ovine enzootic nasal tumor virus, an exogenous retrovirus associated exclusively with contagious intranasal tumors of sheep, was determined. The genome is 7,434 nucleotides long and exhibits a genetic organization characteristic of type B and D oncoviruses. Enzootic nasal tumor virus is closely related to the Jaagsiekte sheep retrovirus and to sheep endogenous retroviruses.

Amino Acid Sequence↗
PubMed1994

Evaluation of a feline leukemia virus vaccine in a controlled natural transmission study.

Twenty-six 8-week-old specific-pathogen-free cats were vaccinated subcutaneously with 2 doses of a commercially available FeLV vaccine, and 26 age-matched specific-pathogen-free cats were similarly vaccinated with a placebo vaccine containing the same adjuvant as the FeLV vaccine. Cats then were randomly assigned to 2 groups of 26 cats (13 FeLV-vaccinated cats and 13 control cats), and each group was housed with 5 cats previously inoculated with FeLV. All cats were tested biweekly for the next 26 weeks for evidence of FeLV antigenemia. Five of the 26 control cats developed antigenemia. However, 4 of these cats were only transiently antigenemic (positive results for 3 consecutive biweekly samples) and only 1 was persistently antigenemic. None of the FeLV-vaccinated cats developed antigenemia. Preventable fraction was calculated to be 100%.

Animals↗
PubMed1988

Comparison of simian immunodeficiency virus and human immunodeficiency virus encephalitides in the immature host.

The simian immunodeficiency virus (SIV) is closely related to the human immunodeficiency virus (HIV) in genomic organization and morphology. More important, SIV and HIV are both primate lentiviruses that cause transmissible immunodeficiency and encephalitis, with an apparently increased virulence in the immature host. The neuropathological features in common between SIV encephalitis in juvenile macaque monkeys and HIV encephalitis in children include the invasion of brain with virus-laden macrophages, the formation of multinucleated (syncytial) giant cells, and white matter lesions and subtle white matter astrocytosis. Important differences include giant cell leptomeningitis and evidence of necrosis and karyorrhexis in brain macrophage infiltrates in SIV-infected monkeys. These changes probably represent a more acute inflammatory process. The importance of future studies to define pathogenetic features of SIV encephalitis, using molecularly characterized isolates with varying neurovirulence and host range, are emphasized.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Analysis of the determinants of neurotropism and neurotoxicity of HFV in transgenic mice.

The Bel-1 protein of human foamy virus (HFV) is a transactivator acting on the U3 region of the long terminal repeat and on an internal promoter (IP) immediately upstream of the bel genes. An HFV transgene called delta gpe, containing both promoters and all bel genes, is expressed in the central nervous system and induces neurodegeneration in mice. To dissect the role of individual promoters and bel genes on transgene expression and neurotoxicity we generated transgenic mice with a construct termed pL-bel1, which lacks the IP and the ancillary genes except bel-1. L-bel1 mice transcribed the HFV transgene in more tissues than delta gpe mice, suggesting that CNS specificity is dictated by cis-acting elements not present in the pLbel-1 construct. Unlike delta gpe mice, L-bel1 mice did not develop neurodegenerative changes and did not show induction of nitric oxide synthase expression, although both strains expressed Bel-1 in the brain. Therefore, Bel-1 expression is not sufficient for neurotoxicity. Our results suggest that Bet, a fusion protein between bel-1 and bel-2 which is highly expressed in delta gpe but not in L-bel1 mice, is a candidate for neurotoxicity.

Animals↗
PubMed2000

Neural stem cells as tools for understanding retroviral neuropathogenesis.

The discovery within the past decade that neural stem cells (NSCs) from the developing and adult mammalian brain can be propagated, cloned, and genetically manipulated ex vivo for ultimate transfer back into the CNS has opened the door to a novel means for modifying the CNS environment for experimental and therapeutic purposes. While a great deal of interest has been focused on the properties and promise of this new technology, especially in regard to cellular replacement and gene therapy, this minireview will focus on the recent use of NSCs to study the neuropathogenesis of the murine oncornaviruses. In brief, the use of this NSC-based approach has provided a means for selective reconstitution within the brain, of specific retroviral life cycle events, in order to consider their contribution to the induction of neurodegeneration. Furthermore, by virtue of their ability to disseminate virus within the brain, NSCs have provided a reliable means for assessing the true neurovirulence potential of murine oncornaviruses by directly circumventing a restriction to virus entry into the CNS. Importantly, these experiments have demonstrated that the neurovirulence of oncornaviruses requires late virus life cycle events occurring specifically within microglia, the resident macrophages of the brain. This initial application of NSC biology to the analysis of oncornavirus-CNS interactions may serve as an example for how other questions in viral neuropathogenesis might be addressed in the future.

Animals↗
PubMed2003

Non-primate foamy viruses.

Foamy viruses (PFVs), also called spumaviruses, are complex retroviruses inducing a characteristic cytopathic effect in cell culture, leading rapidly to cell lysis. These viruses have been isolated mostly in non-human primates, but three non primate PFVs were characterized, namely the bovine foamy virus, the feline foamy virus and more recently the equine foamy virus. In their hosts, PFVs seem to be apathogenic, mirroring an efficient control of virus replication in vivo. Comparing the biology of the different virus isolates will certainly help to unravel the biology of these retroviruses.

Amino Acid Sequence↗
PubMed1987

Sequence relationships of type D retroviruses which cause simian acquired immunodeficiency syndrome.

Simian acquired immunodeficiency syndrome (SAIDS) in macaque monkeys is caused by type D retroviruses; three independent virus isolates are identified as SRV-1 (SAIDS retrovirus-serotype 1), SRV-2, and MPMV (Mason-Pfizer monkey virus). Virions from these three isolates have serologically related core antigens, but distinct surface proteins. Also, SRV-2 is unique since it apparently induces retroperitoneal fibromatosis in addition to SAIDS. The complete DNA sequence of molecularly cloned SRV-2 is presented and compared to the sequences of SRV-1 and MPMV and to the sequences of other retroviruses and retroviral-related elements in the genomes of eucaryotic cells. SRV-1 and MPMV show fewer than 6% differences in predicted amino acid sequences encoding gag, prt, pol, and the C-terminal env domain; SRV-2 displays about 15-18% differences in these regions when aligned with SRV-1 or MPMV. Greater variation of predicted amino acid sequences is noted in the externally located N-terminal env domains; SRV-1 and MPMV have 83% homology whereas SRV-2 has 58% homology with either SRV-1 or MPMV. Nucleotide sequences of the LTRs of SRV-1 and MPMV are 88% homologous; SRV-2 shows 70% homology with the LTRs of SRV-1 and MPMV. Comparisons of the predicted pol region amino acid sequences of these simian type D retroviruses with the pol gene of a type B retrovirus, mouse mammary tumor virus (MMTV), reveal about 50% homology. A human endogenous element related to the pol region of MMTV shows about 25% homology of amino acids with the pol sequences of SRV-1 or SRV-2. The prt genes of the simian type D retroviruses are similar in size and predicted amino acid sequence with the prt genes of MMTV and the hamster intracisternal type A particle genome. The C-terminal env domains of the avian type C retrovirus reticuloendotheliosis virus (REV) and the type C baboon endogenous virus (BaEV) have 60 and 85% predicted amino acid homology, respectively, with the C-terminal env domains of SRV-1, SRV-2, and MPMV. Within the gag and pol genes of the simian type D retroviruses there are striking homologies with the rat IgE-binding protein gene. Sequence relatedness of these type D retroviruses with type A, type B, and type C retrovirus genomes and with cellular sequences supports the notion that recombinational events contribute to the genesis and variation of retroviruses.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1989

Feline immunodeficiency virus infection.

Feline immunodeficiency virus (FIV) (formerly feline T-lymphotropic lentivirus or FTLV) was first isolated from a group of cats in Petaluma, California in 1986. The virus is a typical lentivirus in gross and structural morphology. It replicates preferentially but not exclusively in feline T-lymphoblastoid cells, where it causes a characteristic cytopathic effect. The major structural proteins are 10, 17 (small gag), 28 (major core), 31 (endonuclease?), 41 (transmembrane?), 52 (core precursor polyprotein), 54/62 (reverse transcriptase?), and 110/130 (major envelope) kilodaltons in size. The various proteins are antigenically distinguishable from those of other lentiviruses, although serum from EIAV-infected horses will cross-react with some FIV antigens. Kittens experimentally infected with FIV manifest a transient (several days to 2 weeks) fever and neutropenia beginning 4 to 8 weeks after inoculation. This is associated with a generalized lymphadenopathy that persists for up to 9 months. Most cats recover from this initial phase of the disease and become lifelong carriers of the virus. Complete recovery does not occur to any extent in nature or in the laboratory setting. One experimentally infected cat died from a myeloproliferative disorder several months after infection. The terminal AIDS-like phase of the illness has been seen mainly in naturally infected cats. It appears a year or more following the initial infection in an unknown proportion of infected animals. FIV has been identified in cats from all parts of the world. It is most prevalent in high density populations of free roaming cats (feral and pet), and is very uncommon in closed purebred catteries. Male cats are twice as likely to become infected as females. Older male cats adopted as feral or stray animals are at the highest risk of infection, therefore. The infection rate among freely roaming cats rises throughout life, and reaches levels ranging from less than 1% to 12% or more depending on the area. Clinically affected cats tend to be 5 years or older at the time of hospitalization. Experimental and seroepidemiologic studies suggest that FIV is transmitted mainly by bites. Intimate, non-traumatic contact (mutual grooming, shared use of food, water and litter pans) is inefficient in transmitting the infection. In utero and venereal transmission could not be demonstrated in laboratory settings. There is no statistical linkage between FIV and feline leukemia virus (FeLV) infections in nature. The FeLV infection rate in FIV-infected animals is the same as it is for non-FIV-infected cats.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed2005

Resistance against Friend leukemia virus-induced leukemogenesis in DNA-dependent protein kinase (DNA-PK)-deficient scid mice associated with defective viral integration at the Spi-1 and Fli-1 site.

Retroviral DNA integration is mediated by the viral protein integrase. However, elements of the host DNA repair machinery such as the phosphatidylinositol 3-kinase (PI-3K)-related protein kinase family system would play a role in the integration of viral DNA into the host DNA. Here, we show that a host PI-3K-related protein kinase, DNA-dependent protein kinase (DNA-PK), plays a role in the specific integration of retroviral DNA and induction of retroviral diseases in vivo. DNA-PK-deficient scid mice inoculated with Friend leukemia virus (FLV) exhibited a random integration into their genomic DNA and expressed the viral envelope protein gp70. However, the specific integration of FLV at Spi-1 or Fli-1 sites did not occur in association with the significant resistance of scid mice to FLV-induced leukemogenesis. In contrast, the knockout of another member of the PI-3K-related protein kinase family, encoded by the ataxia telangiectasia mutated (ATM) gene, resulted in mice as sensitive to FLV-induced leukemogenesis as the wild type mice. FLV was specifically integrated into the DNA at Spi-1 and Fli-1 sites with significant expression of these transcription factors. These findings indicated that DNA-PK would be essential for controlling the in vivo integration of FLV at specific sites as well as the susceptibility to FLV-induced leukemogenesis.

Animals↗
PubMed2005

Antiviral reactivities of gammadelta T cells.

The complex antiviral immune mechanisms involve both adaptive and innate reactions mediated by gammadelta T lymphocytes, whose unique immunosurveillance contributions are analyzed here in different clinical and experimental settings. It is beyond any doubt that the fast, potent, cytotoxic as well as non-cytolytic antiviral activities of gammadelta T cells are critical in protecting the host against diverse viral pathogens.

Animals↗
PubMed2003

Detection of viral infection in the respiratory tract of virus antibody free mice: advantages of high-resolution imaging for respiratory toxicology.

Using a highly sensitive membrane permeability assay, a viral infection was discovered in the lungs of virus antibody free (VAF) Swiss-Webster mice purchased for respiratory toxicology studies. The assay is based on the uptake of a charged fluorescent compound by cells lacking an intact plasma membrane. Lungs from 74% of the untreated animals from a single vendor tested positive for injury in this assay. High-resolution histopathologic analysis of 1-microm epoxy resin sections from affected animals identified increased peribronchiolar lymphocytic infiltration and markers of epithelial cell injury. Viral particles were directly observed to be budding from the membranes of infiltrating lymphocytic cells by transmission electron microscopy. Standard histological analysis of paraffin-embedded tissues from lungs of the same mice failed to detect obvious pathology. Serological analyses failed to detect the presence of a virus in the affected mice. Therefore, we conclude that (1) a pathogenic condition was present in the respiratory systems of mice judged pathogen free by standard methodologies, (2) the observed condition produced a pattern of injury comparable to those caused by pulmonary toxicants, (3) high-resolution histopathology and advanced imaging techniques can increase the potential for detection of pathological conditions, and (4) apparently healthy animals can have unrecognized infections with the potential for confounding respiratory toxicology studies.

Animals↗