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PubMed1975

Concurrent and consecutive infection and immunisation with yellow fever and UGMP-359 viruses.

Concurrent and consecutive infection and immunisation with yellow fever virus and UGMP-359 virus was investigated in mice, using identical doses of both viruses. In double infection it was shown that both viruses could multiply independently of one another, when both were inoculated simultaneously by the intracerebral route. On the other hand, there was mutual exclusion between them when the inoculation of one antedated the other, by the same intracerebral route. Both viruses multiplied to similar titres, in single infection, in the target organ (brain). By the intraperitoneal route, the outcome was influenced byhe relative sensitivity of this route of inoculation to support and sustain the replication of either virus. Thus, because yellow fever virus replicated more than UGMP-359 after intraperitoneal inoculation, the latter is always excluded, even when the inoculation ofUGMP-359 preceded that of yellow fever. In the double immunization studies it was shown that comparative specific antibody titres to both viruses were obtained either when both viruses, as immunogens, were given simultaneously, or when the inoculation of one was alternated, at weekly intervals, with the other.

Animals↗
PubMed1976

Genetic exclusion and stable complementation of Sindbis virus.

In an effort to enhance genetic interactions by eliminating spatial or physical barriers between variants of Sindbis virus MgCl2 was used to aggregate infecting viral particles. Mixing viral samples in a 1:1 ratio with 0.5 M MgCl2 produced maximal reduction in plaque forming units (PFU) with minimal cell damage due to MgCl2. Aggregate size was determined to be about 7 PFU. Samples taken at 3,5 and 10 hours after infection with mixed aggregates composed of large and small plaque forming virus indicated that only one type of genome was represented among the progeny particles. In addition, aggregation enhanced complementation and the progeny were stable after several cycles of sonication and passage.

Culture Techniques↗
PubMed1988

Avian adeno-associated parvovirus and Marek's disease virus: studies of viral interactions in chicken embryo fibroblasts. Brief report.

Using growth kinetics we demonstrate two effects based on interactions between the chicken herpesvirus, Marek's disease virus (MDV), and the dependovirus, avian adeno-associated virus (AAAV), in coinfected chicken embryo fibroblasts (CEF): (i) MDV provides helper activity for an efficient multiplication of AAAV; (ii) a high multiplicity of coinfecting AAAV inhibits completely the growth of MDV as well as AAAV.

Animals↗
PubMed1976

The growth of respiratory syncytial virus in organ cultures of bovine foetal trachea.

Respiratory syncytial (RS) virus grown in organ cultures of bovine foetal trachea at 37 degrees C and pH 7.2 reached maximum titres of up to 1 X 10(5) PFU/ml between 11 and 21 days after inoculation. Virus yield was increased three fold by incubation at 33 degrees C, but depressed by the addition of RS virus antiserum, with or without bovine complement, or by the addition of alveolar macrophages. Variation in pH or the concentration of foetal calf serum and magnesium chloride did not affect the virus yield. Virus growth did not affect ciliary activity of the cultures. Histological changes involved slight flattening of the epithelium and the appearance of phloxinophilic inclusion bodies. Fluorescent antibody staining showed more virus antigen in the peri-tracheal connective tissue than in the ciliated epithelium. The presence of non-cytopathic mucosal disease (MD) virus in RS virus infected organ cultures slightly depressed RS virus growth but did not influence ciliary activity. These in vitro experiments suggest that the tracheal epithelium may not be an important target in the pathogenesis of RS virus infection in vivo.

Animals↗
PubMed1996

Isolation of a human rotavirus containing a bovine rotavirus VP4 gene that suppresses replication of other rotaviruses in coinfected cells.

Bovine-human reassortant strains containing ten human rotavirus gene segments and segment 4, encoding VP4, of a bovine rotavirus were isolated from the stool of an infected Bangladeshi infant during cell culture adaptation. Two plaque purified variants of this reassortant, one making very large (429-L4) and the other tiny (429-S4) plaques, were further analyzed. The electropherotypes of these variants were identical except for slight mobility differences in segment 4. The predicted sequence of amino acids (aa) 16-280 in VP4 proteins revealed four differences between variants even in this limited region, so no single difference could be linked to plaque size. The small plaque variant S4 was phenotypically unstable and mutated to a large plaque-former within a single cell culture passage. The predicted sequence of aa 16-280 of a large plaque variant derived from S4 revealed six changes, only one of which was common to that of the L4 strain, thus suggesting that multiple amino acid changes in VP4 may affect plaque size. Although the large plaque variant L4 grew faster and was released from cells more rapidly than S4, its replication and that of other rotaviruses tested (i.e. RRV, NCDV and Wa) was suppressed by S4 in coinfected cells. Using an RRV x S4 reassortant containing only RRV segment 4, it was established that suppression was linked to the S4 VP4 protein. This suppression could not be associated with inhibition of viral adsorption and, therefore, appeared to occur following internalization. Thus, a new property of the rotavirus VP4 protein has been identified in a bovine-human rotavirus reas-sortant.

Amino Acid Sequence↗
PubMed1976

Persistent infection of tissue culture cells by RNA viruses.

In this paper, the characteristics of cultured cells persistently infected with RNA viruses, other than leuko viruses are described. The roles that the host cell, interferon, virus mutants and defective interfering particles may play in the establishment and maintenance of persistent infection are discussed. It is proposed that the interaction of viruses with certain types of host cells can lead to persistent infection. The differences in virus-host interactions may be attributable to differences in membrane properties of various cells. Defective interfering particles may play a role in the establishment of persistent infections in cells which normally undergo lytic virus development. Mutant types of virus appear to be prominent in the virus released from persistently infected cells, but the role that various mutants play in the maintenance of persistent infections remains unclear.

Antibodies, Viral↗
PubMed1990

Arachidonic acid regulates the binding of human interferon in human skin fibroblasts.

The induction of the antiviral state in human fibroblasts by human interferon is inhibited by arachidonic acid, its analogues 5,8,11,14-eicosatetraynoic and 5,8,11-eicosatriynoic acids, as well as by sodium arachidonate. The fatty acids myristic or oleic acid and sodium palmitate do not inhibit the antiviral action of interferon. Experiments were conducted to investigate the mechanism by which arachidonic acid could inhibit the action of interferon. No correlation between cellular lipoxygenase activities and the inhibition of antiviral action of interferon was observed in the fatty acid treated cells. Likewise, the cyclooxygenase inhibitors indomethacin and oxyphenylbutazone do not inhibit the interferon-induced antiviral state. Taken together, the inhibition of interferon action by arachidonates is unlikely to be mediated by cyclooxygenase or lipoxygenase-generated intermediates, even though arachidonates are known to affect the activity of these enzymes in vitro. Measurement of interferon receptors in the fatty acid treated cells showed that arachidonic acid, sodium arachidonate and its analogues decreased the number of human type I interferon receptors available for binding, and inhibited the transcription of the interferon-induced 6-16 gene and the induction of cellular (2'-5')-oligoadenylate synthetase, suggesting the mechanism of inhibition is mediated at the level of the interferon receptor. The significance of the finding that arachidonic acid, a common fatty acid of cells and serum, can affect the antiviral action of interferon is discussed.

2',5'-Oligoadenylate Synthetase↗
PubMed1990

Development of the interferon system. I. In chicken cells development in ovo continues on time in vitro.

When confluent monolayers of cells derived from chicken embryos of different gestational age were cultured for several days without a medium change, a condition termed in vitro aging, the cells' developed an increased capacity to express the interferon (IFN) system. The capacity to both produce IFN and to respond to its antiviral action were enhanced up to 1000- and 100-fold, respectively. Remarkably, the programmed development of the IFN system in these cells seemed to continue virtually uninterrupted after monodispersion of the cells and seeding at high cell density. Cells prepared from young embryos required more time to develop the IFN system than cells from older embryos with the yield of IFN, and sensitivity to its action, related directly to the total in ovo and in vitro age of the cells in culture. For example, essentially the same yields of IFN were obtained from cell cultures made from 5-d-old embryos "aged" for 10 d in vitro, as were obtained from 10-d-old embryos whose cells were aged in vitro for 5 d. In contrast, inducibility of 2'-5' oligoadenylate synthetase by IFN and the induction of heat shock genes by elevated temperature are not enhanced with in vitro aging. The programmed development of the IFN system that starts in ovo seems to continue on schedule in vitro, making the development of the IFN system in chick embryo cells appear as a time-dependent process.

2',5'-Oligoadenylate Synthetase↗
PubMed1999

A conservative triple antioxidant approach to the treatment of hepatitis C. Combination of alpha lipoic acid (thioctic acid), silymarin, and selenium: three case histories.

BACKGROUND: There has been an increase in the number of adults seeking liver transplantation for hepatitis C in the last few years and the count is going up rapidly. There is no reliable and effective therapy for chronic hepatitis C since interferon and antivirals work no more than 30% of the time, and liver transplant surgery is uncertain and tentative over the long run. This is because, ultimately, residual hepatitis C viremia infects the new liver. Furthermore, liver transplantation can be painful, disabling and extremely costly. TREATMENT PROGRAM: The author describes a low cost and efficacious treatment program in 3 patients with cirrhosis, portal hypertension and esophageal varices secondary to chronic hepatitis C infection. This effective and conservative regimen combines 3 potent antioxidants (alpha-lipoic acid [thioctic acid], silymarin, and selenium) that possess antiviral, free radical quenching and immune boosting qualities. CONCLUSION: There are no remarkably effective treatments for chronic hepatitis C in general use. Interferon and antivirals have less than a 30% response rate and because of the residual viremia, a newly transplanted liver usually becomes infected again. The triple antioxidant combination of alpha-lipoic acid, silymarin and selenium was chosen for a conservative treatment of hepatitis C because these substances protect the liver from free radical damage, increase the levels of other fundamental antioxidants, and interfere with viral proliferation. The 3 patients presented in this paper followed the triple antioxidant program and recovered quickly and their laboratory values remarkably improved. Furthermore, liver transplantation was avoided and the patients are back at work, carrying out their normal activities, and feeling healthy. The author offers a more conservative approach to the treatment of hepatitis C, that is exceedingly less expensive. One year of the triple antioxidant therapy described in this paper costs less than $2,000, as compared to mor than $300,000 a year for liver transplant surgery. It appears reasonable, that prior to liver transplant surgery evaluation, or during the transplant evaluation process, the conservative triple antioxidant treatment approach should be considered. If these is a significant betterment in the patient's condition, liver transplant surgery may be avoided.

Adult↗
PubMed2003

The envelope glycoprotein of human endogenous retrovirus HERV-W induces cellular resistance to spleen necrosis virus.

Human endogenous retrovirus type W (HERV-W) envelope glycoprotein (Env) has recently been reported to induce fusion in cells expressing the RD-114 and type D retrovirus receptor (RDR) and to serve as a functional retroviral envelope protein. In this report, another biological function for HERV-W was demonstrated by testing its ability to protect cells against retroviral infection. Spleen necrosis virus (SNV), a gammaretrovirus was chosen for testing resistance because it uses RDR to enter cells. An HERV-W Env expression plasmid was transfected into canine osteosarcoma cells (D-17), which are permissive for SNV infection. Cell fusion assays were performed to demonstrate biological function of HERV-W Env in D-17 cells. The presence of HERV-W env sequences was confirmed in stably transfected cell clones by using polymerase chain reaction. Viral infectivity assays were performed with SNV and amphotropic Murine leukemia virus (MLV-A) pseudotyped vector viruses to measure titers in D-17 cells expressing HERV-W Env and in negative control cells. The HERV-W Env caused fusion of D-17 cells in culture and greatly reduced infection by SNV vector virus. A 1000- to 10,000-fold decrease in SNV infectivity was observed for D-17 cells expressing HERV-W Env as compared to D-17 cells that were not expressing HERV-W Env. In contrast, infection by MLV-A pseudotyped vector virus was not significantly reduced. Thus, HERV-W Env confers host cell resistance to infection by SNV. This is the first report of a human endogenous retrovirus gene product blocking infection by any exogenous retrovirus.

Animals↗